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Medical Records

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0% found this document useful (0 votes)
250 views

Medical Records

Uploaded by

sgekara cyber
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PDF, TXT or read online on Scribd
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TOPIC: MEDICAL RECORDS

MEDICAL RECORDS
INTRODUCTION

 The terms medical r ecor d and health r ecor d are used somewhat interchangeably
to describe the systematic documentation of patient's medical history and care in
the hospital
 Doctors, nurses and other health care professionals write up medical/health
records so that previous medical information is available when the patient returns
to the health care facility. This is vital for their continuing care. The
medical/health record must therefore be available.
 This is the job of the medical record worker. They keep record of all the patients
who are in or have been in the hospital. They also ensure forms are available for
new patients.
 The medical record/ health record contains the patient’s medical history, past and
present illness, history of the illness, progress notes, diagnoses, x­rays, therapies
and treatments by a particular physician, nurse, dentist, nutritionist etc. They are
filled out on the first visit of the patient and then updated as necessary
 They also include the “notes” that the patient moves with to specialists, labs,
pharmacies etc.

Types of medical r ecor ds based on the type of stor age

1. Paper­based medical records


2. Electronic medical records/ Computer­based medical records
3. Hybrid record (where health care record exist in both paper and computer records)

In Kenya many health care facilities use hybrid medical records (where health care record
exist in both paper and computer records. It is not fully electronical as the patient’s
information cannot be accessed in all the hospital in Kenya, a patient has to carry his
medical report from one hospital to another hospital e.g. when going for a referral, for
that referral hospital to see the progress of his treatment.

Most developed countries use electronic medical records (a patient can move from one
hospital to another and find all his medical information in that hospital. He does not need
to carry e.g. any x­ray report, a card showing his medical history, medications, or referral
note. The doctor in the new hospital will be able to log in and see the patients past
medical history, vital signs, progress notes, diagnoses, medications, immunization dates,
allergies, lab data and imaging reports. Electronic medical records is the digital version of

pg. 1
the patient’s chart/information.

Paper medical records is where paper is used to record the patients information and files
are used for each and every patient in the ward

Advantages of electr onic medical r ecor ds

 Better data tracking over time­it is fast and accurate


 Patient information is clearer, no more illegible scribbles
 Improved information access/delivery makes prescribing medication and
therapies safer and more reliable­ensures that the inform, results are not
duplicated nor tampered with
 Better health care as the information walks with patient to specialists, nursing
home e.tc.
 You can talk in cyberspace with your patient
 Patient support­allows you to engage your patients by allowing them to receive
educational materials and allows the patient to engage you
 More than one person can use the record at a time.
 Information can be accessed in a variety of physical locations.
 Records can often be accessed from another city or state.
 Complete patient information even in emergency situations.

Disadvantages

 They are more expensive to implement initially as the providers must invest in the
proper hardware, software, training and support
 Unless properly built, the system may malfunction and destroy all the information

Disadvantages of Paper ­Based Medical Recor ds

 Only one person can use the record at a time, unless multiple people are
crowding around the same record.
 Items can be easily lost or misfiled or can slip out of the record if not securely
fastened.
 The record itself can be misplaced or be in a different area of the facility when
needed
 The patient’s information cannot be accessed in emergency situations.

Types of medical r ecor ds based on the or ganization/r ecor ding of the Medical
Recor d

1. Source­oriented medical records


2. Problem­ oriented medical records

pg. 2
Sour ce or iented medical r ecor ds (SOMR).

 It is a method of recording the medical forms in which each health care team( a
doctor, a nurse, a pharmacist, a nutritionist, lab technologist, physiotherapist etc.)
has his/her separate form where he records his/her daily assessment, progress
notes and treatment of the patient. The forms are then filed together and kept for
future reference i.e. they do not feel the same forms
 Separate sections are established for laboratory reports, x­ray films, radiology
reports and so on
 It is a traditional method of recording
For matting

 Progress notes are always written in paragraph form


Advantages

 It allows more room for use by more health care professionals including the
nutritionist in the health care
 Each department can easily find and chart pertinent data
 It is advantageous for filling a report from respective department in an orderly
fashion. It also saves time when filling these reports

Disadvantages
Fragmented­making it hard to track patients problems chronologically when one wants to
follow up on the treatment process of the patient

Pr oblem or iented medical r ecor ds (POMR)

 Organized around a patients problems rather than around sources of information


i.e. all the care team (a doctor, a nurse, a pharmacist, a nutritionist, lab
technologist, physiotherapist etc.) write their daily assessments or progress notes
and treatment of the patient on the same form (there is no separate forms for each
health care team.
 A number is a signed to each problem
 Most health care facilities currently use this format
For matting
Progress notes/care plan for the treatment of the patients is written by the physician in a
standardized format known as the “SOAP for mat”(S=subjective­chief complainant i.e.
the information on present illness, how he fills, and other symptoms are recorded;
O=objective­information on physical examination, lab tests, x­ray report and any other
reports from the health care team is recorded; A=assessment­diagnosis(interpretation of
the problem is done and recorded); P=plan­treatment or information on how to manage

pg. 3
the problem is recorded. e.g in planning for nutritional care, goals and objectives must be
established )
Advantages of pr oblem or iented medical r ecor ds (POMR)

 Entire health care team works together in identifying a master list of patient
problems and contributes collaboratively to the plan of care
Major par ts of the POMR

 Defined database
 Problem list
 Care plan/ treatment plan
 Progress notes
Example of POMR

Components/sections of the medical r epor t

 Patient infor mation for m/ Per sonal identification/Demogr aphics. It is filled


out on the first visit of the patient and it is then updated as necessary. It provides
data that relates to the patient e.g. name of the patient, gender, date of birth,

pg. 4
marital status, date of birth, place of birth, patient’s permanent address, and
medical record number;
 Medical histor y (Hx)­Document describing past and current history of all medial
conditions experienced by the patient e.g. diagnoses, medical care, family history,
surgical history and treatments. It tells the medical personnel a great deal about
your symptoms
 Tr eatment ­physical examination, assessment, plan and treatment. It is written by
the health care professionals
 Clinical data on the patient whether admitted to the hospital or treated as an
outpatient or an emergency patient.

 Consultation r epor ts. Documentation given by specialists whom the physician


has asked to evaluate the patient
 Labor ator y r epor ts. Provides the results of all diagnostic and laboratory tests
performed on the patient
 Consent for m. Signed document or legal guardian giving permission for
treatment e.g. to perform surgery. It also includes a signed consent for treatment
by appointed doctors and authorization for the release of information; Consent for
treatment is often on the back of the Front Sheet and must be signed by the patient
at the time of admission. There are two parts to this form. The first half of the
form is a general consent for treatment and the bottom half is consent to release
information to authorized persons;
 Dischar ge summer y. Outline summary of the patients care, including date of
admission, diagnosis, treatment, follow ­ups plans and date of discharge

The main uses of the medical r ecor ds/Impor tance of medical r ecor ds

 To document the course of the patient's illness and treatment;


 To track the patient’s medical history and identify problems or patterns that may
help determine the course of health care
 To communicate between attending doctors and other health care professionals
providing care to the patient; for communication with external health care
providers, and statutory and regulatory bodies
 For the continuing care of the patient: It allows other health care providers to
access quickly and understand the patient’s past and current health status.
 To enable physicians (and other health care providers) to provide quality health
care to their patients; facilitating patient safety improvements
 For research ((subject to ethics committee approval, as required)) of specific
diseases and treatment;

pg. 5
 Investigation of complaints/ Evidence of care: The record may become an
important piece of evidence in protecting the legal interests of the patient / client,
health care personnel or other personnel.
 Medical records are also legal documents and may provide significant evidence in
regulatory, civil, criminal, or administrative matters when the patient care
provided by a physician is questioned.
 The collection of health statistics
 Financial reimbursement(compensation paid to somebody for damages or losses
money already spent

Some Impor tant Points about For ms in the Medical Recor d

 Forms should all be the same size, usually A4.


 The patient's name and medical record number, and the name of the form should
be in the same place on EVERY form.
 Only official forms approved by the administration or Medical Record Committee
(if there is one) should be included in the medical record.

The following is a sample medical record form. Sections A, B, C, D and E of the sample
form (see below) remain the same on all forms. Section F is different for every form, as it
is where the content of each form is written

B Top margin 1 cm

A C Name & logo of hospital Patient D Medical Record Number. U


Names Ward:
Nam
Other patient details e of
MAR
GIN F form

Sections A, B, C, D and E remain the same for all forms. 2 cm

Content of each different form recorded in this section.

2cm

pg. 6
i. Clip or Fastener

Forms should be held in the medical record either by a clip or fastener. Staples should
NOT be used as they tend to rust and additional forms cannot be easily added.

It is best to use plastic rather than metal clips. Metal clips can cut fingers or rust.

ii. Medical Recor d Folder

All medical record forms should be kept in a medical record folder. This should be a
manila folder and, if possible, stronger cardboard folders should be purchased. Patients
may obtain copies upon request
Sample medical r ecor d folder :

Number tab

12­34­56

MR Number

Patient’s full name

Year of last attendance

2004

2005

2006

Etc.

0 0

Spine

↑ 0­­­Clip hole­­­
0

pg. 7
The following should be written on the medical record folder:

 patient's name;
 patient's medical record number; and
 Year of last attendance.

Remember: MEDICAL INFORMATION SHOULD NOT BE


RECORDED ON THE FOLDER.

Pr ivacy and confidentiality

All information in a patient / client’s health care record is confidential and subject to
prevailing privacy laws and policies. Health care records contain health information
which is protected under legislation.

Secur ity and Stor age

Medical records must be stored in a safe and secure environment to ensure physical and
logical integrity and confidentiality. Health care providers must develop records
management protocols to regulate who may gain access to records and what they may do
according to their role, responsibilities, and the authority they have.

TOPIC: DIET MODIFICATION

M ODIFIED DIETS
MORDIFICATION OF DIETS
Introduction: Modified diets are diets that have been qualitatively or quantitatively
altered as per patient’s special needs and in line with general principals of meal planning.
i.e. normal diet may be modified and become a specific therapeutic diet

pg. 8
Factor s that may deter mine dietar y modification
a. Disease symptoms
b. Severity of the symptom or disease (Condition of the patient)
c. Nutritional status of the patient
d. Metabolic changes involved
e. Physiological state
THERAPEUTIC MODIFICATION OF NORMAL DIET
Modification can be done in the following ways

 Modification in consistency (to provide change in consistency) e.g. fluid and soft
diets
 Modification in fibre content e.g. low fibre or high fibre

 Modification in energy e.g. high (increase) or low (decrease) calorie diet

 Modification in the content of one or more nutrients

 Modification in flavor (foods bland in flavor)

 Modification by including or excluding specific foods

 Modify the intervals of feeding e.g. frequent feeding

 Modify the mode of feeding e.g. Parenteral feeding and enteral feeding

1. MODIFICATION IN CONSISTENCY
LIQUID DIETS
Liquid diets are commonly ordered for patients with conditions requiring nourishment
that is easily digested and consumed or that has minimal residue.
The two varieties of oral liquid diets are:
f. Clear liquid diet
g. Full liquid diet

C LEAR L IQUID DIET


Pur pose
This is a diet modified to provide oral fluids to prevent dehydration, provide small
amount of electrolytes, relieve thirst and provide a small amount of energy in a form that
requires minimal digestion and stimulation of the gastrointestinal tract.

This diet is served at frequent intervals to supply the tissue with fluid and relieve thirst.

pg. 9
It is an inadequate diet composed chiefly of water and carbohydrates; therefore it should
be used for a very short time (It is indicated for short term use ­24hrs to 48hrs).
Nutritionally depleted patients should receive additional nutritional support through use
of nutritionally complete minimal residue supplements or parenteral nutrition.

NB: Additional modifications may be necessar y when used in some clinical


conditions such as car diac disease or pr ior to some tests. Indication and
char acter istics for clear liquid diet

Diet Indications Char acter istics of the diet


 E.g. Black tea, broth,  Used in Pre­ and  Composed of water and
apple juice, coffee, Post­operation, carbohydrates.
strained fruit/ vegetable  As a transition from  Clear liquid at room
juices, carbonated intravenous feeding temperature
beverages etc. to a full liquid diet,  Leaves minimal amount
 Foods to be avoided  When other liquids of residue in the
include milk and milk and solid foods are Gastrointestinal (GI)
products not tolerated, tract.
 During bowel  Provides approximately
preparation prior to 400­500kcals, 5­10g
diagnostic proteins, 100­120g CHO
visualization or and no fat.
surgery  Should be of low
 In the initial concentration
recovery phase after  Milk and milk drinks are
abdominal surgery omitted
 Following acute  Improve energy level by
vomiting or diarrhea addition of sugar
 Are nutritionally
inadequate in all nutrients

FULL LIQUID DIET

Pur pose

pg. 10
The full liquid diet is an adequate diet designed to provide nourishment in liquid form
and facilitate digestion and optimal utilization of nutrients in acutely ill patients who are
unable to chew or swallow certain foods. The diet is often used as a transition between
the clear liquid diet and a soft regular diet. Patients with hypercholesterolemia full liquid
diet to be modified to have low fat by substituting high saturated fats with low fat dairy
products and polyunsaturated fats and oils. Increasing protein and caloric value of full
liquid diet becomes necessary when the diet is used for a period extending over 2­3
weeks. Table 24 below provides indications for and characteristics of full liquid diet.
Indications and char acter istics of full liquid diet

Diet Indications Char acter istics of the diet


 Soft desserts  For post­operative patients  Foods should be liquid at
from milk and  For acutely ill patients or room temperature
eggs, those with esophageal/GIT  Free from condiments and
 Pureed and disorders and cannot spices
strained soups, tolerate solid foods  Provides between 1500­
ice creams, milk  Following surgery of the 2000kcal/day
or yoghurt, etc. face­neck area or dental or  Large percentage is milk
jaw wiring based foods; lactose
intolerant individuals need
special consideration.
 The diet may be
inadequate in
micronutrients and fiber

Thick Liquid Diet (Blended or Semisolid Diet)


This diet is moderately low in cellulose and connective tissue to facilitate easy digestion.
Tender foods are used to prepare the diet. Most raw fruits and vegetables, coarse breads,
cereals, tough meats and nuts are eliminated. Fried and highly seasoned foods are
omitted.
Pur pose of the diet
The blended liquid diet is designed to provide adequate calories, protein and fluid for the
patients who are unable to chew, swallow or digest solid foods. The diet prescription
should be individualized to meet medical condition and tolerance. Patients with wired
jaws may use a syringe, spoon, or straw to facilitate passage of liquid through openings in
the teeth, depending on the physician’s recommendation
Blended foods should be used immediately but can be refrigerated up to 48hrs or frozen
immediately after blending to prevent growth of harmful bacteria.

pg. 11
Indications and char acter istics of thick liquid diet

Diet Indications Char acter istics of the diet


 After oral surgery or plastic  Fluids and food blended to a liquid form
surgery of the face or neck  Viscosity ranges from the thickness of
area with chewing or fruit juice to that of cream soup
swallowing dysfunctions  All liquids can be used to blend foods.
 For acutely ill patients and However, nutrient dense liquids with
those with oral, esophageal similar or little flavor are preferable. Use
or stomach disorders who are of broth, gravy, vegetable juices, cream
unable to tolerate solid foods soups, cheese and tomato sauces, milk
due to stricture or anatomical and fruit juices is recommended
irregularities  Multivitamin and mineral
 Those progressing from full supplementation is recommended
liquid to a general diet.
 Patients who are too weak to
tolerate a general diet.
 Those whose dentition is too
poor to handle foods in a
general diet.
 ­Those for whom a light diet
has been indicated e.g. post
operative

SOFT OR LIGHT DIET


This is an adequate diet soft in consistency, easy to chew and is moderately low in
cellulose and connective tissue. This diet is designed to provide nutrients for patients
unable to physiologically tolerate a general diet in which mechanical ease in eating,
digestion or both are desired. The diet should be individualized based on the type of
illness or surgery and the patient’s appetite, chewing and swallowing ability and food
tolerance.
Indication and char acter istics of soft diet

Diet Indications Char acter istics of the diet


 Fruit juices or  Post operative patients  Moderately low in
cooked fruits,  Patients with mild gastro cellulose and
 Well­cooked intestinal problems connective tissues
cereals, strained if  Non­surgical patients  Tender foods
necessary; whose dentition is too  Fluids and solid foods
 Fresh spinach weak or whose dentition is may be lightly
 Amaranth inadequate to handle a seasoned
(Terere); general diet|(patients with  Food texture ranges
 Pumpkin leaves; few or no teeth) from smooth and
 Managu  For transition from thick creamy to moderately

pg. 12
 Strained peas; liquid to a general diet crispy
 Potatoes, baked,  Most raw fruits and
boiled, or mashed. vegetables, course
 Fats: butter, thin breads and cereals gas
cream. producing foods and
 Milk: plain, in tough meats are
scrambled egg, in eliminated
cream soups, in  Fried and highly
simple desserts. seasoned foods, strong
 Eggs: soft­cooked, smelling foods should
omelettes, custards. be omitted
Simple desserts;
custards, ice cream,
gelatine desserts,
 Cooked fruits or
cereal puddings
 Minced meat, soft
fish

2. MODIFICATION IN FIBER CONTENT


Fiber is the portion of carbohydrates not capable of being digested by enzymes in the
human digestive tract, thus contributing to increased fecal output. There are two types of
fiber; soluble and insoluble fiber. Diseases affecting digestive system generally require
modification in fiber content. This can be high or low fiber diet.

F IBER RESTRICTED (LOW RESIDUE ) DIET


This diet is composed of foods containing low amounts of fiber which leave relatively
little residue for formation of fecal matter. Residue is the dietary elements that are not
absorbed and the total post digestive luminal contents present following digestion. The
diet excludes certain raw fruits, raw vegetables, whole grains and nuts high in fiber and
meats high in connective tissue. The diet is modified to meet the clients caloric, protein,
fat as well as vitamins and minerals requirements.

Pur pose of the diet


The fiber (low residue) restricted diet is designed to prevent blockage of an inflamed
gastrointestinal tract and reduce the frequency and volume of fecal output while
prolonging intestinal transit time.

pg. 13
Indications and char acter istics for fiber r estr icted diet

Diet Indications Char acter istics of the diet


 Gastro­intestinal disorders colitis,  Low in complex
colostomy carbohydrates
 Inflammatory bowel disease, diarrhea,  Has refined cereals and
hemorrhoids, etc grains
 Acute phase of diverticulosis  Legumes, seeds and whole
 Ulcerative colitis in initial stage nuts should be omitted
 Partial intestinal obstruction
 Pre and post­operative periods of the large
bowels
 convalescents from surgery, trauma or
other illnesses before returning to the
regular diet
 post ­ perennial suturing

pg. 14
H IGH FIBER DIET
This diet contains large amounts of fiber that cannot be digested. Fiber increases the
frequency and volume of stools while decreasing transit time through the gastro­intestinal
tract. This promotes frequent bowel movement and results in softer stools. The
recommended fiber intake for women aged 50 years and below is 21­25g/day and for
men aged 50 years and below is 30­38g/day. Men over 50 years should consume at least
30g/day while women above 50 years should consume 21g/day.

Pur pose
The diet is designed to prevent constipation and slow development of hemorrhoids,
reduce colonic pressure and prevent segmentation. The diet also reduces serum
cholesterol levels by decreasing absorption of lipids, reduces transit time and can be used
to control­ glucose absorption for diabetic patients and overweight clients. Dietary fiber
reduces the risk of cancer of the colon and rectum.
Indications and char acter istics of high fiber diet

Diet Indications Char acter istics of the diet


 Gastro­intestinal disorders:  High in complex
 Diverticular disease: high carbohydrates
 Cardiovascular disease  Has less of refined cereals
(hypercholesterolemia):
 Cancer prevention:
 Diabetes mellitus:
 Weight reduction:

NB: Intake of excessive dietary fiber may bind and interfere with absorption of calcium,
copper, iron, magnesium, selenium and zinc. This results in their deficiency. Therefore,
excessive intake of dietary fiber is not recommended for children and malnourished
adults.
3. MODIFICATION IN ENERGY INTAKE

This may be high or low energy depending on the metabolic activity patterns and the
weight of a patient.

H IGH ENERGY DIET


High energy diet is recommended to provide an energy value above the total energy
requirement per day in order to provide for regeneration of glycogen stores and spare
protein for tissue regeneration. Energy dense foods are used to avoid complication of
bulky diet. For effective metabolism, an extra of 500kcal of the RDA is recommended
per day. If there is poor appetite small servings of highly reinforced foods should be
given. The diet may be modified in consistency and flavor according to specific needs.
Excessive amounts of low calorie foods, fried foods or others which may interfere with

pg. 15
appetite are avoided.

Indications and char acter istics of high ener gy diet

Diet Indications Char acter istics of the


diet
Energy dense foods  Hyperthyroidism  Increased kilocalorie
include butter, sugar,  wasting energy 35­
honey and ghee which  Typhoid 40kcal/kg/day in
are added to the normal  Malaria adults
diet to increase energy  HIV/AIDS
content  All cases of prolonged
degenerative illnesses

C ALORIE R ESTRICTED DIET


These diets are prescribed for weight reduction. The recommended kilocalorie level is
20­25kcal/kg/day. The diet should comprise of complex carbohydrates and should
provide 50­60% of the total calories. Fats should provide <30% of the total calorie.
Pur pose
To provide adequate nutrition, maintain desirable body weight, maintain normal glucose
and lipid levels and to prevent, delay and treat diabetic related complications.
Indications and char acter istics of calor ie r estr icted diets

Diet Indications Char acter istics of the diet


 Vegetables,  Overweight and  The diet should provide20­
 carbohydrates obesity 25kcal/kg Bodyweight/day
 Hypertension with  Complex carbohydrates
excess weight  High in dietary fiber
 Hyper lipidemia  Proteins should be within the DRI
 Diabetes mellitus with
excessive weight
 Gout
 Gall bladder diseases
preceding surgery

4. MODIFICATION IN THE CONTENT OF ONE OR MORE NUTRIENTS


There are four ways to modify the content of one or more nutrients as listed below:
 Moderate fat diet/fat restricted diet
 High protein, high calorie diet
 High or low protein diet
 Low sodium diet
 High carbohydrates

pg. 16
F AT RESTRICTED DIET
The diet is designed to restrict fat intake for patients who experience symptoms of
nutrient losses when high fat foods are eaten. A fat restricted diet limits the amount of fat
you can consume each day and may be prescribed conditions that make it difficult for the
body to digest fat. Provision of fat restricted diet will minimize the unpleasant side
effects of fat malabsorption such as diarrhea, gas and cramping.

Indications and char acter istics of fat r estr icted diet

Diet Indications Char acter istics of the diet


 Gall bladder  The diet provides overall fat between 25­
diseases 50g/kg/day
 Biliary tract and  This diet is tailored to provide <30% of total
lymphatic system calorie and < 10% saturated fat acids. Levels of
 Hepatic cirrhosis restriction are as follows:
(liver cirrhosis)  Mild restriction­25­30% of total calories
 Pancreatic  Moderate restriction­20­25% of total
insufficiency calories
 Malabsorption  Severe restriction­15­20% of total calories
syndromes  The base of the diet should be composed of
 Intestinal resections grains, vegetables and fruits
 Overweight and  Meat fish, poultry and eggs should be limited to
obesity 180g per day
 Cardiovascular
diseases (CVDs
 bloating, diarrhea,
steatorrhea

Adequacy
It is possible to meet nutrient requirements on this diet, but depending on how long you
follow it and how much fat you can digest a supplement may be recommended. Patients
with prolonged stearrhoea or diarrhea may develop vitamin or mineral deficiencies.
Vitamin A, D, E and K are fat soluble which means they need fats to be absorbed and this
requires advice from the nutritionist/dietitian or doctor.

H IGH PROTEIN­H IGH CALORIE DIET


This diet is tailored to provide higher amounts of calorie and protein than usual diet. It is
prescribed where tissue regeneration is required. Its purpose is to help heal wounds,
maintain or increase weight, promote growth, decrease respiratory complications, resist
or fight infections and support the immune system. For a high protein diet, adequate
energy from carbohydrates and fats must be supplied.

pg. 17
Pur pose
The diet is designed to maintain a positive nitrogen balance, promote normal osmotic
pressure, promote body tissue repair, prevent excessive muscle atrophy in chronic disease
states and build or repair worn out tissues of severely malnourished individuals. This diet
can also be used to meet increased energy and protein demands during illness, during
certain periods like pregnancy and lactation. Table 32 below shows indication for and
characteristics of the diet.
Indications and char acter istics of high pr otein­high calor ie diet

Diet Indications Char acter istics of the diet


 Febrile conditions  The diet must provide adequate
 Cancer protein carbohydrates ratio of (2:1).
 Wounds  The diet should provide i.e.35­
 Burns 40kcal/kg body weight/day 1.5­
 Tissue injuries and trauma 2.0g/kg body weight/day
 After surgery  Consist more of high biological value
 Acute and chronic fever e.g. TB, protein
Malaria and Typhoid.
 Certain physiological alteration
­ pregnancy and
lactation/infancy

pg. 18
L OW P ROTEIN DIET
A low protein diet is temporarily indicated/ prescribed to avoid breakdown of tissue
protein which can lead to undesirable levels of nitrogen constituents in the blood. It is
essential that the calorie intake from carbohydrates be sufficient to avoid excessive
breakdown of tissue protein. Low protein may range from (0.6g­0.8g/kg/day).
Indications and char acter istics of low pr otein diet

Diet Indications Char acter istics of the diet


 Hepatic coma  Low biological value protein can be
 Acute and chronic renal used during this time.
failure  The amount can be reduced to 20­
 Liver cirrhosis 35gms per day.
 Acute and chronic
glomerulonephritis

pg. 19
pg. 20
pg. 21
pg. 22
pg. 23
pg. 24 by Osonga
L OW SODIUM DIET
Sodium is a mineral that naturally occurs in some foods. However it can also added to food in
form of salt to help preserve them and add flavor. Limit sodium intake to less than 3000mg per
day. RDI should be limited to 2400mg
3000mg (130mEq) ­Eliminate or eat sparingly processed foods and beverages such as fast foods,
salad dressings, smoked and salted meats. Omit 2000mg (87mEq)­prepared foods high in sodium
do not allow salt in preparation of food or table.
1000 (45mEq) eliminate processed foods and prepared foods and beverages high in sodium.
Omit many frozen foods and fast foods. Limit milk and milk products to 16oz per day. Do not
allow any salt in food preparation or table use. This meal plan used in the inpatient setting for a
short term basis
500 (22mEq) omit processed or canned foods high in sodium. Omit vegetables containing high
amounts of natural sodium limit milk to 16 oz daily and meat to 5 oz daily and meat products.
Use low sodium bread and distilled water for cooking where available.
Allow up to ¼ tsp table salt in cooking or at the table
Pur pose
The purpose of a low sodium diet is to aid control of blood pressure (BP) in salt sensitive people
and to promote the loss of excessive fluids in edema and assist and manage hypertension. Table
34 below shows the indications for and characteristics of low sodium diet
Indications and char acter istics of low sodium diet

Diet Indications Char acter istics of the diet


 Unprocessed  Impaired liver  A diet low in processed foods and beverages
foods and functions  Diet should be low in canned foods,
beverages  Cardiovascular margarine, cheeses, and salad dressings.
 Low sodium diseases
bread  Severe cardiac
failure
 Acute and chronic
renal diseases

5. MODIFICATION IN FLAVOR (FOODS BLAND IN FLAVOR)

BLAND DIET
This is a diet modified to avoid irritation of any kind to the alimentary tract. Such diets are
chemically, mechanically and thermally modified. In bland diet, strong spices, stimulants and
strongly flavored vegetables and fruits that irritates should be avoided. The food should be served
at room temperature.
6. MODIFICATION BY INCLUDING OR EXCLUDING SPECIFIC FOODS

pg. 25 by Osonga
E XCLUSION OF C ERTAIN F OODS (ALLERGIES)
In allergic conditions certain specific foods to which the individual is extremely allergic should
be excluded from the diet. Some people are allergic to protein foods like milk, eggs, peanut, soya
and seafood e.g lactose free diet or gluten free diet in allergic conditions

Diet for r enal conditions


The purpose of diet for renal cases is to control protein, potassium, sodium and fluid levels in the
body.
It is used in acute and chronic renal failure and in hemodialysis.
Foods allowed include high­biological proteins such as meat, fowl, fish, and cheese
Vegetable such as cabbage, cucumber, and peas are lowest in potassium and are so advocated.
Potassium is usually limited to 500 mg/day
Fluid intake is restricted to the daily volume plus 500 ml, which represents insensible water loss.
Foods avoided include bread, macaroni, noodles, spaghetti, avocados, kidney beans, potato chips,
raw fruit, yams, soybeans, nuts, gingerbread, apricots, bananas, grapefruit, oranges, coca­cola

7. MODIFY THE INTERVALS OF FEEDING E.G FREQUENT FEEDING

I NCREASING F REQUENCY OF F EEDING


In some disease conditions patients may not be able to eat very large amounts of food at one
time. It may thus become essential to give smaller meals at frequent intervals as in the case of
fevers, diarrhea and ulcers. In such cases provide small but frequent meals at each interval.
8. MODIFY THE MODE OF FEEDING E.G. PARENTERAL FEEDING AND
ENTERAL FEEDING

TOPIC : DRUG – NUTRIENT INTERACTIONS


Definition of ter ms
a) Dr ug – A substance that is used as a medicine or narcotic.
b) Medicine – Something that treats, prevents or alleviates (provides relief from e.g. pain)
the symptom of a disease.
c) Nar cotic – Drug taken for pleasure, numbness or reduce pain and extensive use can lead
to addiction.
d) Dr ug abuse – Excessive use of a drug.
e) Absor ption ­ the process of movement of a drug from the site of administration into the
systemic circulation
f) Bioavailability ­ the degree to which a drug or other substance reaches the general
circulation and becomes available to the target organ or tissue
g) Dr ug­nutr ient inter action ­ the result of the action between a drug and a nutrient that
would not happen with the nutrient or the drug alone or it refers to changes to a drug
caused by a nutrient, or changes to a nutrient as a result of the drug

pg. 26 by Osonga
Functions of dr ugs
1. Prevents occurrence of a disease.
2. Treats a disease.
3. Alleviates or provides relief from pain.

Stages of how dr ugs pass into the body


1. The drug dissolves in the stomach if taken orally.
2. The drug is absorbed into the bloodstream and goes into the area that needs it.
3. The body reacts with the medicine.
4. The kidney or liver, or both get rid of the drug and this is called detoxification.

Effects of food on dr ugs /Impacts of food on effectiveness of dr ugs


Just like foods, drugs or medicines also have ingredients. Some foods may interact with
ingredients of drugs preventing the drug from working properly by; Delaying or speeding up its
absor ption into the body, Speeds up the absor ption into the blood., Also speeds up the r ate
of elimination in the body, thus, inter fer ing with the effectiveness of the dr ug e.g. Acidic
foods can decrease the power of antibiotics such as penicillin. Alcohol also interferes with the
absorption of some drugs.

Examples of effects of food on dr ugs


i) Drug Aspirin is absorbed more slowly when taken with food. Vitamin C can alter
urinary PH and limit the excretion of aspirin.
ii) Foods that stimulate secretion of digestive juices increases absorption of some drugs
e.g. Gr iseofulvin. (an antibiotic)
iii) Some foods e.g. Candy can change the acidity of the GIT thereby causing the slow
acting asthma medication to dissolve too quickly.
iv) Alcohol produces prolonged hypoglycemic effects when taken with insulin and oral
hypoglycemic agents.
v) Foods rich in dopamine e.g. (Cheese, chicken, liver, red wine, bread etc) cause
hypertensive crisis when taken alongside certain anti­depressants and thus can result
into accidents.
vi) Pyr idoxine in food, blocks the effects of levodopa used in the treatment of Parkinson
disease.

Effects of dr ugs on foods

pg. 27 by Osonga
Effect of dr ug on food intake:
1. Dr ugs that may stimulate one’s appetite;

Appetite may be stimulated by certain drugs resulting in an increase in nutrient intake due to
more food being taken/eaten. On the other hand, drugs may also cause a decrease in nutrient
intake thus drugs affect nutritional status.
The following drugs may stimulate appetite and result into weight gain;
a) Anti – histamines (antibiotics); treat cold or allergies.
b) Anti – anxiety dr ugs; Relieves tension.
c) Tr icycle anti – depr essants.
d) Insulin: Hypoglycemia that may lead to a coma or death can occur in a person with type 1
diabetes, if food is not taken immediately after an insulin injection. If excess food is consumed to
avoid or treat hypoglycemia, weight gain may occur.
d) Ster oids.
2. Dr ugs that may depr ess one’s appetite;
a) Alcohol

It can lead to loss of appetite; reduce food intake and malnutrition due to effects of alcoholism
such as gastritis (inflammation of the lining of the stomach), cirrhosis etc.
b) Amphetamines (depress appetite)

Effects of dr ugs on change of smell and taste


Change of smell or taste may stop people from eating or overeating and this affects their
nutritional status e.g. Antibiotics such as ampicillin, tetracycline etc., flagyl that may cause
metallic taste in the mouth. Anesthetics such as cocaine. Anti­coagulants, Anti­histamines,
Anti­hyper tensive agents, toothpaste ingr edients – sodium laurym sulphate.
Dr ugs that may lead to Gastr o Intestinal effects
Drugs such as non – steroidal anti­inflammatory drugs (NSAIDS) e.g. Aspir in, Ibupr ofen,
Antihistamines. {They cause stomach irritation. Sometimes the irritation is so severe and can
result into serious gastric bleeding.
Effect of dr ugs on nutr ient / food absor ption
A number of drugs can increase nutrient absorption thus benefit nutritional status while others
can decrease nutrient absorption in the body e.g.
Anti­acids can interfere with iron absorption in the body.
Alcohol abuse can result into malsabsorption of thiamine and folic acid causing anemia.

pg. 28 by Osonga
Some anti­acids bind phosphorus thus hindering its absorption.
Chemother apy dr ugs can damage mucosal cells thereby affecting nutrient absorption.
Neomycin may reduce lipase activity hence interfering with fat digestion.
Some drugs may also interfere or result into mineral depletion e.g.
Diur etics – taken to increase amount of water and aslant secreted from the body through
urine. Alcohol – may result to loss of potassium, magnesium and zinc.
Anti­acids – may result to phosphate deficiency, muscle weakness, convulsions and
calcification.
Other may also result into vitamin deficiency e.g.
Or al contr aceptives that may result into loss of foliate, riboflavin, vitamin C and B12.
Some cancer dr ugs may also result into foliate deficiency.
Effect of dr ugs on nutr ient excr etions e.g.
Diuretics may result into increased excretion of sodium and potassium.
Aspirin may result into increased excretion of plasma protein carrier hence affecting
excretion of the protein.

TOPIC: DIET PLANNING

THERAPEUTIC DIETS
Therapeutic diet is a diet prescribed to a person with a disease or a disorder such as
injury, infection, nutritional deficiency, liver cirrhosis, diabetes etc to hasten
recovery. A therapeutic diet controls the intake of certain foods or nutrients. It is
part of the treatment of a medical condition and are normally prescribed by a
physician and planned by a dietician. It is usually a modification of a regular diet.
It is modified or tailored to fit the nutrition needs of a particular person. .
Therapeutic diets can be grouped into two types namely:

a) Nor mal diet

b) Modified diet

NORMAL DIET

This is a regular diet either vegetarian or non­vegetarian well balanced and


adequate for nutrition. It is the foundation of all diets and is designed to provide
adequate nutrition for optimal nutrition and health status in persons who do not

pg. 29 by Osonga
require medical nutrition therapy. This diet is used when there is no required diet
modification or restrictions. Individual requirements for specific nutrients may vary
based on age, sex, height, weight, activity level and different physiological status.

A normal diet consists of three (3) main meals and may include various snacks
depending on individual needs. In planning the meal, there are six principles which
should be considered.

Pr inciples in meal planning

Adequacy

An adequate diet should provide enough energy and enough nutrients to meet the
needs of healthy people. For example, a person whose diet fails to provide enough
iron­rich foods may develop the symptoms of iron deficiency anemia.

Balance of foods and nutr ients in the diet

This means not over consuming any one food. The art of balance involves the use
of enough but not too much or too little of each type of the seven food groups for
example use some meat or meat alternatives for iron, use some milk or milk
products for calcium and save some space for other foods. The concept of balance
encompasses proportionality both between and among the groups.

Ener gy contr ol/density

This is the amount of energy in kilocalories in a food compared with its weight.
Examples of energy dense foods are nuts, cookies, and fried foods. Low energy
density foods include fruits, vegetables and any food that incorporates a lot of
water during cooking. They contribute to satiety without giving much calories.
This principle involves the management of food energy intake.

Nutr ient density

This means eating foods that deliver the most nutrients for the least energy.
Nutrient density is a relative ratio obtained by dividing a food's contribution to the
needs for a nutrient by its contribution to calorie needs. This is assessed by

pg. 30 by Osonga
comparing the nutrient content of a food with the amount of calories it provides. A
food is nutrient dense if it provides a large amount of nutrient for a relatively small
amount of calories.

Moder ation .

This mainly refers to portion size. In planning the diets, the goal should be to
moderate rather than eliminate intake of some foods. Foods rich in fats and sugar
should also be eaten in moderation they provide few nutrients with excess energy

Var iety

This means choosing a number of different foods within any given food group
rather than eating the same food daily. People should vary their choices of food
within each class of food from day to day. This makes meals more interesting,
helps to ensure a diet contains sufficient nutrients as different foods in the same
group contain different arrays of nutrients and gives one the advantage of added
bonus in fruits and vegetables as each contain different phytochemicals

NUTRITION GUIDE/TOOLS FOR A HEALTHY DIET

Knowledge of the nutritive content of a diet is meaningless unless it can be


compared to some standards. This lead to the development of nutrition tools which
serve as reference values for intakes of essential nutrients that will maintain health
in practically all healthy individuals. They assist individuals to meet their
nutritional needs, in prevention of under nutrition and over nutrition that results in
chronic disease.

Nutrition guides are of three types

1. Nutrition/Dietary standards

2. Dietary guidelines

3. Food guides

pg. 31 by Osonga
1. Nutr ition/Dietar y standar ds

Dietar y standar ds ar e guidelines that help us under stand how much of a


par ticular nutr ient is needed by a healthy human being. These are amounts of
essential nutrients considered sufficient to meet the physiological needs of
practically all healthy persons in a specified group and food sources of energy
needed by members of the group. These figures are derived from compilation of
experimental studies designed to determine the nutrient requirements of human
beings. Quantitatively, dietary standards are not requirements but rather are
estimates of reasonable levels of nutrients intake that should support normal
function in most healthy people. Dietary standards are obtained by:

 Survey of food intake of large numbers of apparently healthy individuals.


 Surveys that include both food intake and nutritional status.
 Controlled metabolic experiments (with limited number of individuals).
 Relevant studies on several species of animals.
Most developed countries have developed their own nutrient standards and these
differ slightly for individual nutrients partly because populations, environmental
conditions and available food supplies differ. The following are some of the
different dietary standards for some countries.

Recommended dietar y allowances (RDA).

These standards were developed for use in America. They represent quantities of
nutrients to meet known nutritional needs of practically all healthy people.
Allowances refer to the amount of nutrients to be actually consumed.

pg. 32 by Osonga
Recommended nutr ient intakes (RNI)

This is the Canadian own version of the RDA. It estimates nutrients needed to
support good health.

Safe intake of nutr ients (SIN)

These dietary standards were developed by the FOOD and Agriculture


Organization (FAO) and the World Health Organization (WHO) for
underdeveloped countries where supply of protein and other sources may be
limited

pg. 33 by Osonga
Recommended intakes of nutr ients (RIN)

These standards were developed for use in the United Kingdom (UK)

Uses of RDA

1. Evaluating the adequacy of the national food supply; setting goals for food
production

2. Setting standards for menu planning for publicly funded nutritional


programme e.g. school feeding programmes

3. Establishing nutrition policy for public assistance, nursing homes and


institutions

4. Interpreting the adequacy of diets in food consumption studies

5. Developing materials for nutrition education

6. Setting patterns for normal diets in hospital

7. Establishing labeling regulation

8. Setting guidelines for formulation of new products or the fortification of


specific foods

Limitations and misuse of RDA

1. They are complex for direct use by consumers.


2. They do not state ideal or optimal levels of intakes.
3. Allowances for some age categories e.g. adolescents and elderly are based
on limited data.
4. Data on food content of some nutrients especially the trace minerals are
limited.
5. They do not evaluate nutritional status.
6. They may not apply to sick people.

pg. 34 by Osonga
Nb...In 1990, nutrition experts recommended the framework of the RDAs be
expanded to address the following three emerging issues
a. The growing population of older people
b. The dangers of inappropriately high intakes of specific nutrients
c. The health benefits that might be achieved with higher intakes of certain
nutrients even though research was limited
­The expanded set of standards that evolved was given the working title of dietary
reference intakes (DRIs)

The Dietary Reference Intakes (DRIs)


DRIs reference values that are quantity estimates of nutrient intakes to be used for
planning and assessing diets for healthy people. The DRIs consist of four reference
intakes:

 Recommended Daily Allowances (RDA)­it serves as a reference for all


healthy

 Tolerable Upper Intake Level (UL)­It is the highest amount of nutrient that
can be safely consumed with no risk of toxicity/likely pose no danger to
most individuals in the group. It helps health care providers when advising
individuals on the use of dietary supplements

o Tolerable Lower Intake Level (LL)­It is the lowest amount of a


nutrient likely to pose no danger to most individuals in the group.

 Estimated Average Requirement (EAR)­ It is the nutrient intake estimated to


meet the requirement of half of the healthy individuals in a particular life
stage and gender group

 Adequate Intake (AI) ­ It is the level thought to meet or exceed the


requirements of almost all members of a life stage/gender group. It is used
when there is not a sufficient amount of research to develop RDA

2. Dietar y guidelines

pg. 35 by Osonga
They were 1st developed in 1980.It is developed from the RDIs and other research
evidence describing the types and amount of food to eat and the physical guidelines
for optimum health and growth e.g in weight management

3. Food Guide/Daily food guide


It helps individuals in day to day meal planning. They give a practical
interpretation of both dietary standards and dietary guidelines. Most food guides
group foods into a particular categories based on their nutrient content and
recommends a certain number of servings from each group. The mostly used food
guides are
a) Food pyramid
b).Food exchange list
c).Food composition table
d).Signal system(Healthy food choices)
e). Hand jive
f). Plate model
g). Glycemic index

a). Food composition tables


These are charts or tables showing the relative nutrient content found in a given
quantity of food. They were developed by FAO/WHO for developing countries.
The nutrient compositions of foods were obtained in laboratory after food analysis.
The food composition tables:

 Serve as a basis for comparing one food with another in terms of nutrient
content. For example, when you examine different foods for calcium
content, you will discover that that milk is the best source of calcium.
 Enable the calculation of the nutritive value of any diet and compare these
values with the standards.

pg. 36 by Osonga
 Are valuable in planning diets that meet requirements for specific needs such
as low sodium and high protein diets.
 They provide a ready reference to answer numerous questions concerning
the nutritive value of foods.

b). Food gr oup plan (Food pyr amid)


This is a diet planning tool that sort out food of similar origin and nutrient content
into groups and then specifies that people eat a certain number of servings from
each group every day. The number of servings to be consumed from group depends
on a person’s age and energy needs. In the six food group plan, foods are classified
into six groups in which the breath/base of the pyramid shows that grains deserve
most emphasis in the diet. The tip is smallest and so these foods­fat, oils and
sweets­ should be used sparingly, Figure 1.1. shows the six food group plan. In this
pyramid foods are classified into six groups.

Group 1: Breads, cereals, rice and pasta (6­11 servings)

Group 2: Vegetables (3­5 servings)

Group 3: Fruits (2­4 servings)

Group 4: Meat, poultry, fish, dry beans, eggs etc

Group 5: Milk, yoghurt, cheese (2­3 servings)

Group 6: Fats, oils and sweets (use sparingly).

pg. 37 by Osonga
c). Food exchange system
This refers to a system of classifying foods into numerous lists based on their
macro­nutrient composition and establishing serving sizes so that one serving of
each food on a list contains the same amount of carbohydrates, protein, fat, and
energy (kilocalories). Any food on the list can be exchanged or traded for any
other food on that same list without affecting a plan’s balance or total kilocalories.
It was originally developed for planning diabetic diets.

The system organizes food into seven exchange lists.


1. Starch/Bread
2. Milk
3. Meat
4. Fruits
5. Vegetables

pg. 38 by Osonga
6. Fats
7. Sugar

The six exchange list


All the foods listed together are approximately equal in proteins, carbohydrates and
fat value. Exchange lists provide additional help in achieving kilocalorie control
and moderation. Originally developed for people with diabetes, exchange systems
have proved so useful that they are now in general use for diet planning.
The number of kilocalories is calculated given the number of grams of
carbohydrates, fats and proteins in a food (1g of carbohydrate/ protein yields 4
kcal; 1g of fat yields 9 kcal). To apply the system successfully, users must become
familiar with portion sizes. The table below shows exchanges for carbohydrates,
proteins, fat and energy values that pertain to each list
List Por tion size per ser ving Amount CHO Pr otein Fats Kcal/se
(ml or g) r ving
Starch  1/3 cup arrowroots 30 g  15  2  ­ 80
 1/3 cup ugali  15  2 Trace
 1 slice bread  15  2
 1/3 cup cassava  15  2
 ½ cup cooked bananas  15  2
 ½ cup dried cooked beans  15  7
 ½ cup cooked rice  15  2
 ½ cup cooked pasta  15  2
 ½ cup sweet potatoes  15  2
 ½ cup porridge  15  2
 ½ cup Irish potatoes  15  2
 ½ chapatti  15  2

Milk  ½ cup fresh milk  250  12  8  Trace  90
 Nonfat  ¼ cup ice cream ml  12  8  5  120
 Low 75 ml or one scoop  250  12  8  8  150
fat  1 cup yoghurt ml 
 Whole  250
ml

Meat  Size of matchbox meat  30 g ­  7  3  55

pg. 39 by Osonga
 Lean  Palm size of fish  30 g  7  5  75
 Mediu  A leg, thigh or breast  30 g  7  8  100
m fat chicken  30 g  7  3  75
 High  2 tbsp peanut
fat  ½ cup fresh bean
 Egg  ½ cup omena
Vegetable  ½ cup cooked vegetable 100­150 5 2 ­ 25
s  1 cup raw vegetable g
Fruits  1 small apple, peach, Varies 15 ­ ­ 60
orange, apple or grape
fruit juice (pure juice)
 ¾ cup diced fruits
Fats  1 tsp margarine or oil ­ ­ 5 45
 10 large peanuts
 1/8 medium avocado
 1 slice bacon
 1 tbsp shredded coconut
 1 tbsp cream cheese
 1 tbsp salad dressing
 5 large olives
Sugar 1 tsp 5 20

Procedure for calculating diets using exchange lists


Suppose that 1,200 – calorie diet is to be planned with the following levels, CHO
120g, protein 70g, and fat 30g.Estimate the amounts of milk, vegetables and fruits
to be included. The amounts are dictated somewhat be the preferences of the clients
but the following are minimum levels that should ordinarily be included: Milk 2
cups for adults, 3­4 cups for children and for pregnant/lactating mother; fruits – 2
exchanges; vegetables – 2 exchanges
1. Fill the carbohydrate, protein and fat values for the tentative amount of milk,
vegetables and fruit.
2. Determine the number of bread exchanges. Add up the CHO value of milk,
vegetables and fruit. Subtract this total from the total amount of CHO
prescribed. Then divide the remainder by 15 (the CHO value of one bread
exchange). Use the nearest whole number of bread exchanges. Fill in the
bread.

pg. 40 by Osonga
3. Total the CHO column. If the total deviates more than 3­4 from the
prescribed amount, adjust the amounts of vegetable, fruit and bread. No diets
should be planned with fractions of an exchange, since awkward measures of
food would sometimes be encountered.
4. Determine the number of meat exchanges. Add up the protein value of all
food so far calculated. Subtract this total from the amount of proteins
prescribed. Divide remainder by 7 (the protein value of one meat exchange).
Fill in the protein and fat values
5. Determine the number of fat exchange. Add up the fat value from the milk
and meat. Subtract this total from the amount of fat prescribed. Divide the
remainder by 5 (the fat content of one fat exchange). Fill in the fat value.
6. Check the entire diet for the accuracy of the computations. Divide the day’s
food allowances into a meal pattern suitable for the client.

List Food Measure CHO (g) Protein Fat (g) Calories


(g) Kcal
1. Milk, low 2 24 16 10 250
fat exchanges
2. Vegetable 2 10 4 ­ 56
exchanges
3. Fruits 3 30 ­ ­ 120
exchanges 64
4. Bread 4 60 8 ­ 272
exchanges 124 24
5. Meat, Low 7 49 21 385
fat exchanges
6. Fat 2 ­ ­ 10 90
exchanges
TOTAL 124 70 40 1173

Signal System: Pr inciple of Healthy Food Choices and Cooking Methods


This system is based on traffic light concept of red for ‘stop’ which also denotes danger, yellow
for ‘go slow’ or cautious, and green for ‘go’ or safer road (see table 63 below). It uses
universally understood symbols which makes it simple and highly useful way for a person to
make an informed choice. Importantly it focuses attention on processing and cooking, lays stress

pg. 41 by Osonga
on the Glycemic Index (GI), fiber content of food, the amount and type of fat used and the mode
of cooking. It removes negative feelings about being on a diet and avoiding certain foods. It
empowers the person to make a behavior change towards healthy eating. Table 63: Pr inciples of
Healthy Food Choices, Signal system
Pr inciples Gr een Yellow Red
Refined cereals Low Moderate to high High
and sugars
Saturated fat Low Low High
Total fat Low Moderate High
Glycemic index low Moderate high High GI
Fiber High Low Negligible
Cooking method Steaming, boiling, Pan fried, sautéed, stir Deep fried, extra butter,
roasting, grilling, fry; moderate amount ghee added, rich
tandoor, dry heat, of fat in cooking sauce/dressing, rich in
less fat in cooking added sugar
Processing Rich fiber, parboiled, Low fiber, refined, Low fiber processed, ready
hand pounded. milled to eat
How much to Eat as permitted Moderation Restrict
eat

Hand J ive
The Zimbabwe hand jive shown in figure 14 below, suggested by Dr K Mawji, illustrates how to
measure the amount of food 'imaginatively', in a reasonably accurate manner, without scales etc.
Hand J ive Pr otein : Choose an amount
the size of the palm of your
hand and the thickness of
Carbohydrates ( starch and fruit):
Choose an amount the size of
your little finger .
your 2 fists.

Fat : Limit fat to an amount


Vegetables: Choose as much as you can the size of the tip of your
hold in both hands. Choose low thumb.
car bohydr ate vegetables (e.g. gr een or Dr ink no mor e than 250 mL
yellow beans, cabbage, lettuce). of low­fat milk with a meal.

Figur e 14: The Zimbabwe Hand J ive

Plate model method

pg. 42 by Osonga
The Plate Method is a simple method for teaching meal planning. A 9­inch dinner plate
serves as a pie chart to show proportions of the plate that should be covered by various
food groups. This meal planning approach is simple and versatile. Vegetables should
cover 50 percent of the plate for lunch and dinner. The remainder of the plate should be
divided between starchy foods, such as bread, grains, or potatoes, and a choice from the
meat group. A serving of fruit and milk are represented outside the plate. Figure 15
below shows how a sample basic meal should appear in the plate for a normal healthy
individual.

Sample Basic Meal


Planning Guide

Fruit Meat/ Milk


Protein
Starch/
bread
Vegetables

American
Diabetes 31
Association®

Figur e 15: Simple Basic Meal Planning Guide for Healthy individual

Figure 16 shows a sample plate for a diabetic patient. Note the difference in the portion
sizes of vegetables.

Model Plate

pg. 43 by Osonga
Fruit

Milk/ Yoghurt
Protein

Vegetable

Vegetable

Starch /cereal

Figur e 16: Model Plate for a Diabetic Patient

Combined with the plate model the signal system is a practical and easy way to
implement diet advice for a newly diagnosed person with type 2 diabetes
Figure 17 shows plates usually seen for many people which are not in line with the
principles of meal planning

Plate For mats Usually Seen


Milk/yoghurt Milk / yoghurt

Vegetable Vegetable

Starch /cereal
Protein

Starch /cereal Protein

Rich in star ch/cer eals, low in vegetablesRich in pr oteins, low in vegetables and cer eals

Figur e 17: Plate For mats usually seen not in Line with Meal Planning

TOPIC: NUTRITION SUPPORT


Enteral and Parenteral Nutrition
This refers to the provision of food and nutrients to the patient when the conventional
feeding methods are not adequate or cannot meet nutrition needs. These include Enteral

pg. 44 by Osonga
and parenteral nutrition. Selection of the mode of feeding is dependent upon several
factors. Figure 4.2 below outlines the factors to consider in selection of a feeding method.

Figure: Choice of route of nutrition administration Adopted from JPEN 1993; 17 (4):
1SA.
Enter al Nutr ition
Enteral nutrition is a way of providing nutrition to the patients who are unable to
consume an adequate oral intake but have at least a partially functional GI tract. Enteral
nutrition may augment the diet or may be the sole source of nutrition. It is recommended
for patients who have problems chewing, swallowing, prolonged lack of appetite, an
obstruction, a fistula or altered motility in the upper GIT; are in coma or have very high
nutrient needs.

pg. 45 by Osonga
Types of Enter al Nutr ition For mula
There are various types of enteral feeds available as ready to use or powdered mixes
specifically designed to meet the needs of the patient. The formulas are commonly
categorized by the complexity of the proteins they contain. There are two major types of
Enteral feeds namely: standard and hydrolyzed.

Standar d For mulas


These are also known as polymeric or intact formula. They are made from whole proteins
as found in the diet (e.g. eggs, meat) or protein isolates [semi­purified high biological
value proteins that have been extracted from milk, soybean or eggs]. Because they
contain whole complex molecules of protein, carbohydrate and fat, standard formulas are
used for patients who have normal digestive and absorptive capacity. They come in
variety such as standard, high protein, high calorie and disease specific.

Hydr olyzed For mulas


Partially hydrolyzed formulas contain proteins that are partially digested into small
peptides. Completely hydrolyzed formulas are commonly known as elemental formula
and they contain protein in its simplest form; free amino acids. Hydrolyzed formulas also
provide other nutrients in simpler forms that require little or no digestion e.g. very low fat
in form of medium­chain triglycerides (MCT). Hydrolyzed formulas are meant for
patients with impaired digestion or absorption such as people with inflammatory bowel
syndrome, short gut syndrome and pancreatic disorders.
Indications for Enteral Nutrition
During periods of decreased oral intake, anticipated less than 50% of required nutrient
intake orally for 7­10 days as seen in severe dysphagia (difficulty swallowing), metabolic
stress, major bowel resections, low­output fistulas and coma. Neurological disorders and
psychological conditions.
Malnourished patients expected to be unable to eat > 5 days
Normally nourished patients expected to be unable to eat >5 days
Adaptive phase of short bowel syndrome
Following severe trauma or burns
Contr aindications
 Intestinal obstruction that prohibits use of intestine
 Paralytic illus
 Intractable vomiting

pg. 46 by Osonga
 Peritonitis
 Severe diarrhea
 High output fistulas between the GI tract and the skin
 Severe acute pancreatitis
 Inability to gain access
 Aggressive therapy not warranted

Deter mining nutr ient r equir ements


The type of formula, volume and hence the total nutrient required are determined by the
patients physiological condition. Several equations are available for estimating nutrient
requirements of patients depending on their clinical condition.
The calorie to nitrogen ratio should be >150:1 (1g nitrogen is equivalent to 6.25g
protein). If the C: N ratio is less than 200:1, then the protein supplied by such a feed will
be inadequate for critically ill patients.

Tube feeding
This is the delivering of food by tube in to the stomach or intestine. It is indicated
whenever oral feeding is impossible or not allowed.
Tube feeding routes
The decision regarding the type of feeding route/tube depends on the patient’s medical
status and the anticipated length of time that the tube feeding will be required.

Mechanically inser ted tubes;


Nasogastric tubes where by a feeding tube is pushed through the nose into the stomach
Orogastric tubes whereby a feeding tube is pushed through the mouth into the stomach
Nasoduodenal tubes – the tube is pushed through the nose past the pylorus into the
duodenum
Naso­jejunal tube – the tube is passed during the endoscopy from the nose past the
pylorus into the jejunum
Sur gically inser ted tubes
Oesophagostomy: A surgical opening is made at the lower neck through which a feeding
tube is inserted to the stomach
Gastrostomy: A surgical opening is made directly into the stomach

pg. 47 by Osonga
Jejunostomy : A surgical opening is made into the jejunum
Figure 7 below illustrates different routes of enteral nutrition administration, while table
35 shows methods of administration.

Figure2: Different route of enteral nutrition administration


Advantages of Enteral nutrition
There is a stimulation of GI hormones and consequent regulated metabolism and
utilization of nutrients.
It ensures adequate nutrient supply to the mucosal wall, and protection against atrophy of
intestinal Villi.
It offers physiological protection against ulcers due to its buffering effect from gastric
acids.
Table1: Methods of administration
Method Administration Remarks
Bolus Initially – 50ml then Most appropriate when feeding in to the
feeding increase gradually up to a stomach
maximum of 250 to 400ml
Check aspirate before each feeding
over approximately 30
minutes, 3 to 4 hourly daily Feeds may poorly tolerated causing nausea,
(in 24 hrs) vomiting, diarrhea, cramping or aspiration
Intermittent 400 – 500ml infused by Patient retains freedom of movements in
slow gravity over approximately between feeds

pg. 48 by Osonga
gravity 20 ­30 minutes to 1 hr. 3 to Improved tolerance of feeds
feeding. 4 hourly daily (in 24 hrs)

Continuous Total volume of feed Most suitable when feeding in to the


required is slowly duodenum or jejunum where elemental
administered; approximately diets are most appropriate
100ml/hour over 18 – 24hrs
May also be suitable for feeding in to the
stomach
Method may slow peristalsis
Feeds are better tolerated

Tube feeding instr uctions


 Tube feeding should be used at room temperatures, cold mixtures can cause
diarrhea
 Ensure proper placement of tube and feed at slow constant rate
 Prescribed intervals and volumes of feeding should be adhered to
 Care should be taken to ensure that the tube feeds meet the patient’s nutrient
requirements
 Prepared mixture should be well covered, properly labeled including time of
preparation and stored in a refrigerator for up to 24 hours
 In the absence of refrigeration, quantities lasting only six to twelve hours should
be prepared
 All feeding equipment should be cleaned before and after each feed
 Shake/stir well before use

Commonly used equipment in enteral feeding


Feed preparation equipment for kitchen made feeds and powder feeds include measuring
jars and cups and spoons, mixing bowls, blender, flask, sterile water
Ready to hang (RTH) feeds: giving sets for gravity or giving sets for the pump system,
Enteral feeding pumps, dual port connector and a feeding bag where applicable
Liquid diets in easy bags: giving sets (gravity or pump), feeding pump and/or dual port
connector where applicable
Feed delivery equipment; funnel especially in gastrotomy and Jejunostomy for
controlling viscous flow, syringe for naso­gastric bolus or intermittent feeding and the
feeding tubes where applicable
NB: Feeding pump is recommended as it eases feeding workload because it flows
without constant supervision, enhances accuracy, hygiene and sanitation.

pg. 49 by Osonga
The table below shows methods of estimating daily fluid allowance
Table2: Methods of estimating daily fluid allowance
Basis of estimation Calculation
Body weight
Adults
Young active :16 – 30 years 40 ml/kg
Average: 25 – 55 years 32 ml/kg
Older: 55 – 65 years 30 ml/kg
Elderly:> 65 years 25 ml/kg
Children
1 – 10kg 100 ml/kg.
11 – 20kg An additional 50ml per each kg > 10kg.
21kg or more An additional 25ml per each kg > 20kg
Energy intake 1 ml per Kcal.
Nitrogen plus energy intake 100 ml/g nitrogen intake plus 1 ml per Kcal*
* Useful with high protein feeding

Tube feeding complications


Sometimes a client does not respond to a tube feeding as expected. If the client continues
to lose weight, for example health care professionals must find out why. Perhaps they
have underestimated energy and nutrient requirements.
Commonly seen complications can be classified into: gastro­intestinal, mechanical,
metabolic, and pulmonary. Table 37 and 38 provides a summary of the complications
alongside prevention/management strategies.
Table3: Gastrointestinal complications of tube feeding
Gastro intestinal Prevention/management
complications
Diarrhea Slow feeding rate
Supplemental fluid and electrolytes

pg. 50 by Osonga
Use lactose free formula
Prevent formula contamination
Consider different formula
Check antibiotic/drug therapy
Check flow rate of feed
Consider Enteral nutrition with added fiber
Use ant diarrheal agent
Check osmolarity of feeds (< 500mosl/l recommended
Constipation Give supplemental fluid.
Check if fiber inadequate or excessive
Check physical activity
Nausea or vomiting Reduce flow rate
Discontinue feeding until underlying condition is managed
Change to polymeric feeds if on elemental diet
Check gastric emptying and review narcotic medications,
initiate low fat diet, reduce flow rate
Malabsorption/Mal­ Identify the cause (crohn’s disease, radiation enteritis, HIV,
digestion pancreatic insufficiency etc)
Select appropriate Enteral product
PN may be necessary in selected patients
Abdominal distension Assess the cause
Check feed temperature (give at room temperature)
Do not give rapid formula administration

pg. 51 by Osonga
Table4: Other Medical Complications of tube feeding
Mechanical Prevention/management
complications
Tube placement To be placed by trained personnel using defined protocol to
reduce complications

Feeding tube Use small bore feeding tube to minimize upper airway
problems
Tube clogging Select appropriate tube size
Flash with water
Dilute formula with water
Dislocation of tube Ascertain tube placement before each feed
Clearly mark tube at insertion
Nasopharyngeal Use small lumen tube.
irritation
Use pliable tube
Esophageal erosion Discontinue tube feeding
Recommend parenteral nutrition
Metabolic Pr evention/management
complications
(Fluid and electrolyte Check adequacy of daily nutrient supply of macro and
imbalance, trace micronutrients during EN.
element, vitamin and
Check possibility of Malabsorption
mineral deficiencies,
essential fatty acid
deficiencies
Hyperglycemia Reduce flow rate.
Give oral hypoglycemic agents or insulin.
Change formula
Tube feeding syndrome Reduce protein intake or increase water intake.
For conscious patients education and counseling is needed
Hypernatremia Increased water intake and reduce sodium
(dehydration)

pg. 52 by Osonga
Replace sodium loses
Hyponatremia (over­ Replace sodium loses
hydration)
Re­asses nutrient requirement, check volume administration,
change to nutrient dense formula
Pulmonar y Pr evention/management
complications
Pulmonary aspiration Incline head of bed 300 – 450 during feeding 1 hr after
feeding.
Check tube placement.
Monitor symptoms of gastric reflux.
Check abdominal distension.
Check residual volumes before feeds.
Change to jejunal feeding.
Reduce volume of feed.
Change from bolus to continuous feeding

When a patient has been put on enteral feed, it is important that the administration is
monitored regularly to avoid or identify any complications early and address them. The
table below provides a checklist for monitoring clients/patients recently put on tube
feeding.

pg. 53 by Osonga
Table5: Checklist for monitoring patients recently placed on tube feeding
Action Check
Before starting a new Complete a nutrition assessment
feeding
Check tube placement
Before each intermittent Check gastric residual
feeding:
Check gravity drip rate when applicable
Every half hour
Check pump drip rate, when applicable
Every hour
Check vital signs, including blood pressure, temperature,
Every 4 hours pulse, and respiration
Every 6 hours Check blood glucose, monitoring blood glucose can be
discontinued after 48hrs if test results are consistently
negative in a non­diabetic client
Every 4 to 6 hours of Check gastric residual
continuous feeding
Every 8 hours Check intake and output
Check specific gravity of urine
Check tube placement
Chart clients total intake of, acceptance of, and tolerance
to tube feeding
Every day Weigh clients where applicable
Check electrolytes and BUN when needed
Clean feeding equipment
Check all laboratory equipment
Every 7 to 10 days Check all laboratory Findings
Re­assess nutrition status
As needed Observe client for any undesirable responses to tube
feeding; for example delayed gastric emptying, nausea,
vomiting, and diarrhea
Check nitrogen balance
Check laboratory data

pg. 54 by Osonga
Chart significant details

As had been highlighted earlier there are different enteral formula classifications. Table
40 below shows the enteral formula classifications.

pg. 55 by Osonga
Table6: Enteral formula classifications
Enteral formula Sub­category Characteristics Indications
Polymeric Standard Similar to average diet. Normal digestion
High nitrogen Protein > 15% of total Catabolism Wound
Kcal. healing
Calorie dense 2 Kcal/ml Fluid restriction
Volume intolerance
Fiber containing Fiber 5 – 15/l Regulation of bowel
function
Monomer Partially One or more nutrients Impaired digestive
hydrolyzed are hydrolyzed, and absorptive
elemental peptide composition varies. capacity
based
Disease specific Renal Whole protein with Renal failure
modified electrolyte
content in a caloric
Hepatic High BCAA, low AA, Hepatic
encephalopathy
Pulmonary High % of calories ARDS
from fat.
Diabetic Low carbohydrate Diabetes mellitus
Immune Critically ill Arginine*, glutamine, Critically ill.
enhancing omega­3 fatty acids,
Formulas anti­oxidants
* is contraindicated in critical illness
There a wide range of enteral feeds available in the market. The table below further
highlights some examples of enteral feed formulations. However, it is worth noting that
this is not a complete list of all the formula’s currently available in the market.

pg. 56 by Osonga
Table7: Examples of enteral feed formulations
Feed Composition – 100g powder Indications
Infant feeding CHO­55.9% mainly lactose and For low birth weight,
formulas maltodextrin. premature or light for
date babies when breast
PRO­14.4% mainly whey
milk is not available.
protein and casein.
FAT­24.0% MCT, milk, fat,
corn oil, soybean.
CHO­56.2% For infants of normal
birth weight (mature,
PRO­12.5%
normal for date) when
FAT­27.7% breast milk is not
available.
CHO­55.4% For infants and low birth
weight, light for date
PRO­11.4%
babies when breast milk
FAT­27.7% corn oil, soy oil, is not adequate or not
coconut oil. available

Lactose free infant CHO­55.4% mainly For infants


formulas maltodextrin
PRO­14.0%
Soy protein isolate.
FAT­25% palm, soya and
coconut oil.
CHO­52% For infants and adults
when lactose or cow’s
Corn syrup solids
milk should be avoided.
PRO­14%
Soy protein isolate
FAT­27%
Blend of vegetable oils.
CHO­50% corn syrup, sucrose. For infants and adults
when lactose or cow’s
PRO­15.6% soy protein isolate.
milk should be avoided.
CHO­40% For infants and adults

pg. 57 by Osonga
Glucose polymer and corn when lactose or cow’s
syrup solids. milk should be avoided.
PRO­12% Soy isolate.
FAT­48% soy oil, coconut oil.

pg. 58 by Osonga
Feed Composition – 100g powder Indications
High protein powder CHO­37.4% A protein caloric
supplements supplement that can be
PRO­25%
incorporated in liquid or
Full cream powdered 2. CHO­54% A protein caloric
milk supplement useful where
PRO­36.4%
Dried skimmed milk CHO­68% low fat dietfat
Controlled is required
diets
powder (DSM)
Corn syrup solids, glucose,
lactose.
PRO­24%
CHO­54% Glucose and tapioca For oral or tube feedings.
starch Useful in Malabsorption
and low fat modified diets
PRO­11% Hydrolyzed casein and
amino acids
FAT­35% corn oil, MCT oil
CHO­6.7% Useful in high protein, low
calorie low fat, fat residue
Lactose, sucrose
diets
PRO­17.1%
Calcium caseinate
FAT­0.6%
CH0­30% A protein, vitamin and
mineral supplement ideal
PRO­55%
for high protein diets, low
FAT­1% fat diets and cases of
malabsorption useful for
Calories per 100g – 366g patient allergic to
lactalbumins
Nutritionally CHO­13.8g = 55% of total Cal. Nutritionally complete
complete liquid diets liquid diet for total or
PRO­3.8g = 15% total Kcal.
supplemental feeding, tube
FAT – 3.4g = 30% of total Kcal l. feeding or oral feeding
CHO­17g = 54.6% of total Kcal. High caloric formula
suitable for tube or oral
PRO­7.5g = 15.1% of total Kcal.
feeding especially where
FAT­68g = 30.3% of total Kcal. energy intake is increased,
where fluid is restricted

pg. 59 by Osonga
ENERGY­1Kcal per ml. and or fat malabsorption

CHO­12g = 53% of total Kcal. Nutritionally complete feed


for oral or tube feeding in
PRO­3.4g = 15% of total Kcal
diabetics.
FAT­3.2g
CHO­58%=of32%
totalofKcal.
total Kcal Nutritionally complete feed
for oral or tube feeding as a
PRO­15% of total Kcal.
total diet or supplemental
FAT­30%
CHO­61.5gof=total
54%Kcal.
of total Kcal. diet. Lactose free
Nutritionally with fiber
complete feed
for oral or tube feeding as a
PRO­15.8g = 14% of total Kcal.
total or supplemental diet.
FAT­15.8g = 32% of total Kcal. Lactose free feed, low in
cholesterol and sodium
ENERGY = 100 Kcal per 100ml.

Par enter al Nutr ition


This refers to nutrition directly into the systemic circulation, bypassing the gastro­
intestinal tract (GIT) and the first circulation through the liver. The primary objective of
parenteral nutrition is to maintain or improve the nutritional and metabolic status of
patients who have temporary or permanent intestinal failure.
Char acter istics of par enter al nutr ition
Patients on TPN (Total Parenteral Nutrition) have similar requirements as enterally fed
patients
The six major nutrients covered are: carbohydrates, proteins, fats, vitamins, minerals and
water
Feeds must provide adequate calories
Nutrient form must be specialized for infusion into blood count prior to digestion
Standardized concentration may be modified to suit individual requirements
Indications for Par enter al Nutr ition
Patients who are candidates for parenteral nutrition cannot eat adequately to maintain
their nutrient stores. These patients are already, or have the potential of becoming
malnourished.
Peripheral Parenteral Nutrition (PPN) may be used in selected patients to provide partial

pg. 60 by Osonga
or total nutrition support for up to 2 weeks in patients who cannot ingest or absorb oral or
enteral tube delivered nutrients or when central­vein parenteral nutrition is not feasible.
Parenteral nutrition (PN) support is necessary when parenteral feeding is indicated for
longer than 2 weeks, peripheral venous access is limited, nutrient needs are large, or fluid
restriction is required, and the benefits of PN support outweigh the risks. Patient has
failed Enteral Nutrition (EN) trial with appropriate tube placement (post­pyloric).

pg. 61 by Osonga
EN is contraindicated or the intestinal tract has severely diminished function due to
underlying disease or treatment. Specific applicable conditions are as follows:
Paralytic ileus
Mesenteric ischemia
Small bowel obstruction
GI fistula except when Enteral access may be placed distal to the fistula or volume of
output (<200 mL/d) supports a trial of EN
Diseases of the small intestine
Intractable vomiting/diarrhea
Massive small bowel resection
Trauma
Inflammatory Bowel Disease
Enterocolitis (AIDS, chemotherapy, radiotherapy)
Pancreatitis
Burns
Cancer
Immaturity (premature babies)
As occurs in postoperative nutrition support, the exact duration of starvation that can be
tolerated without increased morbidity is unknown. It has been suggested that wound
healing would be impaired if PN is not started 5–10 days. This is for postoperative
patients unable to eat or tolerate enteral feeding.
The patient’s clinical condition is considered in the decision to withhold or withdraw
therapy. Conditions where nutrition support is poorly tolerated and should be withheld
until the condition improves are severe hyperglycemia, azotemia, encephalopathy and
hyperosmolarity and severe fluid and electrolyte disturbances.
Contr aindications
Functional GIT
Existence of an advanced terminal condition for which aggressive therapy is not provided
Parenteral nutrition in infants Very preterm infants, who often have relatively delayed
gastric emptying and intestinal peristalsis, may be slow to tolerate the introduction of
gastric tube feeds. These infants may need intravenous nutrition while enteral nutrition is
being established or when enteral nutrition is not possible—for example, because of

pg. 62 by Osonga
respiratory instability, feed intolerance, or serious gastrointestinal disease.

pg. 63 by Osonga
Examples of feeds for pediatrics
Protein source: Amino venous
CHO source: dextrose
LIPIDS (Fat) source: Lipovenous 10%
Total parenteral nutrition consists of a glucose and amino acid solution with electrolytes,
minerals, and vitamins, plus fat as the principal non­protein energy source. Bloodstream
infection is the most common important complication of parenteral nutrition use.
Delivery of the solution via a central venous catheter rather than a peripheral catheter is
not associated with a higher risk of infection. Extravasation injury is a major concern
when parenteral nutrition is given via a peripheral cannula. Subcutaneous infiltration of a
hypertonic and irritant solution can cause local skin ulceration, secondary infection, and
scarring. Extravasation injury may occur when a peripheral cannula is used to deliver the
parenteral nutrition solution
Routes of administration of parenteral nutrition
Intravenous solutions can be provided in different ways. The methods used depend on the
person’s immediate medical and nutrient needs, nutrition status and anticipated length of
time on IV nutrition support. They include:
Peripheral Parenteral Nutrition (PPN)
Central Parenteral Nutrition (TPN)
The general decisions to use PPN instead of CPN are based on comparative energy
demands and anticipated time of use.

Per ipher al Par enter al Nutr ition


This refers to use of peripheral veins to provide a solution that meet nutrient needs for
infusion. It has lower dextrose (5% to 10% final concentration) and amino acid (5% final
concentration) concentration than CPN. It may provide full or partial nutritional
requirements to patients.
PPN can be administered in to peripheral veins if solutions used have osmolarity below
800 ­ 900mosm/l for a brief period of less than 14 days. Short catheters (cannulas) and
mid­way catheters are normally used. However, PPN administration is possible for
several weeks with fine bore catheter.
PPN may be used in patients with mild or moderate malnutrition to provide partial or
total nutrition support when they are not able to ingest adequate calories orally or
enterally or when central vein PN is not feasible.
All in one admixture are highly recommended compared to the single bottle system

pg. 64 by Osonga
during PPN.
Centr al Par enter al Nutr ition (CPN)
CPN is often referred to as “Total Parenteral Nutrition” since the entire nutrient needs of
the patient may be delivered by this route. It requires a central venous system for long
term infusions.
The sites mainly used are the Vena jugularis external, Vena jugularis internal, Vena
subclavia, Vena cephalica and Vena basilica for solutions with osmolarity above 800 ­
900 mosm/l.
Peripherally Inserted Central Catheters (PICC) for short ­ and long term infusions are
possible. Implantable system for central venous access (Ports) Lasts for years after
implantation and patients may go on TPN for years with the catheters being changed
every 5 ­ 10 years. Central Parenteral Nutrition is complete nutrition similar to
physiological nutrition and can be provided for unlimited period (weeks to years). PN can
be used in hospitalized patients and those who have returned home or are in assisted
living, extended care facilities or nursing homes.
Access routes for parenteral nutrition include:
Peripheral Access Routes
One of the easiest and safest ways to access the vascular system is to place a cannula into
a peripheral vessel. The adequacy of the vein limits the use of the peripheral system for
infusion. Catheter tips that are located in a peripheral vessel are not appropriate for the
infusion of PN formulas > 900 mosm/L.
The indications for peripheral infusion are short­term access needs. Specially formulated
PN may be administered by peripheral access. These solutions are based on a decreased
dextrose concentration and osmolarity and have been reported to be used for short­term
therapies (<­10–14 days) when fluid restriction is not necessary.
The leading complication associated with peripheral access is peripheral venous
thrombophlebitis. The hallmark symptoms of infusion phlebitis (an inflammation of the
cannulated vein) are pain, erythema, tenderness or a palpable cord. Peripheral devices
have the lowest risk of catheter related infections.

pg. 65 by Osonga
Centr al Venous Access
Central venous access is defined as a catheter whose distal tip lies in the distal vena cava
or right atrium. The most common sites of venipuncture for central access include the
subclavian, jugular, femoral, cephalic, and basilic veins.
Figure 8 below illustrates administration of PN through the sub­clavian vein.

Figure 3: Administration of parenteral nutrition through sub clavian vein

pg. 66 by Osonga
Calculating the nutrient content of Intra Venous (IV) formulas
The energy/nutrient requirements of patients on parenteral nutrition comprises of a
complete nutrition similar to physiological nutrition. These requirements can be
calculated using several different available formulas and no standard prescription
provides an answer for all patients. Nutrient requirements are also adjusted at all times to
suit the patient’s current medical or surgical condition. One of the standard parenteral
nutrition regime that is suited for 80% of patients and calculated as per the kilogram body
weight is as shown in table 42 below:
Table8: Nutrient requirements for IV formulas
Nutrients Requirements
Amino acids 1 ­ 1.5g
Energy (as fat and glucose) 25 ­ 30 kcal (NPE ­ 3 ­ 5g (>2g/kg, <7g/kg)
Non Protein Energy)of which glucose
Fat (LCT) 1­ 2g (<0.3g/kg, <3g/kg)
Vitamins and trace elements Basic needs
Water and electrolytes Basic needs

Note:
Protein Energy (NPE): Stand for energy from carbohydrate and fat only, excluding the
energy from protein. The protein requirements are then calculated separately as per the
patient’s body weight.
The proportion of carbohydrate to fat is then calculated at a proportion of 70: 30 or 50: 50
depending on the patient’s condition. This means that 70% of the NPE will be the
required energy from Carbohydrate and 30% of NPE will be the required energy from fat.
Total energy (TE) requirements can also be calculated from e.g. the Harris Benedict
Equation (HBE) or any other equation or formulas available. The ratio of energy to
nitrogen is then calculated as follows:

pg. 67 by Osonga
Calorie nitrogen ratio – An adequate energy provision is necessary to support the use of
protein for anabolism. The recommended non­protein calorie nitrogen ratio (C: N) for the
different conditions is calculated as shown in the table below.
Table9: Recommended non­protein calorie nitrogen ratio (C: N) for the different
conditions
Conditions Calorie: Nitrogen Ratio (gN)
For normal body maintenance 300:1
Stressful conditions 150:1
Renal failure 250: 1
PPN 70:1
Children 300:1

The percentage of nutrient requirements can also be calculated from the TE as follows:
50 – 60% of the TE from Carbohydrate
15 – 20% of TE from Protein
25 ­ 30% of TE from FAT

Pr ecautions in Par enter al Nutr ition


 Osmolarity – ensure appropriate osmolarity is infused via the appropriate veins to
avoid thrombosis and small blood vessel damage. E.g. osmolarity > 900 should be
administered centrally.

Calculation of the osmolarity of parenteral nutrition solutions


Multiply the grams of dextrose per liter by 5 mosm/g
Example: 50g of dextrose x 5 = 250mOsm/L
Multiply the grams of protein per liter by 10 mosm/g
Example: 30g of protein x 10 = 300mOsm/L
Fat is isotonic and does not contribute to osmolarity
Electrolytes further add to osmolarity for example: 1 mosm/me of individual electrolyte
additive
Total osmolarity is then derived from the sum of the osmolarity of all nutrients infused

pg. 68 by Osonga
 Infusion rate – always check label and package inserts. The maximum infusion
rate recommended for specific solutions should not be exceeded in order to avoid
complications

Vital signs should be monitored daily


Discontinuation should also be gradual to avoid hypoglycemia
Infuse parallel, it is best to infuse parallel. If parallel infusion is not possible then infuse
directly
First carbohydrates with electrolytes, second amino­acid with electrolytes, third fat

pg. 69 by Osonga
Administr ation of par enter al nutr ition
Parenteral Nutrition feeds can be administered in the following forms:
1). Single bottle system: These are single products/bottles providing either one of amino
acid solution, dextrose solution or lipid emulsions or vitamins or trace elements or a
combination of Amino acid and dextrose. The single bottle system may also contain
electrolytes.
2). All in One (AIO) admixtures: These formulations may be prepared as a single product
by the hospital pharmacist or industrial admixtures. The industrial admixtures are mixed
up at the factory and delivered to the hospital. Refrigeration is required and they have a
short shelf life.
3). Chamber bags: Two and three chamber bags. These AIO parenteral nutrition feeds
have a much longer shelf life and are mixed prior to administration.
Complications of Par enter al Nutr ition
These complications are mainly divided into two main categories as follows:
Catheter r elated complications which involve:
Occlusion of the catheter
Catheter blockage (check the type, diameter, period of use)
Catheter related infections ­ these infections may come from the skin or systemic
circulation (gram negative organisms and fungi)
Catheter related sepsis ­ there is need to use antiseptic techniques at all times
Metabolic Complications
Hepatibiliary or Gastrointestinal complications
Abnormal liver function (caused by underlying diseases, i.e. sepsis, malignancy, IBD,
pre­existing liver disease) bacterial overgrowth in the intestines, biliary sludge and
gallstones. Steatosis which may be caused by sole infusion of dextrose as an energy
source without fat emulsions or excessive glucose load (above or equals to 7g of
glucose/kg/day). Sole glucose infusion without fat may also cause essential fatty acid
deficiency (EFAD).
Macr onutr ient Complications
These are risks associated with underfeeding or overfeeding. |:
Hyperglycemia ­ several factors may cause hyperglycemia including overfeeding
Hypoglycemia ­ this may occur mainly if weaning off parenteral nutrition is not done
appropriately or if there is excess insulin administration

pg. 70 by Osonga
Azotemia can result from dehydration, excessive and/or inadequate non protein calories.
Omission of fat emulsions during PN may cause EFAD
Too much infusion may cause hyperlipidemia

pg. 71 by Osonga
Micr onutr ient Related Complications
Fluid imbalance (Dehydration from osmotic diuresis, fluid overload)
Electrolyte imbalance
Vitamin, mineral and trace elements deficiency may only occur

The above complications can greatly be reduced and avoided if there is a multi­
disciplinary nutrition team with experienced clinicians available to insert the central
feeding catheters, designated nurses to care for the catheters, and an experienced
registered dietician to prescribe the right parenteral nutrition formulation and make the
necessary follow ups, monitoring and necessary adjustments. The table below shows
complications of total parenteral nutrition.
Table10: Complications of total parenteral nutrition
Catheter related complications Metabolic complications
Bacteraemia (staphylococcal) Cholestatic jaundice
Invasive fungal infection Hyperglycaemia or glycosuria
Thrombosis Vitamin deficiencies or excesses
Extravasation injuries Hyperammonaemia
Cardiac tamponade

Examples of parenteral nutritional formulations:


You can have confidence in IV solutions if you know what they contain. The basic thing
to remember is that the percentage of a substance in solution tells you how many grams
of that substance are present in 100mL e.g. a 5% dextrose solution contains 5g of
dextrose per 100 ml; a 3.5% amino acid solution contains 3.5g of amino acids per 100ml.
A 0.9% normal saline solution contains 0.9g of NaCl per 100mL. Table 45 shows
examples of parenteral formula feeds. Table 46 on the other hand, shows pediatric
parenteral nutrition formulations.

pg. 72 by Osonga
Table11: Examples of parenteral formula feeds
Amino acid solutions Features Presentation
These are standard Amino acids for 200ml,500ml and
parenteral nutrition which contain 1000ml bottles
Standard Amino
WHO recommended ratio for
Acids
essential and non essential amino
5% (50g AA/L) acids and may contain electrolytes or
may be electrolyte free
10% (100g AA/L)
Essential nitrogen balance
15% (150g AA/L)
Special Amino Acids May be balanced AA solution 200ml, 500ml bottle
containing Glutamine and tyrosine ,
Arginine
Special Amino Acids Disease specific formulation 50ml, 100ml, 200ml
containing AA glutamine bottles
Special AA for These are disease specific 200ml, 500ml bottles
Hepatic insufficiency formulations.
8% (80g AA/L) Specially designed to compensate the
AA disorders in hepatic insufficiency,
rich in BCAA and quite low in AAA.
Special AA for renal Adapted to the metabolic AA disorder 200ml, 250ml and
insufficiency in renal failure and contains a 500ml bottles
balanced profile of EAA and NEAA
7% (70g AA/L)
and the dipeptide glycyl­tyrosine
10% (100g AA/l)
Well balanced AA pattern specifically
designed for infants (preterm, new
born, babies) and young children.
Contains EAA and NEAA similar to
human breast milk.
Contains taurine an EAA for neonates
Carbohydrates Features Presentation
solutions
5% (50g /L) These carbohydrate feeds mainly 50ml, 100ml, 500ml,
contain glucose but some may contain 1000mls bags or bottles
6% (60g/ L)
xylitol and or sorbital
10% (100g/L)

pg. 73 by Osonga
20% (200g/L)
25% (250g/L)
50% (500g/L)
Solutions with both These parenteral nutrition solutions 200ml, 500ml, 1000ml
Carbohydrate and contain both carbohydrate and amino bottle
Amino acids. acid including electrolytes and may be
administered peripherally. e.g.
3% AA and 6% carbohydrate plus
electrolytes.
5% AA and 5% sorbital.

pg. 74 by Osonga
Lipid Emulsions Features Presentation
10% These are lipid emulsions for 200ml, 250ml and
parenteral nutrition with different 500ml bottle or bag
20%
special functions
30%
different lipid formulations may
20% MCT­LCT contain the following:
contains soybean oil (LCT) rich in
EFA
contain EFA, MCFA & LCFA
contain mixture of MCT and LCT
Rapid clearance and energy
production preference fuel in
conditions like carnitine
Isotonic
Mean globule size similar to
chylomicrons
Lipid Emulsion Contain fish oil 50ml and 100ml bottles
(fish oil)
Rich in EPA and DHA
Has anti­inflammatory and
immunomodulatory effect
All in One Features Presentation
All in One Three (triple) chamber bags with 1000ml, 15000ml,
Parenteral Nutrition separate compartments for amino 2000ml, 25000ml. bags
formulations acids, fat and a combination of
glucose or sorbital and electrolytes for
central or peripheral parenteral
Nutrition, depending on the
osmolarity and specifications.
Vitamins and minerals are added into
the bag prior to infusion.
Two chamber bags Two chamber bags with separate 1000ml, 1500ml,
compartments for amino acid and 2000ml bags
glucose with or without electrolytes.

pg. 75 by Osonga
Other nutrients may be added i.e. fat,
vitamins, trace elements as per the
specifications
Vitamins Contains all the water soluble and or 10ml vials
fat soluble vitamin based on
9 water soluble 10ml ampules.
international recommendations.
vitamins
These are added into the parenteral
4 fat soluble
nutrition product prior to infusion,
vitamins
once daily.
Water soluble vitamins to be added
into water base products e.g.
Dextrose, amino acids or the all in
One PN bags but NOT to be added
into the single bottle of fat emulsion.
The fat soluble vitamins can only be
added into the fat emulsion bottle or
the All in One PN bags
follow instructions as specified
Trace element in adults for parenteral 10ml ampoule
nutrition based on international
Trace elements 1ml, 3ml, 10ml vials
recommendations e.g. zinc, copper,
chromium, manganese, selenium.

pg. 76 by Osonga
DIET THERAPY UNIT III: MEDICAL RECORDS

Table12: Pediatric Parenteral Nutritional Formulations


Feed Composition per 10 0mls Presentation
Special AA for Well balanced AA pattern 100ml, 250ml and 500ml
pediatrics specifically designed for infants bottles.
(preterm, new born, babies) and
6.5% (65g AA/l)
young children
7% (70g AA/L) Dosage: As per the child’s
Contains EAA and NEAA
age, weight and
10% (100g AA/L)
Similar to human breast milk recommendations
Contains taurine an EAA for
neonates
Special Amino acids As above for children above 6 As above
for hepatic and renal months of age
Dosage: As per the child’s
failure
age, weight and
recommendations
Carbohydrate The carbohydrate solutions 100ml, 500ml bottles
solutions mainly contain glucose
Dosage: As per the child’s
(presentations as age, weight and
Above for adults) recommendations
Lipid emulsions As Adults 100ml bottles
Dosage: As per the child’s age,
weight and recommendations
Vitamins: As Adults 10ml vial
Water soluble Dosage: As per the child’s age,
vitamins weight
Requirements will be calculated
as per the child’s weight
Fat soluble vitamins A multivitamin preparation of 10ml ampoule
for infants lipid soluble vitamins for
Dosage: As per the child’s
parenteral nutrition for infants
age, weight and
recommendations
Trace elements for Trace element additive for 10ml vial
children in parenteral nutrition
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children based on international Dosage: As per the child’s


recommendations, to meet the age, weight and
basal requirements of trace recommendations
elements during intravenous
nutrition in infants and children

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Current formulations in the market have the three chamber bags for peripheral and central
parenteral infusion.
Vitamin requirements in Parenteral Nutrition
It is recommended that all adult/pediatrics PN patients, be supplemented daily with a standard
multivitamin package. Table 47 below provides the standard vitamin package/requirement for
parenteral nutrition.
Table13: Vitamin requirements in parenteral nutrition
Vitamins Daily Requirements
B1 3.0 mg
B2 3.6 mg
Niacin 40.0 mg
Pantothenic Acid 15.0 mg
B6 4.0 mg
Biotin 60,0 mg
Folacin Acid 400.0 mg
B12 5.0 mg
C 100.0 mg
A 3,300 IU
D 200 IU
E 10 IU
K 300­500 mg
* AMA Recommendation, JPEN 1979
** Nutritional advisory group, JPEN 1998
Note: Vitamin supplementations for pediatrics are calculated as per the child’s weight.

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Determining trace element requirements


The trace elements zinc, copper, chromium, manganese, iodine, iron, and selenium must be
provided in PN to prevent clinical deficiency. It is recommended that all adult PN patients be
supplemented daily with a standard trace element package as shown in the table below.
Table14: Recommendations for trace elements in parenteral nutrition
Adult patients mg/day µmol/day
Chromium (Cr) 0.010­0.015 0.19­0.29
Cobalt (Co)
Copper (Cu) 0.5­1.5 8­24
Fluorine (F) 1­3 53­158
Iron (Fe) 1­2 18­36
Iodine (I) 0.1­0.2 0.79­1.6
Manganese (Man) 0.15­0.8 2.7­ 15
Molybdenum (Mo) 0.015­0.030 0.16­0.31
Selenium (Se) 0.03­0.06 0.38­0.76
Zinc (Zn) 2.5­4.0 38­61

Monitoring of Parenteral Nutrition


This is necessary to assess whether the regimen is suitable for the patient and also to confirm
and, if necessary correct the prescribed regime. To prevent possible complications, for example,
catheter related complications and metabolic related complications
Be careful to check:
The general condition of the patient
Patient’s daily body weight ­ bed weighing scales may be practical to check body weight daily at
the same time.
Nitrogen balance
Fat elimination ­ check fat tolerance test and plasma triglycerides
Blood electrolytes ­ including phosphate
Blood glucose
Micronutrients in the long­term parenteral nutrition patients
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Summary of Parenteral Nutrition Guidelines in the Critical Care Unit


Source: JPEN 1998
All patients receiving less than target in 3 days enterally to receive PN within 24 to 48 hours of
admission once haemodynamically stable
NPE requirements to be calculated at 25 kcal/kg/d and increased to target over 2 – 3 days
Carbohydrate to be given at a minimum of 2g/kg/d as glucose, monitor blood sugars (BS), BS
>10mmol/l to be avoided
Lipids to be given at a dose of 0.7 – 1.5g/kg/d, EFA, EPA and DHA, live oil based, fish oil
added
Protein to be given at 1.3 –1.5g ideal body weight (IBW)
Amino acid solution should contain glutamine at a dose of 0.2 ­.04g /kg/Bodyweight/d (0.3 –
0.6g alanyl­glutamine dipeptide)
Daily dose of multivitamin and trace element to be adhered to
PN admixtures to be administered as a complete All in One bag. If there is evidence of PEM on
admission and enteral nutrition is not feasible, it is appropriate to initiate parenteral nutrition as
soon as possible following admission and adequate resuscitation
If a patient is expected to undergo major upper GI surgery and EN is not feasible, PN should be
provided under specific conditions: If the patient is malnourished PN to be given 5­7 days
preoperatively and continued into the postoperative period
Wean PN gradually
Discontinue once the patient is able to adequately tolerate 60% of caloric requirements enterally

TOPIC. INBORN ERRORS OF METABOLISM­GENETIC DISORDERS IN IFANCY

GENETIC DISORDRS HAVING NUTRITIONAL IMPLICATIONS

MAPLE SYRUP URINE DISEASE (MSUD)

 It is also called branched chain ketoaciduria


 MSUD is an inherited disorder affecting branched chain amino acids (the building
blocks)
 The condition gets its name from the distinctive sweet oduor of affected infants urine
(particularly prior to diagnosis and during times of acute illness)
 Enzyme affected: Branch chain alpha keto acid dehydrogenase complex that is
responsible for the breakdown of amino acids (leucine, isoleucine and valine)

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SYMPTOMS

Beginning in early infancy this condition is characterized by

 poor feeding
 vomiting
 lack of energy (lethargy)
 developmental delay
 Presence of sweet smelling urine

If left untreated MSUD can lead to:


 seizures
 coma
 hypoglycemia
 keto acidosis
 opisthotonos(severe spasm in which the back arches and the head bends back)
 pancreatititis
 neurological decline

MSUD is caused by deficiency of the branch chain alpha keto acid dehydrogenase complex
(BCKDC) leading to build up of the branched chain amino acids (leucine isoleucine and valine)
and their toxic by­products in the blood and urine

Infants with this disease seem healthy at birth but if left untreated suffer severe brain damage and
eventually die within the first five months in severe cases of the diseases (when left untreated)

Diagnosis
 Presence of sweet smelling urine
 Blood test to determine the levels of leucine, isoleucine and valine
 Urine test for ketones

Management
 Low protein diet (leucine, isoleucine and valine).This is a must as all natural protein
contain these enzymes
 Adequate energy to prevent the body from breaking up muscle protein that may lead to
metabolic stress
 Supplementation of calcium
 MSUD patients with anorexia, diarrhea or vomiting must be hospitalizes for intravenous
infusion of sugars and for nasogastric drip formulae
 Liver transplantation at younger age as it completely and permanently normalize
metabolic function enabling discontinuation of nutritional supplements
 Close dietary monitoring of pregnant women with MSUD to prevent detrimental

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abnormalities in development of the embryo or fetus

PHENYLKETONURIA (PKU)
 It is metabolic genetic disorder characterized by impaired activity of the liver (hepatic)
enzyme, phenylalanine hydrolase (PHA) which oxidizes phenylalanine to tyrosine
rendering it non­ functional
 It is a genetic disorder in which the body cannot process part of a protein called
phenylalanine into tyrosine thus result into a buildup of phenylalanine in the body (blood)
 Phenylalanine is almost in all foods(It is high in animal and plant protein) and in artificial
sweeteners

Complications of PKU

The disease is expressed at 3 to 6 months of age if not treated within 3 weeks of age and result
into accumulation of phenylalanine or deficiency of tyrosine. Accumulation of phenylalanine or
deficiency of tyrosine affects central nervous system and result into
 Mental retardation(lack of normal intellectual capacities)
 Brain function abnormalities
 Microcephaly(abnormally small head and underdeveloped brain)
 Mood disorders
 Eczema(inflammation of the skin)
 Hyperactivity
 Musty oduor( smelling of mold)
 Irregular motor functioning
 Seizures

Diagnosis
 Newborns with blood Phenylalanine concentration greater than 2 mg/dl on screening are
scheduled for confirmation test. In USA all newborns are screened for PKU

Management
 The objective of nutrition therapy is to maintain blood phenylalanine concertation that
will allow optimum growth and brain development.

PKU in br eastfeeding mother with a nor mal baby; PKU in both the mother and
br eastfeeding child; PKU in a baby being br eastfed by a nor mal mother
o In all these scenario, Infants may still be breastfeed to provide all of the benefits of breast
milk
o But in PKU baby’s, the quantity must also be monitored (e.g. breastfed twice a day if the
blood phenylalanine level of the child is high. This should be supplemented with low
phenylalanine milk substitute to prevent clinical manifestations
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o Supplementation for missing nutrient will be required.


o PKU mothers should keep their phenylalanine level low through dietary control

Breast milk is low in phenylalanine than cow’s milk. Blood level of the baby’s phenylalanine
level must be monitored through lab tests

Diet for infants, older childr en and adults

Adequate energy

Provide foods low in phenylalanine that includes


o Restricting or eliminating foods high in protein e.g. meat chicken, fish, eggs, nuts,
cheese, legumes, milk and other dairy products
o Provide 20 to 70 mg/kg of phenylalanine of body weight and this requirement declines as
the child grows
o Provide 180­200 mg/kg/day of tyrosine (an essential amino acid) for infant and 120­150
mg/kg/day for children and adults
o More fruits and vegetables since they provide very low phenylalanine
o Jams, sweets, cooking oils
o Fruits and vegetables (should be taken freely) since they provide very low phenylalanine
o Low protein breads pastas and cereals
o Aspartame, artificial sweetener contains aspartic acid and phenylalanine. It should be
avoided because phenylalanine is released during its metabolism. Aspartame is present in
many diet foods, chewing gums and soft drinks

It’s important that they stay on the diet for the rest of their lives

N/B. Exchanges of foods containing one gram of protein equivalent to 50 mg of phenylalanine

Proving a diet low in protein foods (low in phenylalanine) and supplementing tyrosine intake is
the best treatment for PKU. There are medical foods with low phenylalanine

GALACTOSEMIA

 This is a rare genetic metabolic disorder that affects an individual’s ability to metabolize
the sugar galactose properly thus resulting into accumulation of galactose in the blood
 Although the sugar lactose can metabolize the galactose, galactosemia is not related and
should not be confused with lactose intolerance

Cause
 Lactose in food (dairy products and milk) is broken down by the enzyme lactase into
glucose and galactose

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 In individuals with galactosemia, the enzyme needed for fur ther metabolism of
galactose ar e sever ely diminished or missing entir ely leading to toxic levels of
galactose and phosphate

Management

The only treatment for this is eliminating lactose and galactose from the diet i.e
 All products containing milk
 Milk products
 Omelets

Symptoms
 Speech difficulties
 Learning disabilities
 Neurological impairments e.g. tremors
 Ovarian failure in females

Long ter m complications


 Speech difficulty
 Ataxia/staggering
 Diminished bone density
 Premature ovarian failure
 Cataract

FRUCTOSURIA
 It is a rare hereditary disorder in which about 10­20 % of the fructose taken is excreted in
the urine
 In normal individuals, about 80% of the ingested fructose is converted to glucose and
glycogen when the rest is broken down to form lactic acid. In fructosuria, there is lack of
fructokinase enzyme that is needed for conversion of fructose into glucose.

Symptoms
 In fructosuria, infants are free of symptoms unless sugar (sucrose) is given. Then there
may be vomiting and hypoglycemic fits and a series of episodes may lead to jaundice and
enlargement of the liver. It is potentially fatal as liver failure may develop if the condition
is not recognized and treated

Management
 Sucrose and fruit should be excluded from the diet.
 Vitamin C supplements

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TOPIC: WEIGHT MANAGENT

ENERGY AND WEIGHT MANAGEMENT


 Weight management for a healthy living depends on energy output and input.
 If energy input is more than energy output you get a positive energy balance thus an
increase in weight whereas if energy input is less than energy output you get a negative
energy balance thus decrease in energy.
 For proper weight gain you need a positive energy balance and a negative energy balance
for weight loss therefore
o Energy balance = Energy intake – energy output

Component of weight
 Body weight = Bone + muscle + Organs + body fluids + Adipose tissue.
 Water consistent 60 – 65% body weight whereas adipose tissues varies through weight
gain and weight loss.

Adipose (fat) tissue – The primary form in which energy is stored. (Energy is stored in
the form of glycogen­that last only 12­36 hours; Muscle mass; and adipose (fat)
tissue).Adipose tissue fat is in form of triglycerides in the fat cells. Adult female require
an appropriate body fat of 20 – 25% body weight and 12% of this should be essential
including that of breast, thighs and pelvic region.
Adult male require 12 – 25% of body weight with 5 – 7% as essential fat.
Essential fat is stored both in bone marrow, lungs, kidney, intestines, muscles, brain,
heart and liver.

Stor age fat – Fat that accumulates under the skin and internal organ and prevent them
from traumas.
Fat cell development
 Adipose tissues increases either by increase in the size of the cell (hyper tr ophy) or
increase in the number of fat cell (hyper plasia) or a combination of hypertrophy and
hyperplasia.
 Obesity is usually characterized by hypertrophy and fat deposits can expand up to 1000
times.
 Once fat cells are formed they are permanent and cannot be decreased in their numbers.
 After weight loss, the reduced cell size is unhappy and seeks to restore normal volume
hence the risk of weight gain.

Over weight and Obesity


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 Overweight refers to a state in which the weight exceeds a standard based on height. (It is
a condition of excessive fatness).

Types of obesity
 Obese (equals or more than 30)
 Obese class I (30.0­39.9
 Obese class II (35.0­39.9).
 Obese class III (equals or more than 40)

Central obesity­It is where someone is obese and most of the fat is located in the central
abdominal parts of the body.(Obesity where there is a visceral fat in the body mostly the
abdomen).
N/B. Visceral fat (fat that collects deep within the central abdominal area of the body) may lead
to diabetes, stroke, hypertension and coronary artery disease. The risk from all causes may be
higher for those with central obesity than for those whose fat accumulates elsewhere in the body.
Assessment of weight
Weight can be assessed by the following methods.
 BMI
 Waist Hip r atio Waist cir cumfer ence: It is a good indicator of fat distribution and
the best tool for evaluating central obesity/abdominal fat. Women with a waist
circumference ≥35 inches (88.9 cm) and men with a waist circumference greater than
40 inches (101.6 cm) have a high risk of central obesity – related health problems.
 Ideal body weight
 Per centile Char t for childr en
 Skinfold measur ement­ Provide an accurate estimate of total body fat and a fair
assessment of the fat’s location. About half of the fat in the body lies directly beneath
the skin, so the thickness of this subcutaneous fat is assumed to reflect total body fat.
Measures taken from central body sites (around the abdomen) better reflect changes
in fatness than those taken from upper sites (arm and back).

Causes of pr edisposing/r isk factor s to obesity and over weight


 Overweight and obesity are consequences of energy imbalance due to diet high in
energy/diet high in fat.

Her editar y/Genetics


 Obesity tends to run in families the probability of becoming obese when you have a lean
parents is 9 – 14% and 41 – 50% when you have a lean and obese parent. When you have
obese parents 66 – 80%.

Physiological factor s
 Inability to respond to hunger and satiety may lead to obesity and overweight.

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Hor monal factor s


 Play a role on how a person may eat e.g. during stress you may eat less.

Regulator y dysfunction
 Some people respond to external cues than internal cues e.g. if given appetizing food
some people are unable to resist over eating.

Inactivity
 Poor physical activity is a risk factor to obesity and overweight.

Health Risks Associated with over weight and obesity


Health risks increase as BMI falls rise above 24.9. Independently, factors such as smoking habits
raise health risks, and physical fitness lowers them.
 Excess weight contributes to hyper tension thereby increasing the risk of heart attack and
strokes. Obesity raises blood pressure in part by altering kidney function and promoting
fluid retention.
 Increased risk of type 2 diabetes. Most adults with type 2 diabetes are overweight or
obese, and these cause some degree of insulin resistance.
 High blood lipids
 Cardiovascular diseases
 Sleep apnea (abnormal ceasing of breathing during sleep)
 Osteoarthritis
 Abdominal hernias
 Some cancers
 Varicose veins
 Gout
 Gallbladder disease
 Kidney stones
 Respiratory problems
 Complications in pregnancy and surgery

Management of obesity and over weight


There are ways of management – diet, regular physical activity, behavior modification and
surgery.
1. Diet
 Ener gy­Calorie restricted diet is needed to achieve negative energy balance. It should
be nutritionally adequate except for energy which should be low to a point where fat
stores are mobilized. Most adults will loose weight at intakes of 1200 – 1300kcal/day.
However diet less than 1500 kcals pauses a risk since it is likely to lead to excessive

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loss of lean tissues.


 Pr otein: To preserve lean body mass, daily protein intake should be in the range of
0.8 to 1.2 g/kg of body weight
 Fat: Fat should account for 20% to 30% of total energy. Saturated fats should be
limited to less than 6% to 8% of total fat energy. Diets with low to moderate fat
intake (15% to 30% of total energy) tend be lower in total energy and highest in diet
quality when compared to low­carbohydrate diets.
 Car bohydr ates: Carbohydrates should account for 50% to 60% of total energy.
Carbohydrates can help prevent the loss of lean tissue.
 Calcium: A review of evidence suggest calcium intake lower than the recommended
level is associated with increased body weight. The research suggests that a calcium
rich diet especially one that include dairy sources(with limit to total calories) not only
helps young women keep weight in check may reduce overall levels of body fat.
Calcium may depress certain hormones which consequently improves the body’s
ability to breakdown fat in cells and slow fat production
 High fiber diet.

N/B. Benefits of high fiber­Low in calorie, High in minerals and vitamins especially greens, give
satiety, help in regulating bowel movements, reduce blood cholesterol, promote chewing and
decreases rate of ingestion/constipation
 Adequate water /fluids: in weight management, water is to satisfy thirst. Water helps
with weight management in several ways

o Food with high water content increase fullness, reduce hunger and
consequently reduce energy intake
o Drinking a large glass of water before a meal may ease hunger, fill the
stomach, and reduce energy intake/food intake. Water adds no kcalories, and
it helps the GI tract adapt to a high fiber diet.

2. Regular physical activity


 The burning of kcals is influenced by duration and frequency of physical activity.
Exercise can help increase BMR, manage stress and increase vascularity of blood vessels.

Benefits of r egular physical activity


 Improve cardiovascular functions.
 Increases HDL and lower insulin resistance.
 Lead to weight loss.
 It regulates appetite and increases BMR.
 It decreases stress especially diet related.
 Increases bone mineralization thereby decreasing the risk of bone weakening.

3. Behavior Modification (e.g. watching TV, r ate of chewing)


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 It helps control energy intake and weight loss. It involves self­evaluation to identify the
behavior that is bringing the weight gain.

4. Bar iatr ic sur ger y


 It advised for patients with a BMI of more than 40 or for diabetic obese patients with
BMI of 35­40. Bariatric surgery is where the volume of the stomach is reduced mostly
through gastric bypass

Rate and extent of weight loss


 It’s recommended to loss ½(0.5) kg/weight leading to a loss of approximately 10% of
weight reduction and this can be achieved by reducing kcals intake by 500kcals to
1000kcals/day.
 The final goal should be individualized and realistic e.g. for people with morbid obesity,
ideal body weight or BML may not be realistic.
 WHO recommends a weight loss of 0.5­1kg per week

Advantages of weight loss


 Reduction in blood pressure
 Reduces total cholesterol and LDL cholesterol
 Increases in physical activity that comes with more benefits
 Lower blood glucose level
 Reduced risks of diabetes mellitus, heart diseases and cancer

Theor ies that explain weight gain


1. Lipostatic theor y

It is a long term theory, it involves a feedback mechanism where a signal from the adipose mass
is released when normal body composition is disturbed.
It is higher in younger people than older people and mostly occurs when weight loss has been
experienced.
2. Set point theor y

Each person has an ideal biological weight or set point weight. Once body weight reaches this
point, a whole set of signals/ regulation mechanism is produced that influences the persons food
intake to maintain this weight/ return to the set point weight.
It has been noted that many people who lose weight quickly regain all their lost weight,
suggesting that the body somehow chooses a preferred weight and defends that weight by
regulating eating behaviors and hormonal actions. Research confirms that the body adjusts its
metabolism whenever it gains or loses weight – in the direction that returns to the initial body
weight/set point weight.
If this theory is true some forms of obesity could be due to abnormally established set points.
3. Glucostatic theor y
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It is a short term mechanisms and involves factors governing hunger, appetite and satiety. In a
fed state blood glucose level can raise as high as 100mg/dl while during hunger it can be as low
as less than 70mg/dl.
4. Hor monal factor s theor y

Hormonal imbalances such as reduction in thyroxin hormone will result in decreased BMR and if
food intake remains the same, this may lead to weight gain.
5. Fat cell theor y

Number of fat cells is determined early in life to provide space to store fat. Once they have been
formed, fat cells have a tendency to remain full of fat. A child onset obesity or overweight may
be because of increased number of fat cells while an adult onset obesity or overweight may
because of an increase in size of fat cells
Body types /Types of fat deposits/Regional distr ibution of adipose tissue
Each one of us inherits a unique body type
i. Ectomor phs ­ are generally tall and thin and have long arms and legs.

These people have difficulty gaining weight and muscle no matter how much they eat or how
hard they weight train. They have the body type you tend to see in ballet dancers, runway
models, long­distance runners, and some basketball players. A very small proportion of the
population has this type of body.
ii. Mesomor phs ­ are generally muscular, shorter, and have stocky arms and legs.

These people are strong and tend to gain muscle mass when they do strength training. They may
find it difficult to lose weight. They excel in power sports like soccer, softball, vaulting in
gymnastics, and sprinting events in track and field.
iii. Endomor phs ­ are generally shaped like apples or pears and carry more body fat.
Gynecoid type (pear shape)/female type
Common in women. Characterized by pear shape with heavier deposits around the buttocks, hips
and thighs (heavier deposit below the waist than above the waist) and are assumed to be energy
reserve to support pregnancy and lactation.
Andr oid type (Apple shape)/male type
Common in men. Characterized by apple shape with heavier fat deposits around the waist, above
the waist and around the abdomen and is associated with significance risk of cardiovascular
diseases and non­insulin dependent, diabetes mellitus and heart attack.
Their bodies resist losing weight and body fat no matter how restrictive they are with their
eating. In fact, the more they “diet,” the more their metabolisms slow down to resist weight loss.
These people are better able to handle long periods of starvation and famine (which was a benefit
to our ancestors). In sports they excel at are distance swimming, field events, and weight lifting

N/B. Weight gain in the area of and above the waist (apple type) is more harmful than weight
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around the hips (pear type

UNDERWEIGHT
This is when a patient, adult has BMI less than 18.5
Health risk factors of low body weight.
 Increase in morbidity and mortality due to lowered resistance and infection and injuries.
 Under functioning of some glands e.g. Pituitary, thyroid adrenal and gonads which could
lead to infertility and loss of menstruation.
 Chronic fatigue.
 Anemia
 Psychological problems e.g. Anorexia, bulimia, depression, anorexia nervosa.

 Underweight and significant weight loss are also associated with osteoporosis and bone
fractures

Causes of under weight


1. Inadequate intake of calories to meet activity needs.
2. Excess activities or compulsive athletic training.
3. Poor absorption and utilization of food.
4. Metabolic and pathological condition/diseases e.g. HIV, cancer, TB
5. Psychological or emotional stress e.g. nervosa and bulimia

Management of under weight


Assessment of the cause and extent of the underweight should be done before starting any
treatment. The diet should be high in energy and protein to build the muscles.
Str ategies of weight gain
Ener gy. For increasing weight the total calorie intake should be in excess of the energy
requirement. An additional 500kcals per is recommended this will result into a weekly
gain of 1/2kg or
Limiting low calorie foods or by enriching the foods/giving energy dense foods e.g.
adding sugar, honey.
Pr otein: Instead of 1 g of protein, over 1.2 g per kg is recommended for tissue building
Fats: Increased fat is recommended. Easily digestible fats are recommended. Fried foods
and fatty foods are not recommended as they may cause diarrhea. Fatty foods should not
be taken at the beginning of a meal as they reduce appetite. High calorie fatty foods such
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as cream, butter, margarine and oils help to increase weight


Carbohydrates: High carbohydrate sources must form the basis of the diet.
Fluids: Fluids should not be taken before or with a meal but only after a meal so that
food intake is not reduced
Regular meals, no skipping of meals at least 3 meals daily and if possible 6 meals a day.
Regular moder ate exer cise to stimulate appetite and build up muscles.

TOPIC: GASTRO INTESTINAL DISEASES


Intr oduction
The gastro intestinal tract also called the alimentary canal; is a long hollow tube that begins at
the mouth and ends at the anus.
It’s made up of the mouth, esophagus, stomach, small intestine, large intestine (colon) and
rectum. Other organs that lie outside the tract but support its work by secretion of important
enzymes and digestive fluids are gall bladder and the liver.
1. Disor der of the mouth/mouth pr oblems

Tissues of the mouth often reflect a person nutritional status. In malnutrition, tissues of the
mouth deteriorate and become inflamed and are more vulnerable to infection, injury, pain and
difficulties with eating. The conditions of the mouth are:
 Gingivitis

This refers to inflammation of the gums and the affected gums bleed during tooth brushing.
 Stomatitis

This refers to the inflammation of the oral mucosa lining of the mouth.
 Glossitis

Refers to inflammation of the tongue whereby there is wounds in the tongue.


 Cheilosis

Refers to the cracking at the corner of the mouth affecting the lips and the corner angers making
opening of the mouth to receive food difficult.

Nutr ition implications


1. Reduced food intake and difficulty in swallowing (dysphagia).
2. Loss of blood.

Management
1. Nutr ition ther apy

Give high protein diet for wound healing

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High caloric liquid and then soft food (diet)


Give non acidic and without strong spices to avoid irritation.
Do not give hot foods which may cause pain
Give foods reach in vitamin C and iron
Give small quantity of food but at a frequent interval
2. Medical ther apy

Use of mouth washes before meals to relieve pain


Use of antibiotics

2. Esophagus pr oblem/disor der s


Esophagus is a long muscular tube lined with mucus membrane that extends from the
pharynx/throat to the stomach. It has 2 sphincters that control the movement of food into the
esophagus and into the stomach that is the upper and lower sphincter and it’s about 25cm long.
Lower esophageal sphincter pr oblems
Achalasia
This is where the lower esophageal sphincter (LES) does not relax normally when presented with
food during swallowing, thus resulting into obstruction at the gastro­esophageal junction ie it’s a
disorder in which the esophagus is less able to move food towards the stomach.
Nutr ition implications and signs
1. Dysphasia (difficulty in swallowing)
2. Regurgitation
3. Chest pain
4. Heart burn
5. Weight loss

Management
1. Give nutrient dense liquid and semi solid foods taken at moderate temperature.
2. Give small quantities of food but at frequent intervals.

Gastr o esophageal r eflux diseases (GERD)


This refers to the backflow/regurgitation of gastric contents from the stomach into esophagus.
The regurgitation of the acid gastric contents into the lower part of the esophagus causes
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irritation (burning sensation) of the walls of the esophagus as its wall do not have linings to
prevent it from the acid.
Signs and symptoms
 Heart burn
 Regurgitation
 Chronic bleeding and aspiration which may result into coughing and dyspnea
 Sour throat
 Excessive belching
 Frequent throat clearing
 Breathing problems (sinusitis)
 Dysphagia

Causes of GERD
1. Pregnancy (estrogen and progesterone) can reduce LES pressure thus causing the valve
separating the esophagus and stomach not to close properly.
2. Hiatel – hernia
3. Obesity
4. Nasogastric tubes can cause aspirations
5. Use of some drugs to treat certain conditions
6. Radiation such as for lung cancer treatment
7. Aging
8. Fungal infection
9. Stress

Aims of nutr itional management


 Prevent irritation of the oesophageal mucosa in the acute phase
 Prevent oesophageal reflux
 Decrease the irritating capacity or acidity of gastric juice

Management of GERD
1. Nutr ition ther apy – nutrition plays a major role in the management of GERD
 Provide low fat food and small frequent meals
 Avoid acidic foods such as citrus fruits, tomato products, coffee, carbonated drinks,
alcohol and spices.
 Iron supplements/iron rich foods for chronic bleeding
 Avoid large meals at night
 Reduce weight if overweight
 Avoid smoking as it triggers acid production

N/B Symptoms are aggravated by lying down or by any increase of abdominal pressure e.g. tight
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clothing
2. Medical ther apy – Many people do use anti acids and other drugs e.g. omeprazole but
the use of antacids has a nutritional complications e.g.

They have effects on the absorption of vitamin and iron and therefore it should be taken at least 2
hours before/after iron supplementation.
Effects of the aluminum containing anti acids may be decreased by high protein meals.
Folate absorption/utilization may be impaired by anti acids thus resulting into neural tube defects
as well as genital abnormalities of the heart, palate and urinary tract. Provide folate
supplementation to offset the increased risk.
Prolonged anti acid used with excessive consumption of calcium may cause high calcium levels
that may result into serious metabolic diseases.
3. Mechanical management
 Reduce weight
 Avoid bending/leaning over or lying down immediately after meals
 Avoid tight clothing
 Elevate head of bed/use pillows

Lifestyle
 avoid smoking as it triggers acid production
 Avoid alcohol

N/B (LES­ is a valve at the entrance of the stomach. LES closes as soon as food passes through
it. If LES does not close all the way or if it happens too often, acid produced by your stomach
can move up into the esophagus causing a burning chest pain called heartburn. If acid reflux
symptoms happens more than twice a week then you have acid reflux disease also known as
GERD

Hiatel – her nia


This is where a portion of the upper part of the stomach protrudes through the hiatus (diaphragm)
into the chest.
Diagr am

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Food is easily held in this herniated area of the stomach and mix with acid, then regurgitated
back up into the lower part of the esophagus. Gastritis (inflammation of the lining of the
stomach) may occur in the herniated portion of the stomach and cause bleeding and anemia
Symptoms as in GERD
Management
As in GERD
Large hiatal hernia may require surgical operation
Other esophagus pr oblem: Esophagitis­This r efer s to the inflammation of the esophagus
usually caused by GERD

3. Pr oblems of the stomach and duodenum


i) Peptic ulcer disease
Definition of ter ms
Mucosa – Mucus secreting membrane lining all body cavities
Mucosal membr ane – a thin sheet of material that covers the organs or cavities
Sub mucosa – the connective tissue that lies below the mucosa membrane.
Ulcer – refers to the loss of tissue on the surface of the mucosa or ulcers are open sores or
lessons. They are found in the skin or mucus membrane of the body.
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Peptic ulcer is the general term for an eroded lining or sore of the lower portion of esophagus,
stomach and first portion of the duodenum (central portion of the GI tract). It occurs when these
central GI tract is corroded by pepsin (an enzyme produced by the cells of the stomach that splits
proteins into peptones. This enzyme is acidic in nature).The pepsin wears away the protective
mucus layer of the central GI tract. Ulcer can also be caused by HCL. A peptic ulcer of the
stomach is called gastric ulcer; of the duodenum, a duodenal ulcer. And of esophagus, an
esophageal ulcer.
Although there is much overlap, symptoms of a gastric ulcer may differ from those of a duodenal
ulcer.
i. Duodenal ulcer
 Pain may occur or worsen when the stomach is empty, usually two to five hours after a
meal.
 Symptoms may occur at night between 11 PM and 2 AM, when acid secretion tends to be
greatest.
 Duodenal ulcers is the most common and normally occur at age 20­30
 Patients with duodenal ulcers may gain weight from frequent eating to counteract pain.
ii. Gastr ic ulcer  
 Symptoms of a gastric ulcer typically include pain soon after eating.
 Symptoms are sometimes not relieved by eating or taking antacids.
 Normally occur at age 45­60
 Weight loss is common
Cause of peptic ulcer s
 Peptic ulcers is caused by helicobacter pylor i (H pylori produces urease which
neutralizes the stomach acid –from HCL and pepsin and allows H pylori to grow in acid
free zone. This enzyme also injure the cells of the stomach or duodenum) or
 Intake of non­ster oidal anti­inflammator y dr ug (NSAIDS) e.g. Aspirin, declophenac,
Panadol, brufen. They damage the stomach lining thus living the stomach vulnerable to
the effects of HCL and pepsin

Other risk factors include; they aggravate the existing ulcer


 Stress which causes vasoconstriction or reduced blood supply to the gastric mucosa
leaving it unprotected.
 Hereditary factors; Family history of ulcers is often in ulcer patients.
 Eating habits; eating hurriedly, improper mastication of food and skipping of meals.
 Irritants e.g. alcohol, cigarettes, caffeine and spices. Smoke has nicotine that concentrate
the HCL and induce increased production

Symptoms of peptic ulcer


 Painful hunger (burning, gnawing, aching) contractions usually in the upper
abdomen
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 Anemia
 Blood in the stools
 Hemorrhage
 Bloating
 Low plasma protein levels
 Vomiting
 Low weight in gastric ulcer and gain weight in duodenal ulcer.

NB: The amount of concentr ation of hydr ochlor ic acid is higher in duodenal ulcer s while in
gastr ic ulcer the amount and concentr ation is nor mal.

Management
Medical ther apy – take medicine regularly as prescribed e.g. Use of anti­ acids, antibiotics and
omeprasoles one to three hours after meals or before bed times.
Nutr itional management –
1. Limit the foods and seasoning that increase acid secretions/inhibit healing.
a) Caffeine (including coffee and strong tea) and chocolate, spices and black pepper
b) Unripe citrus fruits like oranges
c) Sour foods
d) Seasonings such as pepper, garlic, ginger, chilies and strong spices.

2. Avoid foods that are high in fiber that are irritating


3. Eat slowly
4. Give foods high in iron/iron supplements may be provided
5. Fat: a moderate intake of fat is beneficial since fat delays the empting of the stomach but
fatty foods should be avoided e.g. fried foods and fatty foods
6. Give small quantity but frequent meals to ensure that the stomach is not empty, at least 3
regular meals daily.
7. Protein: a high protein intake to promote healing of the wounds and to provide buffering
action
3. Eating less than 2 hours before bed time
4. Use of probiotics

Foods high in vitamin C, A, Protein, zinc enhance the healing of the gut wall

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NB 1: Milk (a historical food for peptic ulcer diseases) does not aid in ulcer healing and
actually pr omote gastr ic acid pr omotion i.e. Milk is an alkaline that neutr alizes the
stomach acid thus pr ovides a tempor ar y r elief however , it incr ease acid secr etion thus
delays the healing of the ulcer s. Other foods that incr ease acid secr etion ar e coffee, soft
dr inks and alcohol.
N/B 2. Fer mented milk is good in the pr evention of ulcer s as the pr obiotic (the live
bacter ia­e.g. lactobacillus bulgar icus) in milk pr events the gr owth of ulcer causing bacter ia,
H­Pylor i. Combining pr obiotic tr eatment with omepr azole, amoxicillin, and clar ithr omycin
in H pylor i–impr oves the tr eatment effectiveness, compar ed with dr ug tr eatment alone.

Some specific foods to be given ar e


 Cabbage­cabbage has anti­inflammatory effects.
 Spinach­ has low fiber.
 Potatoes: nutritive and anti­acid
 Okra: contain mucilage capable of protecting gastric mucosa
 Other vegetables are carrots.
 Fruits: apples, ripe bananas, avocado, pawpaw, pears, guava, orange juice
 Cereals: oat meal, porridge with low fibre, chapatti, macaroni, spaghetti, rice, matoke
 Tea­has flavonoids resposibles for healing effect
 Eggs e.g. scrambled
 However roast beef and lamp, stewed/ baked should be taken in moderation as they
contain pureness (that stimulate gastric mucosa)

Lifestyle habits:
 Avoid alcohol, cigarette smoking and NSAIDS
 Minimize stress as stress cause hyper secretion of gastric acid

N/B. Not everyone with “ulcer” symptoms has an ulcer. Symptoms similar to those of peptic
ulcers can be caused by a wide variety of conditions. The differential diagnoses of peptic ulcers
are:­
 Functional dyspepsia (i.e., the presence of ulcer­symptoms without a specific cause)
 Abnormal emptying of the stomach
 Acid reflux
 Gallbladder problems
 Much less commonly, stomach cancer.

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2. INDIGESTION (dyspepsia)

This refers to any discomfort in the digestive tract or it refers to a feeling of fullness or
discomfort during or after meal
It’s mainly caused by gall bladder disease, chronic appendicitis, ulcer, stress, rapid eating, poor
mastication etc.
Symptoms
 Discomfort in the digestive tract
 Feeling of fullness or discomfort during or after meal

Nutr itional implication


 Inadequate food and nutrient intake

Nutr ition ther apy/dietar y management


 Provide a well­balanced diet
 Avoid rapid eating and poor mastication of food
 Give plenty of water

3. Acute Gastr itis

This is a temporary inflammation of the gastric mucosa (the lining of the stomach). Unlike
chronic gastritis that develop slowly, acute gastritis occurs suddenly
Causes
 Overeating
 Overuse of alcohol and tobacco
 Chronic and excessive uses of aspirin/non­steroidal anti­inflammatory drugs (NSAIDS),
trauma and shock, fever, renal failure, burns, food poisoning, H pylori and chronic
vomiting etc.

Symptoms
 Nausea
 Vomiting
 Feeling of fullness in the upper part of abdomen
 Burning pain in your upper abdomen

Nutr ition implications


 Anemia
 Loss of nutrients
 Increased metabolism

Dietar y management
1. To allow the stomach time to rest and heal, withhold food for 24 – 48 hours or longer

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depending on whether there is bleeding or not.


2. Give fluids intravenously during this period.
3. Increase the amount of foods according to the patient’s tolerance until a full regular diet
is achieved.
4. Avoid seasoned foods.

4. Chr onic Gastr itis


This refers to a condition (gastritis) that occurs slowly overtime resulting into irreversible
atrophy of the gastric mucosa related to chronic inflammation.
Loss of mucosal cell functions may lead to lack of HCL in the stomach, anemia and malnutrition.
5. Damping syndr ome (r apid gastr ic emptying)
Damping syndrome is a condition where the lower end of the small intestine (jejunum) fills too
quickly with undigested food from the stomach. It develops after a survey to remove part of the
stomach usually pyloric sphincter/after surgery to bypass the stomach to help you loose weight,
bariatric surgery/weight loss surgery.
This causes partially digested food to rapidly enter jejunum too quickly (in an uncontr olled,
abnor mal fast manner ) causing hyperosmolar load.
Fluids from the intestinal capillarities enter the jejunum thus resulting into low blood pressure
and also stimulates peristalisis thus resulting into diarrhea.
Causes of the Dumping Syndr ome
 Gastric surgery – removal of part of the stomach/gastric bypass surgery

Symptoms
 Abdominal cramps
 Diarrhea
 Vomiting
 Bloating
 Sweating
 Rapid pulse rate
 Shortness of breath
 Weakness
 Dizziness and paleness

 Early dumping syndrome­It is where people develop signs and symptoms (diarrhea,
nausea, vomiting, bloating, shortness of breath and abdominal cramps) during or right

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after meal (10­30 minutes)


 Late dumping syndrome­ It is where people develop signs and symptoms 1­3 hours after
eating
 While others have both early and late symptoms

Nutr itional implications


 Loss of nutrients
 Weight loss

Nutr ition ther apy


 All fluids and foods by mouth should be withheld for 3 – 5 days and the patients feed by
Nasogastric tube
 Give pectin, a dietary fibre found in fruits and vegetables as it helps in treating dumping
syndrome by delaying gastric empting and slow carbohydrate absorption.
 Vitamin and mineral supplementation may be necessary.
 Serve liquids between meals rather with meals to slow the passage of the food mass.
 Limit simple carbohydrates
 Lie down immediately after eating to help slow the transit of food to the intestine but
clients with reflux should not lie down after eating.

4. Disor der s of the small intestine


1. Diar r hea and Malabsor ption
Diarrhea refers to an increase in frequency of bowel movements compared with the usual
pattern/excess water content of stools affecting consistency/volume/both.
Diarrhea is not a disease but a symptom of a medical condition either in the small intestine, large
intestine, pancreas or other conditions such as lactose intolerance, HIV, mal absorption and
irritable bowel syndrome etc.
NB: Gener al diar r hea may r esult fr om basic dietar y excess e.g. excess fiber /sugar .
Categor ies of diar r hea
Acute diar r hea – characterized by sudden onset and frequent passage of watery stool. It lasts for
24 – 48 hours.
Symptoms: abdominal pain, fever and vomiting.
Chr onic diar r hea – persist for a longer period of time and may last for several weeks.
Management
Medical ther apy
 Treat the underlying cause
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 Ors may be given in severe acute diarrhea.

Dietar y modification
 Give a low fiber diet, mostly simple carbohydrates
 Low fat diet (to avoid malabsorption)
 Bland diet: Spicy diet may cause irritation of the stomach.
 Plenty of fluids to provide for lost fluids and electrolytes
 Energy – increase energy if the diarrhea is accompanied by fever.
 Increased intake for vitamin for the loss of vitamins
 Increased mineral intake mostly sodium and potassium
 Small quantities of food at frequent intervals. Excess will cause pressure in the GIT

Malabsor ption
This is where there is interference with how nutrients are absorbed/digested
There are 4 malabsorption conditions
1. Celiac disease
2. Cystic fibrosis
3. IBD (inflammatory bowel diseases)
4. Short bowel syndrome

Celiac disease
It’s an inherited disorder that causes damage to the small intestine and interferes with the
absorption of the nutrients.
People who have celiac diseases cannot tolerate gluten, a protein found in cereal grains such as
Wheat, barley etc.
Gluten molecules combine with antibiotics in the small intestine causing the usually brush like
lining of the intestine to flatten thus affecting the digestion and absorption of foods.
Management
 Avoid food with gluten

Cystic fibr osis


It’s an inherited disorder that mostly affects the white people and can be classified as either
gastro – intestinal disorder or respiratory disorder
It’s where there is a high mucus secretion that obstructs endocrine glands, the lungs and ducts.
Symptoms
 Bulky, foul smelling, oily stool
 Malabsorption
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 Excessive sweeting in hot weather


 Thick mucus that accumulates on the endocrine glands, lungs

Nutr ition ther apy


 High energy diet
 High protein diet

Inflammator y bowel disease


The term inflammatory bowel is used to apply to two intestinal conditions that result into
inflammation of the bowel i.e. cr ohn’s disease and ulcer ative colitis
Pr edisposing factor s
 Hereditary
 Environment e.g. crohn’s disease is higher in industrialized areas
 Immune functions

Differ ence between cr ohn’s disease and ulcer ative colitis


Differ ence
Definition Cr ohn’s disease( a chr onic Ulcer ative colitis( a chr onic
inflammation of the intestine) inflammation of the lar ge intestine
that begins in the r ectum)
Cause Inadequate intake of food, zinc Unknown but it’s likely that intestinal
deficiency, malabsorption of fats and allergy caused by some food e.g. Milk
protein, fever may be responsible
Cite of Any part of the GIT (from mouth to Inflammation and ulceration of large
inflammation the anus) but mostly the small intestine(colon) that always begin in the
intestine. rectum .Rectal bleeding is common
The inflammation affects the GIT
from mouth to anus but may skip
certain areas
Symptoms:
Weight loss : common Weight loss: Common

Diar r hea: common (passage of loose Common (alternating periods of


stools with mucus and blood diarrhea and constipation)
accompanied by pain)
Steator r hea: sometimes it can result No steatorrhea
into loss of calcium, magnesium and
zinc.
Fever : yes No

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Other symptoms: anorexia, fatigue Loss of appetite, rectal bleeding,


cramping dehydration, electrolyte imbalance,
anorexia mal absorption

Cr ohn’s disease
Definition
 Cr ohn’s disease is a chronic inflammatory bowel disease that affect any part of the GIT,
from mouth to the anus, but the inflammation mostly occurs in the small intestine.

Cause:
 Inadequate intake of food
 zinc deficiency,
 malabsorption of fats and protein
 fever

Symptoms of Cr ohn’s disease


 Fatigue,
 Anorexia
 variable weight loss
 right lower quadrant pain or cramping
 diarrhoea
 steatorrhea
 Fever.
Nutr ition implications
 Inadequate food and nutrient intake
 Malabsorption and mal­digestion
 Increased nutrient needs
Aims of nutr ition management
 Restoration of good nutritional status
 Relief of discomfort

Management

Dietar y management
 During acute flare­ups bowel rest and parenteral nutrition is recommended
 Later in patients who cannot tolerate whole foods elemental oral formula maybe useful
 Energy and protein content of the diet should be high to promote healing and restore
weight. Provide 40 – 50Kcal/Kg, and for protein 1 – 1.5g/Kg
 Give a low fibber diet to minimize bowel stimulation
 Give small frequent meals that are better tolerated than three large meals, this may help

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maximize intake
 Assess status of calcium, magnesium and zinc since steatorrhea promotes their loss

Medical ther apy


 Drugs e.g. antibiotics
 Surgical operation mostly for people suffering from people suffering from ulcerative
colitis where the colon or rectum may be removed.

Nutr itionther apy


 Low fiber diet
 Give iron because of bleeding
 High protein diet for wound healing 1­1.5g/kg/body weight
 High calorie diet 40­50 kcal/kg body weight
 Low fat diet
 Small frequent meals
 Provision of vitamin A,C, E, B12, and Folate
 Provision of pro­biotic and pre­biotic to promote growth of flora in the colon and
intestine.
 Provision of calcium ,zinc and magnesium since steatorrhea promotes their loss

Ulcer ative colitis

Definition
 Ulcer ative colitis is a chronic inflammation of the large intestine (colon) that begins in
the rectum)

Cause: Unknown but it’s likely that intestinal allergy caused by some food e.g. Milk may be
responsible
Symptoms
 Passage of loose stool with mucus and blood accompanied by pain and spasms
 Loss of appetite
 Rectal bleeding
 Ulcerative lesions in the mucosa of the large intestines
 Dehydration
 Electrolyte imbalance
 Anorexia
 Malnutrition
Nutr ition implications
 Anaemia due to rectal bleeding
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 Increased nutrient needs


 Fluid imbalance
 Food mal­digestion and nutrient malabsorption
Aims of nutr ition management
 To relieve pain and inflammation
 To restore and maintain optimal nutritional status
Dietar y management
 Same as in Crohn’ disease. However, no dietary interventions seem to lessen disease
activity. And unlike Crohn’s disease where intestinal surgery fails to cure the disorder,
removal of the colon and the rectum does cure ulcerative colitis

Gastr oenter itis­This refers to the inflammation of the stomach and intestine
Shor t Bowel Syndr ome
 It is a malabsorptive condition that results after surgical removal of the parts of the small
intestine (usually 2/3 of the ileum and the ileocecal valve) with extensive dysfunction
of the remaining portion of the organ or it refers to malabsorptive condition that results
after surgical removal of more than 50% of the small intestine
 Ileocecal valve is the valve between ileum and the caecum. It prevents the backflow of
materials from the large intestine to the small intestine.
 Removal of some parts of the ileum and the valve promotes a transit time too rapid for
sufficient absorption of nutrients such as water, electrolytes, proteins, fats, carbohydrates,
vitamins and minerals thus resulting into malnutrition. Resection (sur gical r emoval of
about 50% of the small intestine) can be done to conditions such as crohn’s disease,
abdominal injury and traumas.

Management
 Enteral or parenteral nutrition as the small intestine adapts to its function( remaining
villi may enlarge and lengthen to increase the absorptive surface area of the
remaining intestine)
 Reduced fat intake as the remaining intestine adopts.
 Increased electrolyte intake, vitamin and mineral.

Disor der s of the lar ge intestine


1. Flatulence – refers to the condition of having excessive stomach/intestinal gas as a result
of swallowed air (when eating, swallowing and chewing gum) or production in the GIT.
Most swallowed air is expelled from the stomach by belching and is odorless. Some
travel into the large intestines and is mixed with the gas produced by the bacteria in the
large intestine and is expelled through the anus. Increased amount of rectal gas indicate

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excessive bacterial fermentation and suggest malabsorption of a fermentable substance


The unpleasant odor of the flatulence is as a result of the gases that contain sulphur
produced by the bacteria that mix with the odorless CO2, O2, hydrogen, nitrogen and
sometimes methane that are produced in the intestine or swallowed

Management
Medical ther apy
 Use of drugs

Nutr ition ther apy


 Reduction in the amount of gas swallowed(aerophogia)­aerophagia can be avoided by
eating slowly, chewing with mouth closed and refraining from drinking through straws
 Reduction in fiber intake and other foods that results into increased production of gases
eg beans, cabbage, broccoli, whole grains, milk and its products, onions, apples, pears,
potatoes and decrease in intake of food that contains artificial sweeteners e.g gums

NB: Rice is the only star ch that does not pr oduce a gas
2. Ir r itable Bowel Syndr ome
 A disorder where there is a recurrent abdominal pain and diarrhea that often alternating
with periods of constipation
 It differs from one person to another. Some experience only diarrhea or constipation
whereas others experience and alternating patterns of both.
 It’s more common with females than men.

Symptoms
 More than three bowel movements per day or fewer than three
 Lumpy/hard or loose/ watery stool
 Passage of mucus
 Bloating (swelling of the abdomen caused by excessive gas)

Management
 For constipation, give high fiber diet
 For diarrhea give low fiber diet

3. Diver ticular Disease


Diverticulum or diverticular is a small tubular sack that protrudes from the main canal or cavity
in the body (diver ticular r efer s to a small out pouching in the GIT i.e. fr om the esophagus to
the colon)
It is caused by pressure within the intestinal lumen which may be related to chronic constipation
and a low fiber diet
It can either be

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i. Diverticulosis – presence of multiple diverticular in the walls of the GIT mostly colon.
It mostly occurs in older adults.
ii. Diverticulitis – refers to the inflammation of the diverticular

The common term for the conditions is diverticular disease


Symptoms
 Gross bleeding
 Low Hb and albumin level
 Cramping of the stomach
 Alternating periods of diarrhea and constipation
 Bad breath
 Regurgitation and fever
 Dysphagia

Nutr itional implications


 Anaemia
 Increased nutrient needs
Aims of nutr ition management
 To restore nutritional status
 To relieve pain and enhance healing

Management
 Provision of high fiber for the management of the diseases and low fiber diet for the
diverticulitis
 High protein for repair of worn out tissues
 Low fat diets in acute cases, provide clear liquid diet with progression to a very low­
residue diet

5. Constipation
Refers to the retention of feces in the colon beyond normal empting time (or this is where bowel
movement become difficult or less frequent thus resulting into hard stool that is more difficult to
pass.
A person is said to be constipated if he/she goes longer than thr ee days without bowel
movement (without passing a stool) or when he passes dry or hard stool often or often having
difficulty pushing out stool
It is more common in older adults.
Causes
 Low fiber diet
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 Inadequate fluid/water intake


 Lack of exercise
 Changes in social settings
 Inadequate activity or exercise
 Stress/worries
 Overuse of laxatives (stool softeners) which overtime weaken the bowel muscles
 A disruption of regular diet or routine/change of diet
 Excessive/ prolong use of anti­acids containing calcium or aluminum
 Ignoring the urge to pass stool
 Some medications e.g. iron supplements

Management
To manage the problem, you need to make your stool softer by
 Increased fiber intake (both soluble and insoluble fiber), this is found in vegetables,
fruits and cereals
 Increased fluid intake
 Increased physical activities. Avoid sitting or lying down for long
 use of laxatives(medical therapy)

Other management strategies


 You also need to have a good toilet routine­go to the toilet at a regular time and place
where you feel comfortable
 Use the toilet when you feel the urge

Other conditions of lar ge intestine ar e acute and chr onic gastr itis, indigestion and the
hemor r hoids

Hemor r hoids (piles)


Hemorrhoids are swollen (enlarged) and inflamed veins in the rectum and anus that cause
discomfort and bleeding (they occur when the veins in the anus are enlarged)
Types of hemor r hoids
 Inter nal hemor r hoids­located inside the rectum. They cannot be seen or felt
(Not visible from outside). They are normally painless and rarely cause
discomfort. Straining when passing stool can damage the surface of the
hemorrhoid and cause bleeding (The first sign is rectal bleeding)
Occasionally straining can push an internal hemorrhoid through the anal opening.
This is known as protruding or prolapsed hemorrhoid
 Exter nal hemor r hoid­develops under the skin around the anus and therefore not

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visible. They are painful. Straining when passing stool cause them to bleed
Causes of hemor r hoids
 Straining during bowel movement
 Obesity
 Sitting for long period of time on the toilet
 Pregnancy­increases pressure on the anus veins during later period of pregnancy
(as the uterus enlarges, it presses on the vein in the colon, causing it to bulge)
 Chronic diarrhea
 Chronic constipation
 Anal intercourse­ can cause or worsen existing ones
 Aging­It is most common among the adults aged 45­65 years. However the young
people and children can also get it
 Low fiber diet
 Lifting heavy objects repeatedly
 Genetics­Some people inherit tendency to develop hemorrhoids

Symptoms
 Discomfort during bowel movement or sitting
 Swelling around the anus
 Bleeding during bowel movement
 Itching in anal region
 A lump near the anus (protruding from the anal region)
 Feces may leak out unintentionally

Pr evention
 Nutrition therapy­high fiber diet( more fruits, vegetables and whole grains) to
soften stool and increase its bulk thus avoiding the straining caused by
hemorrhoids
 Drink plenty of water
 Fiber supplementation
 Stool softeners
 Do not strain­Straining and holding your breath when trying to pass a stool
creates greater pressure in the veins of the lower rectum
 Go to the toilet as soon as you feel the urge. This prevents the stool from
becoming dry and harder to pass
 Exercise to prevent constipation and reduce pressure on veins
 Avoid long periods of sitting more so on the toilet. Long periods increases
pressure on the veins of the anus
 Sufficient rest
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Tr eatment
 Nutrition therapy­High fiber diet, Increased protein, increased iron intake,
increased vitamin C, increased intake of water
 Use of cream and ointment containing hydrocortisone
 Ice parks and cold compress­ applied to the affected areas may help with swelling
 Moist towelettes­dry toilet paper may aggravate the problem
 Analgesics­painkillers e.g. aspirin, ibuprofen to alleviate pain
 Surgical operation

TOPIC: LIVER DISEASES

TOPIC: DISEASES OF THE LIVER AND THE GALLBLADDER


(A) DISEASES OF THE LIVER
Anatomy of the Liver :
 The Liver is the largest internal organ in the body and the second largest organ of the body
after the skin, located just below the diaphragm.
 The liver lies to the right of stomach and overlies the gallbladder and it weighs about 3.2­3.7
pounds (1.44­1.66 Kgs).It is also the largest gland in the human body.
 It is called a gland because it secretes chemicals that are used by other parts of the body
 The liver is part of the biliary system, which includes the gallbladder and the pancreas.

A diagram of the liver, gallbladder and pancreas in the body

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Note:
1. The liver has an impor tant bear ing on ones nutr itional status as the disease of this
or gan has dir ect effects on metabolism of nutr ients
2. The liver is connected to two lar ge blood vessels. 1. The hepatic por tal vein that
car ies blood containing digested nutr ients fr om the entr e gastr ointestinal tr act,
blood fr om the spleen and blood fr om the pancr eas. 2. The hepatic por tal ar ter y
car r ies blood fr om aor ta

Functions of the liver :

The functions of the liver can be grouped into three main categories.

1. Manufactur ing functions


1. Protein synthesis e.g albumin (protein for the blood stream that is required to
maintain fluid within the circulation system) and blood clotting factors
2. Synthesis of glycogen from glucose. Glucose is synthesized into glycogen when the
supply glucose is in excess and the glycogen can be stored both in the liver and in the
muscle cells.
3. Synthesis of cholesterol
4. Synthesis of triglycerides.
5. Production of bile that is essential for fat metabolism
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6. Production of special proteins that carry lipids in circulation


2. Stor age functions
1. Storage of vitamins ( Vitamin A­for vision and immunity, D­for absorption of
calcium, K­for clotting of blood, B12 and folic acid)
2. Storage of iron (For production of red blood cells)­Most of the iron is stored in the
liver
3. Storage of glycogen­It is released when the extra energy is needed by the body

3. Waste disposal/detoxification

1. The liver plays an important role in detoxifying the body by converting


ammonia, a toxic by­product of metabolism from dietary protein and muscle tissue into
urea that is excreted by the kidneys as urine.

2. Drugs, medicines and alcohol are metabolized and detoxified by the liver

3. Breaking down of insulin, hormones and red blood cells and helps in the
removal of waste products from the breakdown of these products e.g. bilirubin from the
breakdown of red blood cells

Liver Diseases (Liver disease is any condition that affects liver


function.)
1. Hepatitis
2. Liver cirrhosis
3. Alcoholic liver disease
4. Liver cancer
5. Hepatic failure/ liver failure

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1. HEPATITIS
 Hepatitis is an infectious disease characterized by inflammation and degeneration of
the liver cells that affect the livers ability to function. Hepatitis viruses are the most
common cause of hepatitis in the world but hepatitis can also be caused by toxic
substances (e.g. alcohol, certain drugs), other infections and autoimmune diseases
Types of hepatitis
There are five types of hepatitis, hepatitis A, B, C, D and E but the most common
hepatitis are A, B and C.
1. Hepatitis A. It is caused by hepatitis A virus (HAV). Sour ces of
contamination: Contaminated water and food or from close contact with
someone who is infected. It is mild and do not always progress to chronic
state. Most people infected recover without being treated nor showing the
signs.
2. Hepatitis B. It is a serious liver infection caused by hepatitis B virus (HBV)
and it can progress into chronic stage and thus develop into liver failure, liver
cancer and liver cirrhosis (a condition that causes permanent scarring of the
liver.
N/B. There is no cure for hepatitis B but there is a vaccine to prevent it
Mode of tr ansmission of hepatitis B:
1. Sexual contact with infected person, through blood, saliva, semen, or
vaginal secretions, blood transfusion and by sharing of infected needles
2. Mother to child during birth
3. Hepatitis C. It is caused by hepatitis C virus (HCV). .Most people infected
with hepatitis C (HCV) have no symptoms until liver damage shows up after a long period of
time.

Symptoms of hepatitis
Anorexia, weakness and fatigue, joint pain, loss of appetite, jaundice (yellowing of
skin and the whites of the eyes {due to the accumulating of the bile pigment
(bilirubin) in the blood}, vomiting, diarrhea, fever, weight loss and abdominal pain

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Management
1. Nutrition therapy­hepatic diet
 High energy diet because of the degeneration of the organ, fever and for weight gain.
E.g. glucose and honey can be added to food
 Protein intake: Protein intake depends on the extent of liver damage. High protein diet
for mild and moderate cases for repair and synthesis of new tissue. Give low protein
(High biological protein) in a cute cases and when the extent of damage is extensive as
the damage liver may not be able to convert all the ammonia into urea. We also give
low protein diet to minimize the production of ammonia
 Low fat diet because of impaired bile secretion. Emulsified fat like from whole milk,
butter and eggs can be given as less bile is required for their emulsification. Avoid
fried foods, fatty foods
 High vitamins especially A,D,E,K due to decrease and impaired absorption of fat as
this vitamins need fat for their absorption
 Increased vitamin C intake for tissue leaching
 Other diet modification to manage the symptoms such as vomiting, diarrhea
 Tube feeding and parenteral feeding in severer cases
 Avoid alcohol
2. Medical therapy: Use of drugs and medicines

3. Lifestyle
E.g. good hygiene, use of protection during sexual intercourse and by not sharing needles

2.LIVER CIRRHOSIS/ SCARRING (FIBROSIS)


This is a chronic disease of the liver in which a fibrous connective tissues replaces the healthy
functioning cells. It is characterized by destruction of the cells thus resulting into an abnormal
structure. It happens after the healthy cells are damaged over a long period of time, usually many
years. (Cirrhosis is the advance stage of liver disease)

There’s no cure for cirrhosis except a liver transplant, but you and your doctor can slow cirrhosis

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down by treating whatever is causing it.

What Causes Cir r hosis?

Chronic alcoholism is the main cause of liver cirrhosis. This disease can also develop as a result
of other liver conditions or diseases you already have. They include:

 Chronic Alcoholism is the main cause of liver cirrhosis. Alcohol and metabolic
products interfere with liver metabolism and damages liver cells directly. This results
into  fatty liver, inflammation and replacement of liver cells by fibrous connective

 Viral hepatitis mostly Hepatitis C and B

 Obstruction/ blockage of the liver (by e.g. gall stones ) of the bile duct leading to
accumulation of bile in the liver

 Development of fatty liver (fatty cirrhosis) due to malnutrition –Malnutrition


conditions that can result into fatty liver .are­ overweight, diabetes, high cholesterol
levels, and high blood pressure. Continuous fat infiltration causes cellular destruction
and fibrotic tissues changes

 Metabolic conditions e.g. copper and iron overload

 Autoimmune inflammatory conditions. .


 Medications. Some drugs can cause cirrhosis if they’re taken for a very long time.

Symptoms
 The onset of the disease is gradual with initial symptoms of gastro­intestinal disturbances like
nausea, vomiting, anorexia and abdominal distention and pain. This is then followed by
 Bleeding in the GIT leading to anemia
 Ascites (Fluid accumulation in the abdomen/ belly) and edema
 Accumulation of waste products in the body blood leading mental confusion
(encephalopathy).
 Loss of weight
 Jaundice

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 As the diseases progresses, blood circulation through the liver is impaired and blood clotting
mechanism is also impaired as factors such as prothrombin and fibrinogen are not adequately
produced by the damaged liver thus you bleed easily from a small bruise.
 You can also develop gallstones that may block the bile duct

N/B Ascites is the buildup of fluid in the space between the lining of the abdomen and the
abdominal organs (the peritoneal cavity)
Edema is fluid built up in the tissues, usually the feet, legs or back.
Both conditions result from abnormal accumulation of sodium associated with portal
hypertension (High blood pressure) and liver disease.
1MAGE OF A NORMAL LIVER AND ONE WITH CIRRHOSIS

Management
2. Nutrition therapy­hepatic diet
 High energy diet because of the degeneration of the organ, fever and for weight gain.
E.g. glucose and honey can be added to food.35 to 35 Kcal/kg body weight
 Low Protein diet to minimize the production of ammonia and not to over work the

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liver as the diseased liver may not convert all the ammonia into urea: 1 to 2g/kg body
weight. The intake should be adequate to regenerate the liver cells and prevent
infections. Give low protein(High biological protein)
 Carbohydrate: Adequate intake of carbohydrate to prevent catabolism of the of the
body protein for energy, which would further increase blood ammonia. Intestinal
bacteria make ammonia from undigested proteins (proteins from shed mucosal cells,
protein, protein from GI tract bleed, and dietary protein)
 Low fat diet because of impaired bile secretion. Emulsified fat like from whole milk,
butter and eggs can be given as less bile is required for their emulsification. Avoid
fried foods, fatty foods. The fat should be moderate enough as it increases kcalorie
content of food. Restriction should also be ensured when there is steatorrhea
 High vitamins and minerals: The central role of the liver is to metabolize and store
vitamins and minerals. High minerals and vitamins should be ensured as diseased liver
may not be able to metabolize and store enough minerals for the body. High intake of
vitamins especially A,D,E,K should also be ensured due to decrease and impaired
absorption of fat as this vitamins need fat for their absorption
 Increased vitamin C intake for tissue leaching.
 Decreased sodium intake to reduce and manage ascites and edema. Usually ‘no added
salt’ is recommended for patients with severer cirrhosis, however, sodium intake is often
restricted for patients who develop decompensated cirrhosis with ascites. Limit sodium
intake to 2000 mg/day or less or no salt at all in order to prevent fluid buildup and
swelling of the liver. The best salt substitute is lemon juice (it is salt free).
 Fluid: Fluids should be encouraged unless ascites or edema is present. Water is the fluid
of choice
 Alcohol: There should be abstinence from alcohol to protect the liver from further injury
How to reduce salt intake?
1) Choose low salt foods
2) Count your salt
3) Do not add any salt at the table
4) Check labels low salt or “no salt added”
5) Try to avoid processed foods e.g canned meat, vegetables, bread, cheese, mayonnaise
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because they have more salt than the unprocessed ones


3. Medical therapy:
Use of drugs and medicines. Neomycin and Lactulose help to keep ammonia down

N/B: Patient with liver cirrhosis are at increased risk of developing liver cancer

IMAGE OF A PATIENT WITH LIVER CIRROSIS

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3. ALCOHOLIC LIVER DISEASE/ALCOHOLIC HEPATITIS


This refers to the inflammation of the liver caused by drinking alcohol.
Though alcoholic hepatitis is most likely to occur in people who drink heavily over many
years, the relationship between drinking and alcoholic hepatitis is complex. Not all heavy
drinkers develop alcoholic hepatitis, and the disease can occur in people who drink only
moderately.
Symptoms
jaundice, Loss of appetite Nausea and vomiting Abdominal pain and tenderness Weight
loss, Retention of large amounts of fluid in the abdominal cavity (ascites),Confusion and
behavior changes due to brain damage from buildup of toxins
(encephalopathy) Kidney and liver failure

4. LIVER CANCER
 Liver cancer is a cancer that begins in the cells of your liver. Cancer is where there is
a development of abnormal cells that divide uncontrollably and have the ability to
destroy normal body tissue. The most common form of liver cancer is hepatocellular
carcinoma, which begins in the main type of liver cell (hepatocyte). Other types
Risk factor s to liver disease
 Certain inherited liver diseases e.g Wilsons disease , exposure to aflatoxins(poisons
produced by molds that grow on poorly stored crops), Cirrhosis, Chronic infection
with hepatitis B and C viruses, obesity, fatty liver, diabetes, excessive alcohol
consumption
Early cancers can be treated by chemotherapy surgery or a liver transplantation.

5. LIVER/HEPATIC FAILURE
 Liver failure can be grouped as either acute or chronic liver failure
 Acute liver failure is loss of liver function (when liver cells are damaged) that occurs
rapidly­in days or weeks in a person who has no pre­existing liver disease. It is less
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common than chronic liver failure which develops slowly


Causes: Acetaminophen overdose (This drug is the main cause of liver in U.S.A),
Use of herbal medicines, Hepatitis, Autoimmune disease that attacks liver cells, cancer,
Metabolic diseases e.g. Wilson’s disease, acute fatty liver of pregnancy
Symptoms
Jaundice, abdominal pain, abdominal swelling, vomiting, weight loss, confusion and
sleepiness
Functional Foods to incor por ate into the weekly diet for people with liver
diseases
1. Gar lic – Activates liver enzymes that help your body flush out the toxins.
2. Gr apefr uit, citr us fr uits e.g lemon and or anges–They are high in both Vitamin C and
antioxidants, have cleansing abilities for the liver and boost production of the liver
detoxification enzymes that help flush out carcinogens and other toxins.
3. Beets and Car r ots – Both are extremely high in plant flavonoids and betacarotene, that
stimulate and support overall liver function.
4. Gr een Tea­ This liver loving beverage is full of plant based antioxidants known as
catechins compounds known to assist liver function.
5. Gr een Leafy Vegetables – Extremely high in chlorophyll, greens soak up
environmental toxins from the blood stream. With their distinct ability to neutralize
chemicals and pesticides these cleansing foods offer a powerful protective mechanism
for the liver.
6. Avocados – this nutrient dense superfood help the body produce glutathione, a
compound that is necessary for the lives to cleanse harmful toxins.
7. Apples – High in pectin apples hold the chemical constituents necessary for the body to
cleanse and release toxins from the digestive tract. This in turn, makes it easier for the
liver to handle the toxic load during the cleansing process.
8. Alter native Gr ains – e.g Millet can help filter toxins from the liver.
9. Cr ucifer ous Vegetables­ Broccoli and cauliflower are good sources of glucosinalate
which supports enzyme production in the liver. These natural enzymes flush carcinogens
and other toxins from the body and may significantly lower risks associated with cancer.
10. Lemons and Lime – these citrus fruits are high in vitamin C. Drinking freshly squeezed
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lemon or lime juice in the morning can help stimulate the liver.
11. Cabbage – Stimulates liver detoxifying enzymes (that help the liver to flush out toxins

(B) GALLBLADDER DISEASES

GALLBLADDER DISEASE
Intr oduction

 The gallbladder is a small pouch (sac) that is located under the liver.
 The main function of the gallbladder is to store the bile produced in the liver and pass it
along to the intestine. After meals, the gallbladder is empty and flat, like a deflated
balloon. Before a meal, the gallbladder may be full of bile and about the size of a small
pear.
 In response to signals, the gallbladder squeezes stored bile into the small intestine
through a duct.
 Bile helps digest fats but the gallbladder is not absolutely necessary for human survival,
as bile can reach the small intestine in other ways and therefore removing the gallbladder
in an otherwise healthy individual typically causes no observable problems with health or
digestion yet there may be a small risk of diarrhea and fat malabsorption
 The release of bile into the intestine is signaled by a hormone called cholecystokinin ,
which is released when food enters the small intestine. It causes the gallbladder to
contract and deliver bile into the intestine where it emulsifies (breaks down) fatty
molecules. It also enables fat­soluble nutrients (such as vitamins A, D, E, and K), to pass
through the intestinal lining and enter the bloodstream.

Disease of the Gall Bladder


1. Gallstones(cholelithiasis)
2. Choledocholithiasis disease
3. Acalculous Gallbladder Disease
4. cholecystitis disease

1. Gallstones(Cholelithiasis)

 The process of gallstone formation is referred to as cholelithiasis.


 Gallstones are solidified particles (hard deposits) of substances in the bile. They are made of
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a “combination of bile salts, cholesterol, calcium, lecithin(a phospholipid) and bilirubin,”

 The majority of gallbladder diseases are caused by


inflammation due to irritation to the gallbladder
wall (cholecystitis). This occurs when gallstones
obstruct the ducts leading to the small intestine
and may eventually lead to necrosis or gangrene.
 Gallstones can be any size from tiny as a grain of
sand to large as a golf ball.
TYPES OF GALLSTONES
a) Cholester ol Stones.
Although cholesterol makes up only 5% of bile, about three­fourths of the gallstones are
formed when there is too much cholesterol in the bile.
Conditions that may lead to cholelithiasis:
 When the liver secretes too much cholesterol into the bile.
 When the gallbladder is not be able to empty normally, so bile becomes stagnant.
 When the cells lining the gallbladder is not able to efficiently absorb cholesterol and fat
from bile.
 There are high levels of bilirubin. Bilirubin is a substance normally formed by the
breakdown of hemoglobin in the red blood cells. It is removed from the body in bile.
b) Pigment Stones.
 Pigment stones form when there is excess bilirubin in the bile.
 Pigment stones can be black or brown.
c) Mixed stones: Mixed stones are a mixture of cholesterol and pigment stones.
Although it is common to have many smaller stones, a single larger stone or any combination
of sizes is possible.
N/B
 Gallstones are most common among overweight, middle­aged women, but the elderly
and men are more likely to experience more serious complications from gallstones.
 Women who have been pregnant are more likely to develop gallstones. The same is true
for women taking birth control pills or on hormone/estrogen therapy as this can mimic

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pregnancy in terms of hormone levels.

2. Choledocholithiasis (Common Bile Duct Stones)


This is when gallstones are present in the common bile duct, rather than the gallbladder. This
condition is called choledocholithiasis.
 

Symptoms of Stones in the Common Bile Duct (Choledocholithiasis)


 Stones lodged in the common bile duct can cause symptoms that are similar to those
produced by stones that lodge in the gallbladder, but they may also cause the following
symptoms:
 Jaundice (yellowish skin)
 Dark urine, lighter stools, or both
 Rapid heartbeat and abrupt blood pressure drop
Fever, chills, nausea and vomiting, and severe pain in the upper right abdomen.

3. Acalculous Gallbladder Disease


 This is when gallbladder disease occurs without stones, a condition called acalculous
gallbladder disease.
 It is where a person has symptoms of gallbladder stones, yet there is no evidence of
stones in the gallbladder or biliary tract. It can be acute (arising suddenly)
4. Cholecystitis disease
 This is the inflammation of the gallbladder.
 It occurs when gallstones blocks the tube leading the gallbladder. Other causes of
cholecystitis include bile duct problems and
tumors.
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Symptoms

Severe pain in the right abdomen., Pain that radiates from the right shoulder or back.,
Tenderness over your abdomen when it's touched., Nausea., Vomiting and Fever

Cholecystitis signs and symptoms often occur after a meal, particularly a large or fatty
meal.

RISK FACTORS FOR GALL BLADDER DISEASE

Risk Factor s in Women


1) Women are much more likely than men to develop gallstones. In general, women are
probably at increased risk because estrogen stimulates the liver to remove more
cholesterol from blood and divert it into the bile.
2) Pregnancy increases the risk for gallstones, and pregnant women with stones are more
likely to develop symptoms than women who are not pregnant. Surgery should be
delayed until after delivery if possible. In fact, gallstones may disappear after delivery
3) Hormone replacement therapy (HRT) doubles or triples the risk for gallstones,
hospitalization for gallbladder disease, or gallbladder surgery. Estrogen raises
triglycerides, a fatty substance that increases the risk for cholesterol stones.
4) Risk Factor s in Men
1. Advance in age­ About 20% of men have gallstones by the time they reach age 75.
Because most cases do not have symptoms, however, the rates may be underestimated
in elderly men.
Risks in Childr en
Gallstone disease is relatively rare in children. When gallstones do occur in this age group,
they are more likely to be pigment stones. Girls do not seem to be more at risk than boys.
The following conditions may put children at higher risk: Spinal injury, History of abdominal
surgery, Sickle­cell anemia, impaired immune system, receiving nutrition through a vein
(intravenous)
GENERAL RISK FACTORS
1. Ethnicity

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e.g Hispanics and Northern Europeans have a higher risk for gallstones than do people of
Asian and African descent.
2. Genetics
Having a family member or close relative with gallstones may increase the risk.
3. Diabetes
People with diabetes are at higher risk for gallstones and have a higher­than­average risk
for acalculous gallbladder disease (without stones).
4. Obesity
Obesity. Being overweight is a significant risk factor for gallstones. In such cases, the
liver over­produces cholesterol, which is delivered into the bile and causes it to become
supersaturated.

Nutr ition ther apy


Diet may play a role in gallstones. Specific dietary factors may include: ­
1. Fats: e.g lean meat and low dairy fats. Dietary fat is the principal cause of contraction of
the diseased organ and subsequent pain. Energy should come primarily from
carbohydrate foods especially during acute phases. Fats also contributes to weight loss , a
primary goal because obesity and excess food intake is associated with the development
of gallstones
2. Fiber : High intake of fiber has been associated with a lower risk for gallstones It also
helps in weight management e. g whole grains
3. Fruits and vegetable: People who eat a lot of fruits and vegetables may have a lower risk
of developing symptomatic gallstones that require gallbladder removal. Some great ones
are avocados, berries, grapes, cucumbers and beets. Broccoli, bell peppers and oranges
are high in fiber and vitamin C, which if lacking can contribute to gallstones. Pectin­rich
fruits — such as apples, strawberries and citrus — can also help
4. Kcalor ies: Reduced kcals if one is overweight
5. Sugar : High intake of sugar has been associated with an increased risk for gallstones.
Diets that are high in carbohydrates (such as pasta and bread, chips, cakes, sodas Crips,
pastry and biscuits) can also increase risk, because carbohydrates are converted to sugar
in the body

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6. Dr ink plenty of water


7. Alcohol: A few studies have reported a lower risk for gallstones with alcohol
consumption. Even small amounts (1 ounce per day) have been found to reduce the risk
of gallstones in women by 20%. Moderate intake (defined as 1 ­ 2 drinks a day) also
appears to protect the heart. It should be noted, however, that even moderate alcohol
intake increases the risk for breast cancer in women. Pregnant women, people who are
unable to drink in moderation, and those with liver disease should not drink at all.
8. Coffee: Research suggests that drinking coffee every day can lower the risk of gallstones.
The caffeine in coffee is thought to stimulate gallbladder contractions and lower the
cholesterol concentrations in bile. However, drinking other caffeinated beverages, such as
soda and tea, does not seem to have the same benefit.

TOPIC: PANCREATIC DISORDERS

PANCREATIC DISORDERS
ANATOMY OF THE PANCREAS

The pancreas is about 6 inches long and sits across the back of the abdomen, behind the stomach.
The head of the pancreas is on the right side of the abdomen and is connected to the duodenum
(the first section of the small intestine) through a small tube called the pancreatic duct. The
narrow end of the pancreas, called the tail, extends to the left side of the body (Towards spleen)

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Functions of the pancr eas

 The pancreas has two main functions: an exocr ine function that helps in digestion and an
endocr ine function that regulates blood sugar.
 Almost all of the pancreas (95%) consists of exocrine tissue that produces pancreatic
enzymes for digestion. The remaining tissue consists of endocrine cells called islets of
Langerhans that produces hormones that regulate blood sugar and regulate pancreatic
secretions. The pancreas is therefore two glands that are intimately mixed together into
one organ.
Exocrine functions (digestion)
 The exocrine portion of the pancreas plays a major role in the digestion of food( that the
stomach releases slowly into the duodenum as a thick, acidic liquid called chime)
Pancreatic juice is a mixture of
1. Digestive enzymes. The digestive enzymes digest food (carbohydrates, fats, and
proteins) that the stomach realises slowly into the duodenum as a thick, acidic liquid
called chime. These enzymes include
 trypsin , chymotrypsin and carboxypeptidase to digest proteins;
 pancreatic amylase for the digestion of carbohydrates;
 lipase to break down fats
2. The bicar bonate ions that neutralize the acid in the chime to protect the intestinal wall
and create a proper environment for the functioning of pancreatic enzymes

N/B. The pancreatic juice eventually mixes with the bile in the common duct where they act on
the food in the duodenum. Bile is produced by the liver and stored by the gallbladder until need
arises
Endocrine Function (Blood Glucose Homeostasis)

 The endocrine component of the pancreas consists of islet cells (islets of Langerhans) that
create and release important hor mones directly into the bloodstream.
 Blood glucose levels must be maintained within certain limits so that there is a constant
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supply of glucose to feed the cells of the body but not so much that glucose can damage
the kidneys and other organs.
 The pancreas produces 2 antagonistic hormones to control blood sugar: glucagon and
insulin.

1. Glucagon (produced by the alpha cells) that raises blood glucose levels by stimulating the
liver to metabolize glycogen into glucose molecules and to release glucose into the blood.
Glucagon also stimulates adipose tissue to metabolize triglycerides into glucose and to
release glucose into the blood.
2. Insulin is produced by the beta cells of the pancreas. This hormone lowers blood glucose
levels after a meal by stimulating the absorption of glucose by liver , muscle, and adipose
tissues. Insulin triggers the formation of glycogen in the muscles and liver and
triglycerides in adipose to store the absorbed glucose.

 Regulation of Pancr eatic Function


The function of the pancreas is controlled by both the ner vous system and the endocrine
system.
 The endocrine system uses 2 hormones to regulate the digestive function of the pancreas:
secretin and cholecystokinin (CCK).

COMMON DISORDERS OF THE PANCREAS


1. Pancreatitis
2. Cystic Fibr osis
3. Pancr eatic cancer

PANCREATITIS
Pancreatitis is a disease in which the pancreas becomes inflamed. This is caused by digestion
of the organ tissues by enzymes it produces, principally trypsin. (i.e. It is where the pancreatic
tissues are damaged by its own enzymes).Normally enzymes remain in inactive form in the
pancreas until pancreatic secretions reach the duodenum through the pancreatic duct. The
damage happens when these digestive enzymes are activated before they are released into the
duodenum and begin attacking the pancreas tissues causing a cute pain

Causes

The activation of the inactive enzyme to active form may occur as a result of gallbladder disease that may
cause gallstones to enter the common bile duct and obstruct flow from the pancreas or cause a reflux of
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these secretions and bile from the common duct back into the pancreatic duct

Other causes include

 Heavy alcohol use which can lead to blockage of the pancreatic duct.
 Medications, infections, abdominal trauma, metabolic disorders, cystic fibrosis, lupus and
surgery.
 Presence of tumour, infections such as mumps, Hep A/B or salmonella
 A venomous sting of a scorpion.

Forms of pancreatitis: acute and chronic.

Acute pancreatitis
 Acute pancreatitis is a sudden inflammation that lasts for a short time. It may range from mild
discomfort to a severe, life­threatening illness.
 Most people with acute pancreatitis recover completely after getting the right treatment.
 In severe cases, acute pancreatitis can result in bleeding into the gland, serious tissue damage,
infection, and cyst formation. Severe pancreatitis can also harm other vital organs such as
the heart, lungs, and kidneys.

Symptoms of Acute Pancreatitis


 Upper abdominal pain that radiates to your back;
 Abdominal pain that feels worse after eating, especially foods high in fat.
 Swollen and tender abdomen( when touched)
 Nausea and vomiting
 Fever
 Increased heart rate

Chronic pancreatitis
 Chronic pancreatitis is long­lasting inflammation of the pancreas.
Causes:
1. It most often happens after an episode of acute pancreatitis.
2. Heavy alcohol drinking is another big cause. Damage to the pancreas from heavy

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alcohol use may not cause symptoms for many years, but then the person may
suddenly develop severe pancreatitis symptoms.

Symptoms of chronic pancreatitis


 The symptoms of chronic pancreatitis are similar to those of acute pancreatitis.
Other symptoms are:
 Weight loss due to poor absorption (malabsorption) of food. This malabsorption happens
because the gland is not releasing enough enzymes to break down food.
 Also, diabetes may develop if the insulin­producing cells of the pancreas are damaged.
 Oily, smelly stools (Steatorrhea)

Complications associated with Pancreatitis

 Kidney failur e: Acute pancreatitis may cause kidney failure.


 Diabetes: Damage to insulin­producing cells in your pancreas from chronic pancreatitis
can lead to diabetes, a disease that affects the way your body uses blood sugar.
 Malnutr ition: Both acute and chronic pancreatitis can cause your pancreas to produce
fewer of the enzymes that are needed to break down and process nutrients from the food
you eat. This may lead to weight loss, even though you may be eating the same foods or the
same amount of food
 Pancr eatic cancer : Long­standing inflammation in your pancreas caused by chronic
pancreatitis is a risk factor for developing pancreatic cancer.
 Pseudocyst(Pancr eatic cyst):  These are sack like pockets of fluid on or within the
pancreas. Most of them are not cancerous but some can be cancerous. A large pseudocyst
can ruptures and cause complications such as internal bleeding and infection. Signs and
symptoms of pseudocyst are:

o Persistent abdominal pain which may radiate to your back.


o A mass you can feel in your upper abdomen.
o Nausea and vomiting

N/B. A ruptured pseudocyst is a medical emergency. Fluid released by the pseudocycts can
damage nearby blood vessels and cause massive bleeding
Signs and symptoms of a ruptured pseudocyst are: vomming of blood, fainting, severe abdominal
pain, weak heat beat, and decreased consciousness

The pr imar y goals of nutr itional management for chr onic pancr eatitis ar e:
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 Prevent malnutrition and nutritional deficiencies


 Maintain normal blood sugar levels (avoid both hypoglycaemia and hyperglycaemia)
 Prevent or optimally manage diabetes, kidney problems, and other conditions associated
with chronic pancreatitis

The pr imar y goals of nutr itional management in acute pancr eatitis ar e:

 Maintain a healthy body weight: Obesity appears to be a risk factor for the
development of pancreatitis and for an increased severity when it occurs. Gallstones is
also a risk factor for acute pancreatitis

Management

Nutrition therapy

 In early stages (acute pancreatitis), oral feedings are withheld because entry of food into
the intestines stimulates pancreatic secretions and usually causes pain. Enteral nutrient
should be provided.

o Most patients with pancreatitis are able to resume oral feeding in two days.
o Parenteral nutrition is not recommended in pancreatitis unless enteral nutrition
fails. It may fail due to pseudocytes, intestinal and pancreatitis fistulas,
pancreatitis abscesses, and pancreatitis ascites

 A low­fat diet: The amount of fat consumed varies depending on your weight.
 Pr otein: Moderate protein should be given
o A protein diet of 1.0­1.5 g/kg body weight/d is generally sufficient and well
tolerated.
 Calor ies: High energy diet in chronic pancreatitis
 Usually, if 30%­40% of the calories are given as fat this is well tolerated, especially when
the foods are rich in vegetable fats.
 Fibr e: In general, a low fibre diet is recommended, because fibre may absorb enzymes
and delay the absorption of nutrients. An adequate quantity of exogenous pancreatic
enzymes is necessary to correct protein and lipid mal­digestion.
 Vitamins & Miner als: Increased vitamins and mineral intake for patients with chronic
pancreatitis

 Alcohol: Avoid alcohol if pancreatitis was caused by alcohol use. Alcohol should be

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taken in moderation even if it was not the main cause of acute pancreatitis

 Smoking: People with pancreatitis should avoid smoking, as it increases the risk for
pancreatic cancer.

 High intake Foods r ich in antioxidants: They help your body to fight off the free
radicals that cause damage to the tissues and worsen the condition. e.g. green leafy
vegetables, bell peppers, cherries, and berries.

Some foods to be avoid these foods 

 Saturated fats found in shortening, margarine, certain oils, chips, cookies, cakes,
pastries and crackers
 Fried food and junk food
 Refined carbs present in white bread, pasta, snacks and certain cereals
 Sugar and sweets
 Caffeine, present in coffee, tea and chocolate

CYSTIC FIBROSIS (CF)

Cystic fibrosis is an inherited disorder that mostly affects the white population. The leading
characteristic of cystic fibrosis is the hyper secretion of abnormal, sticky, thick mucus (by cells
that produce mucus) that obstructs exocrine glands and ducts, and that also causes severe damage
to the lungs, sweat glands digestive system and in males it causes infertility

An image of a liver with cystic fibr osis

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SYMPTOMS

 Secretion of thick mucus that accumulates and clogs air passages in the lungs and
intestines. This may result into frequent respiratory infections, breathing difficulties, and
chronic lung disease.
 Loss of salt that accompanies the mucus. A loss of salt may cause an upset in the balance
of minerals in the blood, abnormal heart rhythms, and, possibly, low blood pressure and
shock.
 Liver disease
 Diabetes
 Pancreatitis. Inflammation of the pancreas that causes severe abdominal pain.
 Gallstones
  Fatty/oily stool, 
  Infertility in males. 
 Sinusitis( inflammation and swelling of the nasal passage)
 Nasal polyps(soft painless noncancerous growth on the lining of the nasal cavity)
 Clubbing of fingers and toes. A condition marked by extremely thickened fingertips and
toes due to decreased oxygen in the blood

ORGANS AFFECTED BY CYSTIC FIBROSIS

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Management

Nutrition therapy
Enzymes, vitamins, and salt:

 High energy, high protein with no fat restriction

 Increase intake of vitamin A, D, E, K, and extra calcium. There are special formulas for
people with CF.

 People who live in hot climates may need a small amount of extra table salt.

 Give small and frequent meals


 Most people with CF must take pancreatic enzymes to help in the digestion of
carbohydrates, proteins, fats.
o These enzymes help your body absorb fat and protein. Taking them all the time
will decrease or get rid of foul­smelling stools, gas, and bloating. They are taken
with all meals

PANCREATIC CANCER
Two types of cancer can affect the pancreas:

1. The most common is cancer of the exocrine pancreas that originates in the pancreatic
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ducts.
This type of pancreatic cancer, called "pancreatic ductal adenocarcinoma. It is the most
common
2. Another type of cancer consists of a group of tumours that originate from the cells that
make hormones such as insulin. These tumours are called "pancreatic endocrine tumours.

A diagr am of pancr eatic ductal adenocar cinoma.

Causes of Pancr eatic cancer

It's not clear what causes pancreatic cancer in most cases. Doctors have identified factors, such
as smoking, that increase your risk of developing the disease.

How pancr eatic cancer for ms

Pancreatic cancer occurs when cells in your pancreas develop mutations in their DNA. These
mutations cause cells to grow uncontrollably and to continue living after normal cells would die.
These accumulating cells can form a tumour. Untreated pancreatic cancer spreads to nearby
organs and blood vessels.

Pancr eatic cancer symptoms


Pancreatic cancer is often referred to as a “silent cancer” because it is thought that the early
symptoms can be vague and unrecognised.  Most people with pancreatic cancer have pain and
weight loss, with or without jaundice (yellowing of the skin):

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 Pain – Pain is a common symptom. It usually develops in the upper abdomen as a dull
ache that wraps around to the back. The pain can come and go, and it might get worse
after eating.
 Weight loss – Most people with pancreatic cancer lose weight because of a lack of
appetite, feeling full after eating only a small amount of food, or having diarrhoea. The
bowel movements might look greasy tract where and float in the toilet bowl because they
contain undigested fat.
 Jaundice – This causes yellow coloured skin and whites of the eyes. Jaundice is caused
by a block in the flow of bile from the gallbladder, where it is stored, to the intestinal the
bile assists in digestion of food. The block is caused by the cancer.
 Dark urine, nausea, vomiting, and enlarged lymph nodes in the neck.
 Loss of appetite and changes the taste.
 An enlarged gall bladder due to blockage of the bile ducts.
 Elevated blood sugars. Some people with pancreatic cancer develop diabetes as the cancer
impairs the pancreas' ability to produce insulin. 
 Itching: Itchy skin, palms, and soles of feet. People with pancreatic cancer sometimes report
itching all over. Blockage of the bile ducts is often responsible.

N/B Understanding that the tube (duct) carrying bile from the liver passes through the pancreas
on its way to the intestine, helps us understand why some people with pancreatic cancer develop
jaundice (an abnormal yellowing of the skin and eyes).

Risk factor s of pancr eatic cancer


The following factors may raise a person's risk of developing pancreatic cancer:
 Age. The risk of developing pancreatic cancer increases with age.
 Gender.
 Race/ethnicity.

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 Smoking.
 Obesity and diet.
 Diabetes.
 Family history.
 Rare inherited conditions.

Pancr eatic cancer staging

The stages of pancreatic cancer are:

 Stage I: Cancer is confined to the pancreas and can be removed using surgery.

 Stage II: Cancer has spread beyond the pancreas to nearby tissues and organs and may
have spread to the lymph nodes. At this stage, surgery may be possible to remove the
cancer.

 Stage III: Cancer has spread beyond the pancreas to the major blood vessels around the
pancreas and may have spread to the lymph nodes. Surgery may or may not be possible
to remove the cancer at this stage.

 Stage IV: Cancer has spread to distant sites beyond the pancreas, such as the liver, lungs
and the lining that surrounds your abdominal organs (peritoneum). Surgery isn't an option
at this stage.

Dietar y pr oblems that come with cancer


The dietar y pr oblems can be br ought about by
1. Cancer infection

 The main functions of the pancreas are to provide digestive enzymes to help break
down food and hormones such as insulin and glucagon to control blood sugars.
 Cancer of the pancreas can interfere with this, which can lead to digestive problems
and prevent you from absorbing all the nutrients from your food.

2. Treatment methods

 Treatment options such as surgery, to remove all or part of the pancreas and/or radio
and chemotherapy, can also cause dietary problems leading to poor appetite, nausea
and vomiting, diarrhoea and changes in taste and smell.

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The dietar y pr oblems may include:

 Poor digestion and malabsorption of fats, carbohydrates and proteins due lack of digestive
enzymes which help us break down our food and absorb the nutrients from food. Symptom of
malabsorption are: pale, floaty stools which can be oily, foul smelling and difficult to flush
away. Other symptoms include bloating, flatulence and weight loss.
 Poor appetite and weight loss. Due to poor digestion, malabsorption, poor appetite and
diarrhoea
 Nausea and vomiting
 Jaundice can cause loss of appetite, taste changes, nausea, vomiting, and steatorrhea. These
symptoms usually resolve once the jaundice is treated
 Change in taste and smell.
 Mouth sores
 Diabetes that occurs because your pancreas may not be making enough insulin
Management
Medical therapy

 Surgery
 Chemotherapy
 Radiation

Nutrition therapy
 High energy diet: Because of increased metabolic rate
 Sufficient carbohydrate to spare protein for synthesis of tissues and healing process,
production of hormones and enzymes
 High intake of protein
 Sufficient intake of vitamins and minerals especially vitamin A, C,E and B
complex(They are coenzyme agents for protein and energy metabolism

 Nutrition therapy for change in taste and smell


o If your food tastes too sweet, try adding lemon juice or salt – starting with a few
sprinkles/drops and increase until you find the taste acceptable.
o If food tastes metallic or too salty, try adding sugar or honey.
o If you are affected by cooking odours, try to stay out of the kitchen while food is
being cooked if possible.
o Choose foods without a strong smell – sometimes the smell of a food can put you off
eating. Cold foods tend not to smell as much as hot foods.
o Marinate meat or vegetables to add more flavour.
o To add more flavour to your food, add herbs, spices e.tc
 Nutr ition ther apy Nausea
o Eat little and often especially before your treatment (e.g. soup and dry biscuits or
toast), and drink as much fluid as possible.
o Instead of drinking a lot at once, try sipping small amounts of liquid often.
Sucking on ice cubes can also help to increase your fluid intake.
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o If you wake up feeling sick, eat a dry biscuit (ginger biscuits may help with
nausea) or a slice of toast. If you are diabetic, consult your medical team.
o Fizzy drinks such as ginger ale or soda water can often help relieve an upset
stomach.
o It is important to keep up your fluid intake to prevent you from becoming
dehydrated if you have been vomiting a lot. You should contact your medical
team if you are unable to keep fluids down.
o Avoid strong odours and cooking smells, which can trigger nausea and vomiting

TOPIC: CARDIOVASCULAR DISEASE


CARDIOVASCULAR AND LUNG DISEASES
Intr oduction
CARDIOVASCULAR SYSTEM
The cardiovascular system consists of the heart and blood vessels (arteries, veins, and capillaries).
 The Heart is a pumping organ, weighing about between 250 and 350 grams (It is about
the size of a large fist) located slightly to the left of the middle of the chest. The heart is
made of strong muscle tissue and is protected by the rib cage. It is enclosed in a
protective sac, pericardium which also contain a lubricating fluid. The outer wall is made
up of three layers, the epicardium, the myocardium which is the muscle of the heart, and
the endocardium.
All blood vessels are lined with a thin layer, endothelium that keeps blood cells inside of the
blood vessels and prevents clots from forming. The endothelium lines the entire circulatory
system, all the way to the interior of the heart, where it is called the endocardium.

o Ar ter ies and Ar ter ioles: Arteries are blood vessels that carry blood away from the heart.
They carry oxygenated blood except pulmonary artery. Arteries face high levels of blood
pressure as they carry blood being pushed from the heart under great force. To withstand
this pressure, the walls of the arteries are thicker, more elastic, and more muscular than
those of other vessels
o Capillar ies: Capillaries are the smallest and thinnest of the blood vessels in the body and
also the most common
o Veins and Venules: They carry blood to the heart. They carry deoxygenated blood
except pulmonary vein. Because the arteries, arterioles, and capillaries absorb most of the
force of the heart’s contractions, veins and venules are subjected to very low blood
pressures. This lack of pressure allows the walls of veins to be much thinner, less elastic,
and less muscular than the walls of arteries.

Veins rely on gravity, inertia, and the force of skeletal muscle contractions to help push
blood back to the heart. To facilitate the movement of blood, some veins contain many
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o one­way valves that prevent blood from flowing away from the heart.

Definition of ter ms
Ar ter ioscler osis: Blood vessel disease characterized by thickening and hardening of artery
walls, with loss of functional elasticity, mainly affecting the intima (inner lining) of the arteries
Ather oscler osis: Common form of arteriosclerosis, characterized by the gradual formation of
yellow cheese like streaks of cholesterol and fatty materials that develop into hardened plagues
in the intima or inner lining of the major blood vessels. Thickened blood vessel or blood clot as a
result of atherosclerosis may eventually cut off blood supply to the tissues e.g. tissues of the
heart and this may result into heart attack if it affects major coronary vessel
N/B.1 The term atherosclerosis originated from the Greek word “ athera ”( gruel­meaning
porridge like) and “sclerosis” (hardening).
N/B.2 There are two major coronary arteries, the left and the right coronary artery, that branched
from the aorta to the muscles of the heart(myocardium), that branched further into the muscles of
the heart
Intima : inner layer of the blood vessel wall
Plague: Thickened deposits of fatty material, largely cholesterol, within the blood vessel wall
that eventually may fill the lumen and cut off blood supply to the tissue served by the damaged
vessel
Ischemia : Deficiency of blood (oxygen and nutrients) to a particular tissue, resulting from
functional blood vessel constriction or actual obstruction wall as in atherosclerosis
Infar ct : An area of tissue necrosis caused by local ischemia, resulting from obstruction of blood
circulation to the area or infar ct refers to an area of dead tissues as a result of ischemia e.g. acute
myocardium infarction
Ather oma : A mass of fatty plague formed in inner arterial walls in atherosclerosis
Cachexia ­a wasting condition marked or metabolic syndrome marked by weakness, extreme
weight loss (loss of muscle), and malnutrition e.g cardiac cachexia

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CARDIOVASCULAR DISEASES

Cardiovascular disease (CVD) is a gener al ter m for conditions/diseases affecting the hear t or
blood vessels.

Cardiovascular diseases can be divided into

1. Blood vessel diseases (vascular diseases. ) such as


 Coronary artery disease(also known as coronary heart disease and ischemic heart disease)
, Arrhythmias ( Heart rhythm problems), Congenital heart diseases(heart defects you're
born with), Peripheral arterial disease – disease of blood vessels that supply blood to the
arms and legs, Cerebrovascular disease – disease of blood vessels that supply blood to the
brain and head (includes stroke),Renal artery stenosis, Aneurysm
2. Hear t diseases such as.

 Cardiomyopathy – diseases of cardiac muscle, Hypertensive heart disease – diseases of


the heart secondary to high blood pressure or hypertension, Heart failure ­ a clinical
syndrome caused by the inability of the heart to supply sufficient blood to the tissues to
meet their metabolic requirements
 Pulmonary heart disease – a failure at the right side of the heart with respiratory system
involvement
 Cardiac dysrhythmias – abnormalities of heart rhythm
 Inflammatory heart disease

o Endocarditis – inflammation of the inner layer of the heart, the endocardium. The
structures most commonly involved are the heart valves.
o Inflammatory cardiomegaly
o Myocarditis – inflammation of the myocardium, the muscular part of the heart.

 Valvular heart disease


 Congenital heart disease – heart structure malformations existing at birth
 Rheumatic heart disease – heart muscles and valves damage due to rheumatic fever
caused by Streptococcus pyogenes a group A streptococcal infection.

N/B. The term "heart disease" is often used interchangeably with the term "cardiovascular
disease."
Common/Gener al symptoms of car diovascular diseases
Often, there are no symptoms of the underlying disease of the blood vessels. A heart attack or
stroke may be the first warning of underlying disease. Symptoms of a heart attack include:
o pain or discomfort in the centre of the chest;
o Pain or discomfort in the arms, the left shoulder, elbows, jaw, or back.
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o In addition the person may experience difficulty in breathing or shortness of breath;


feeling sick or vomiting; feeling light­headed or faint; breaking into a cold sweat; and
becoming pale. Women are more likely to have shortness of breath, nausea, vomiting,
and back or jaw pain.
o The most common symptom of a stroke is sudden weakness of the face, arm, or leg,
most often on one side of the body. Other symptoms include sudden onset of:
o Numbness of the face, arm, or leg, especially on one side of the body;
o Confusion, difficulty speaking or understanding speech;
o Difficulty seeing with one or both eyes;
o Difficulty walking, dizziness, loss of balance or coordination;
o Severe headache with no known cause; and
o Fainting or unconsciousness.

Risk factor s of CVD /Causes of CVD

 The exact cause of CVD isn't clear, but there are lots of things that can increase your risk
of getting it. These are called "risk factors".
 The more risk factors you have, the greater your chances of developing CVD.

The risk factors can damage the blood vessels (arterial wall) and or can result into development
of plague. The risk factors can be divided into two
1. Lipid risk factors
2. Non­lipid risk factors

Lipid r isk factor s


1. High total cholesterol > 200 mg/dl

Cholesterol is soft, fatlike (a fatty substance) substance found in all the cell membranes and the
blood. High cholesterol in the blood can cause blood vessels to narrow and increase the risk of
developing a blood clot as well as damage the blood vessels thus resulting into increased risk of
heart attack (myocardial infraction) and stroke (thrombosis)

There are two types of cholesterol that is dietary cholesterol contained in food and blood or
plasma cholesterol that is essential from body metabolism.

Animal based foods and products (milk and its derivatives, eggs, fish, shellfish and all types of
meat), variety of meats especially offal (particularly liver and brain), shrimps and eggs have the
highest cholesterol content. Plant based foods do not contain cholesterol. However, there are
minute amounts of cholesterol in vegetable oils that are considered incidental.
2. High triglycerides > 150 mg/ dl

Too much fat, saturated fatty acid, Trans ­unsaturated fatty acids increases harmful cholesterol
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(LDL) levels in the blood and reduces the good cholesterol. The major dietary sources of
saturated fatty acids include animal based foods and products such as butter, cured cheeses,
margarine, bacon, sausages and pork, fresh eggs, cream, hydrogenated vegetable fats, lard, palm
oil and whole cow’s milk. Plant based foods are low in saturated fatty acids with some exception
such as coconut and palm oil.

3. High LDL(harmful) cholesterol > 130 mg/dl


4. Low HDL cholesterol < 40 mg/dl

Non­ lipid r isk factor s

Non­lipid risk factors can be divided into two,


1. Modifiable
2. Non­modifiable

Modifiable non lipid r isk factor s

High blood pr essur e (> 140/90 mm Hg)


 High blood pressure (hypertension) is one of the most important risk factors for CVD. If
the blood pressure is too high, it can damage the blood vessel(arterial walls)

Smoking/Tobacco use/exposur e to tobacco smoke


 Smoking and other tobacco use is a significant risk factor for CVD. The harmful
substances in tobacco can damage and narrow your blood vessels.

Diabetes mellitus
 Diabetes is a lifelong condition that causes blood sugar level to become too high. High
blood sugar levels can damage the blood vessels, making them more likely to become
narrowed.

N/B. Many people with type 2 diabetes are also overweight or obese, which is also a risk factor
for CVD.

Physical Inactivity
 People who do not exercise regularly are more likely to have high blood pressure, high
cholesterol levels and be overweight. All of these are risk factors for CVD.
 Exercising regularly will help keep the heart healthy. When combined with a healthy diet,
exercise can also help you maintain a healthy weight.

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Over weight and obesity

 Being overweight (BMI > 25­29.9 kg/m2or obese (BMI > 30 kg/m2) and having a waist of
94cm (about 37 inches) or more for men , or a woman with a waist measurement of 80cm
(about 31.5 inches) or more for women

 Being overweight or obese increases the risk of developing diabetes and high blood
pressure, both of which are risk factors for CVD. The risk is more if one has an
abdominal/central obesity

Unhealthy Diet

An unhealthy diet can lead to high cholesterol and high blood pressure. This can be as a result
of
o High salt (sodium chlor ide) intake: when sodium is taken in excess more
water is drawn into the circulation, increasing the volume of blood to be
pumped. In addition, excess salt makes the arterial walls to be more rigid
leading to arteriosclerosis. Much of the salt we eat is added to the table during
eating (20%), fifteen percent comes from salt naturally found in foods and
60% comes from salt added to processed foods (hidden salt).
o High fat intake

Alcohol
 Excessive alcohol consumption can also increase the cholesterol and blood pressure
levels, and contribute to weight gain. Alcohol(> 1 drink per day for women and > 2
drinks per day for men)

Dr ugs ­such as cocaine


Str ess
 While stress can affect all the body organs and functions of the body, its effect tends to
be concentrated on the heart and the cardiovascular system which is obliged to work
hard.

Non­modifiable non lipid r isk factor s

Family histor y of CVD

 If you have a family history of CVD, your risk of developing it is also increased.
 You're considered to have a family history of CVD if either:
o Your father or brother were diagnosed with CVD before they were 55
o Your mother or sister were diagnosed with CVD before they were 65

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Ethnic backgr ound/r ace

 CVD is more common in people of South Asian and African (blacks) or Caribbean
background.
 This is because people from these backgrounds are more likely to have other risk factors
for CVD, such as high blood pressure or type 2 diabetes

Age
 CVD is most common in people over 50 and the risk of developing it increases as you get
older. Age (males > 45 years, females > 55 years)

Male gender
 Men are more likely to develop CVD at an earlier age than women

Toxins and viruses can also damage (cause injury) the endothelium tissue of the blood vessel

CVDs can be acute (sudden) or chronic. Myocardial Infarction (MI) is an example of the acute
form. Chronic heart disease develops over time and causes the loss of heart function. If the heart
can maintain blood circulation the disease is classifies as compensated heart disease.
Compensation usually requires that the heart beat unusually fast. Consequently the heart
enlarges. If the heart cannot maintain circulation, the condition is classifies as decompensated
heart disease and congestive heart failure (CHF) occurs. The heart muscle (myocardium) the
valves, the lining (endocardium), the outer covering (pericardium) or the blood vessels may be
affected by the heart muscle.
Pr evention and nutr ition management of CVD
 Ener gy: An obese patient must be reduced to normal body weight with low calorie diet
 Pr otein: A diet of 60g protein is necessary to maintain proper nutrition. In severe
hypertension, protein restriction to 20 g may be necessary as temporary measure since
protein foods are rich in sodium
 Fats: Avoid high intake of animal or hydrogenated fats as they are prone to
atherosclerosis. Instead provide omega 3 fatty acids as they help in regulation of high
blood pressure
 Car bohydr ates: Provide complex carbohydrates
 Diet high in fibr e (Fibr e): Fibre is found exclusively in plant based foods. Provide both
soluble and insoluble fibre. Animal foods such as milk, eggs, fish, meat and their
derivatives contain no fibre. Insoluble fibres are found in higher concentration in
vegetables such as carrots, green leafy vegetables, cereals such as wheat, brown rice, rice
bran, wheat bran, corn bran, whole grain bread and cereals, cabbage family, cauliflower,
green beans, green peas, legumes, mature vegetables, root vegetables, tomatoes, nuts,
fruits such as pears, peaches, plums, seeds, strawberries, apples and bananas. High
concentration of soluble fibre occurs in fruits, oats, barley and legumes such as peas,
beans and lentils
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 Sodium: Increased intake of sodium in diet leads to increased intravascular volume and
thus increases cardiac output by elevating blood pressure
 Potassium: Potassium role in hypertension is its interplay with sodium, calcium and
magnesium in all living cells and in blood. 1. Potassium causes increased excretion of
sodium by the kidney (low levels of potassium cause the body to retain sodium and water
and this can elevate high blood pressure).2. It relaxes the vascular tissues and the arterial
muscle. 3. Reduces secretion of rennin which operates to conserve sodium and blood
fluids. Provide about 3500 mg of potassium daily and this can be provided by high
amounts of fruits and vegetables. Dietary sources of potassium include foods such as
blackstrap molasses, soybeans, wheat germ, pumpkins, bananas, almond, avocado,
spinach, potatoes, sweat potatoes, carrot juice, tomatoes, whole grain bread, melon,
cucumber, prune juice, beans, oranges, mangoes. Others from animal sources include
salmon, cod, beef steak, cheese, cow’s milk and fresh eggs.
 Calcium: Increased calcium intake as calcium is involved in the control of strength with
which blood is pumped by the heart
 Magnesium: High consumption of magnesium reduces the production of prostacyclin
which is vasodilating and increases the release of thromboxane which is vasoconstricting
(Prostacyclins and thromboxanes are hormone like the one compounds referred to as
eicosanoids that regulate BP, clotting and other body functions). Magnesium also
stabilizes calcium channels. Low blood magnesium lowers potassium level and leads to
hypokalemia. The food sources of magnesium ranked by milligram of magnesium per
standard amount include bran, pumpkin and squash seeds kernel roasted, sesame, nuts,
wheat germ, whole wheat flour, soybeans, molasses, spinach, white bean, green leafy
vegetables, potatoes and oranges.
 Physical activity: Physical activity has measurable biological effects affecting
cholesterol levels, insulin sensitivity and vascular reactivity. Moreover these effects are
dose dependant such that the more the exercise, the greater the health benefits. Engaging
in moderate level of physical activities such as intermittent walking for 30 to 45 minutes
is recommended for prevention of CVD. Moderate exercise such as walking may both
lower LDL and raise HDL levels if the activity is constantly pursued for a long time.
Moderate means 30 minutes brisk walking (3­4 miles) per hour, walking upstairs,
dancing, bicycling and any exercise that will expend 200 calories per day.

 CORONARY HEART DISEASE


 Coronary heart/artery disease (CHD) is a disease in which the coronary arteries (the
major blood vessels that supply the heat with blood, oxygen and nutrients) become
damaged or diseased by a waxy substance called plaque (a cholesterol containing
substance) that builds up inside the coronary arteries i.e It is a disease caused by

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atherosclerosis and it is the most common form of CVD


 When plaque builds up in the arteries, the condition is called Ather oscler osis.

Note: This fatty degeneration and thickening (atherosclerosis) narrow the vessel lumen and may
allow a blood to clot. Eventually the clot may cut off blood flow in the involved artery. If the
artery is a critical, such as a major coronary vessel, a hear t attack occurs. Tissue area serviced
by the involved artery is deprived of its oxygen and nutrients supply, a condition called
ischemia, and the cells die. The localized area of dying or dead tissue is called an infar ct.
Because the artery involved supplies cardiac muscle, the myocardium, the result is called
myocar dium infar ction

Symptoms of cor onar y ar ter y disease

 When plaques build up, they narrow your coronary arteries, decreasing blood flow to
your heart. Eventually, the decreased blood flow may cause
o Chest pain due to restricted blood flow to the heart muscle (angina)
o Cardiac/myocardial Ischemia
o Shortness of breath
o Arrhythmias
o Heart failure (where the heart is unable to pump blood around the body properly)
or other coronary artery disease signs and symptoms.

A complete blockage can cause a heart attack.


The buildup of plaque occurs over many years and therefore can go unnoticed until you have
a heart attack

Ather oscler osis

 Atherosclerosis is a condition in which plaque builds up inside the arteries.


 Plaque is made up of fat, cholesterol, calcium, and other substances found in the blood.
 Over time, plaque hardens and narrows and weakens the arteries.
 Atherosclerosis limits the flow of oxygen­rich blood to your organs and other parts of the
body.

Symptoms that may be develop


o Angina(Chest pain or pressure)­ If you have atherosclerosis in your heart you may
develop
o Carotid artery disease and transient ischemic attack (TIA if left untreated, may progress
to a stroke) ­ If you have atherosclerosis in the arteries leading to your brain and neck.
Carotid artery refers to the two major arteries supplying the brain and the neck with blood

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o Peripheral artery disease e.g. Intermittent claudication (leg pain when walking)­If you
have atherosclerosis in the arteries in your arms and legs. Peripheral arteries are the
arteries that supply other parts of the body other than the brain, neck and spinal cord with
blood
o High blood pressure or kidney failure­If you have atherosclerosis in the arteries leading
to your kidneys
o Erectile dysfunction in men ­If you have atherosclerosis in the arteries leading to your
genitals. You may have difficulties having sex.
o In women, high blood pressure can reduce blood flow to the vagina, making sex less
pleasurable.
o Aneurysms­ Aneurysms is a serious complication that can occur anywhere in your body.
An aneurysm is a bulge in the wall of your artery. If an aneurysm bursts, you may face
life­threatening internal bleeding

Causes and r isk factor s


 High cholesterol, often from getting too much cholesterol or saturated fats in your diet
 High triglycerides, a type of fat (lipid) in your blood
 Smoking and other sources of tobacco
 Diabetes
 Inflammation from diseases, such as arthritis, lupus or infections, or inflammation of
unknown cause
 High blood pressure
 High cholesterol
 Obesity
 Smoking and other tobacco use
 A family history of early heart disease and Lack of exercise

Angina/Angina Pector is­It is a symptom or a manifestation of many heart diseases and arteries
that supply the heart with blood e.g. coronary heart disease
 Angina is a term used to refer to chest pain caused by reduced blood flow to the heart
muscle.
 Angina is a symptom of e.g. coronary artery disease. Angina can be a recurring problem
or a sudden, acute health concern.
 Angina is relatively common but can be hard to distinguish from other types of chest
pain, such as the pain or discomfort of indigestion. If you have unexplained chest pain,
seek medical attention right away.

Symptoms associated with angina include:


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o Pressure
o Squeezing (feeling like a heavy weight has been placed on their chest)
o Heaviness, tightness or pain in the center of your chest
o Nausea, dizziness and Fatigue
o Shortness of breath
o Sweating

N/B. Types of anginas. Stable angina and unstable anginas.


 Stable angina is the most common form of angina, and it typically occurs with exertion
and goes away with rest. It develops when your heart works harder, such as when you
exercise or climb stairs
 Unstable angina (a medical emergency)
Occurs even at rest. It is usually more severe and lasts longer than stable angina, maybe
as long as 30 minutes. May not disappear with rest or use of angina medication. Might
signal a heart attack

 CARDIAC ARRHYTHMIA
 This refers to uneven heat rhythm(beats)
 Heart rhythm problems (heart arrhythmias) occur when the electrical impulses that
coordinate the heartbeats don't work properly, causing the heart to beat too fast, too slow
or irregularly.
 Worse heart arrhythmias may be caused by a weak or damaged heart

Symptoms

Arrhythmias may not cause any signs or symptoms. Noticeable arrhythmia symptoms may
include:
o A racing heartbeat (tachycardia)­an abnormal rapid heat beat, over 100 beats per minute
o A slow heartbeat (bradycardia)
o Chest pain
o Shortness of breath
o Lightheadedness
o Dizziness
o Fainting (syncope) or near fainting

Causes/r isk factor s

Many things can lead to, or cause, an arrhythmia, including:


 Cardiomyopathy( a condition where the heart muscle is abnormal making it harder for the
heart to pump and deliver blood to the rest of the body)
 Blocked/narrowed arteries in your heart (coronary artery disease)
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 High blood pressure


 Diabetes
 Overactive thyroid gland (hyperthyroidism) and Underactive thyroid gland
(hypothyroidism)
 Smoking
 Drinking too much alcohol or caffeine
 Drug abuse
 Stress
 Certain prescription medications
 Certain dietary supplements and herbal treatments
 Electrical shock
 Heart attack
 Abnormal heart valves
 Prior heart surgery
 Heart failure
 Congenital heart disease (Being born with a heart abnormality may affect your heart's
rhythm)
 Drugs and supplements.
Complications
 Certain arrhythmias may increase your risk of developing conditions such as Stroke.
Heart failure

 MYOCARDIAL ISCHEMIA/CARDIAC ISCHEMIA/ISCHEMIC HEART


DISEASE
 Myocardial ischemia is a condition in which the blood flow to the heart muscle is
decreased by a partial or complete blockage of the heart's arteries (coronary arteries). The
blood vessels are narrowed or blocked due to the deposition of cholesterol on their walls.
 This result into reduced supply of oxygen and nutrients to the heart, which is essential for
proper functioning of the heart.
 This may eventually result in a portion of the heart being suddenly deprived of its blood
supply leading to the death of that area of heart tissue, resulting in a heart attack.
 Myocardial ischemia may also cause serious abnormal heart rhythms.
o Treatment for myocardial ischemia is directed at improving blood flow to the heart
muscle and may include medications, a procedure to open blocked arteries or coronary
artery bypass surgery and Making heart­healthy lifestyle

Symptoms
Some people who have myocardial ischemia don't experience any signs or symptoms (silent
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ischemia). When myocardial ischemia does cause signs and symptoms, they may include:
o Chest pressure or pain typically on the left side of the body (angina pectoris)
o Neck or jaw pain
o Shoulder or arm pain
o A fast heartbeat
o Shortness of breath(dyspnea)
o Nausea and
o Vomiting
o Heart failure
o Difficulty in breathing or swelling of the extremities due to weakness of the heart
muscle

Causes
Conditions that may cause myocardial ischemia include:
 Coronary artery disease (atherosclerosis) is the most common cause of myocardial
ischemia.
Risk factor s: Factor s that may incr ease your r isk of developing myocar dial ischemia
include:
 Tobacco, smoking and long­term exposure to secondhand smoke can damage the interior
walls of arteries — including arteries of the heart.
 Smoking also increases the risk of blood clots forming in the arteries that can cause
myocardial ischemia
 High cholesterol level that can result into high blood pressure
 Diabetes. Diabetes is linked to high blood pressure. High blood pressure can damage
arteries that feed your heart by accelerating atherosclerosis.
 High blood pressure/ hypertension
 High blood pressure is common in those who are obese.
 High salt intake that may result into high blood pressure
 Stress
Complications
 The condition can result into heart attack (myocardial infarction) and Irregular heart
rhythm (arrhythmia)

 CEREBROVASCULAR DISEASE (STROKE)

 Cerebrovascular disease refers to a problem with the circulation of blood in the blood
vessels of the brain.
 A blockage with effects lasting less than 24 hours is referred to as a tr ansient ischemic
attack. A complete blockage with long­term effects is referred to as a cerebrovascular
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thrombosis (clot) or accident or a stroke. Sometimes, a blood vessel in the brain can burst
resulting in long term effects.

Types of Cer ebr ovascular disease


Cerebrovascular disease refers to cardiovascular disease that affects the blood vessels of the
brain. It occurs when the blood flow in the blood vessel to the brain is cut off or is temporarily
disrupted resulting in the death of nerve cells. The flow of the blood to the brain can be cut off or
can be temporarily disrupted when blood vessel ruptures( hemorrhagic stroke) or when blood
clot is clogged in the blood vessel( ischemic stroke). There are a number of different types of
cerebrovascular disease. The two most common types are:

 Str oke – A stroke is where the blood supply to part of the brain is cut off, which can
cause brain damage and possibly death. The blood supply can be blocked or interrupted
by a blood clot, where the blood thickens and becomes solid. This is the most common
cause of stroke.
 Tr ansient ischemic attack (TIA) – It is also known as a mini stroke, it is similar to
stroke but here the blood flow to the brain is only temporarily disrupted.

Others are:
 Subar achnoid heamor r hage– an uncommon cause of stroke where blood leaks out of
the brain's blood vessels(when blood vessel ruptures)
 Vascular dementia – problems with the blood circulation, leading to parts of the brain
not receiving enough blood and oxygen.

According to some scholars, there are four types of stroke; two are caused by blood clots, and
two are caused by ruptured blood vessels. Cer ebr al thr ombosis and cer ebr al embolism
account for approximately 70% and 80% of all strokes.

Cer ebr al thr ombosis, the most common stroke, occurs when a thrombus ( a blood clot formed
within a blood vessel and remaining attached to its place of origin)) forms and blocks blood flow
in an artery bringing blood to part of the brain. They usually occur at night or first thing in the
morning when blood pressure is low. They are often preceded by transient ischemic attach (TIA
or mini stroke)

Cer ebr al embolism occurs when an embolus (a loos blood clot) forms away from the brain,
usually in the heart. The clot is carried in the bloodstream until it lodges in an artery leading to or
in the brain and blocks the flow of blood

A subar achnoid hemor r hage occurs when a blood vessel on the brain’s surface ruptures and
bleeds into the space between the brain and skull

A cer ebr al hemor r hage occurs when defective artery in the brain busts, flooding the
surrounding tissue with blood

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Paralysis and other symptoms of a stroke or TIA may occur, depending on the site and extent of
brain damage. Patients who experience left­sided stroke most commonly experience sight and
hearing losses e.g. inability to see where food is on the plate. Right hemisphere, bilateral, or
brainstem stroke causes significant problems with feeding and swallowing in addition to speech
problems

The symptoms can be remembered with the word FAS, which stands for:

 Face (usually on one side of the body) – the face may have drooped on one side, the
person may be unable to smile, or their mouth or eye may have dropped.
 Ar ms or legs– the person may not be able to lift both arms or legs and keep them there
because of arm weakness or numbness in one arm (usually on one side of the body)
 Speech – their speech may be slurred or garbled, or they may not be able to talk at all.

Other symptoms include:

 Sudden vision problems in one or both eyes.


 Dizziness.
 Sudden, severe headache.
 Dysphagia

Management
Nutr ition ther apy
o Limit the amount of salt in your daily diet. Recommended: 2400 mg per day
.Sodium may be restricted to 2 to 4 g if there is hypertension or to control edema
o Car bohydr ates. Use of complex carbohydrates to replace saturated fats as this
lowers LDL cholesterol levels. Recommended: 50­60% .
o Pr otein. Plant based proteins e.g legumes, dry beans, nuts, whole grains and
vegetables are the best as they lower LDL cholesterol. Fat free and low­ fat dairy
products e.g. egg white, fish, skinless poultry and lean cuts of beef and pork are also
low in saturated fats and cholesterol
o High fiber diet. Recommended: 20­30 g/day, soluble fiber 10­25 g/day. Adding 5 to
10 g of soluble fiber( oats, barley, pectin reach fruits and beans ) per day is associated
with approximately a 5 % reduction in LDL cholesterol
o Reduce the total fat to no more than 20%, and trans fatty acids in your diet
particularly saturated fat. Saturated fats raises the LDL cholesterol level. For every
1% increase in kcals from saturated fats as a percentage of total energy, serum LDL
cholesterol increases by approximately 2%.On the other hand, a 1% decrease in
saturated fats will lower serum cholesterol by approximately 2%
o Satur ated fats, less than 7% of the total energy intake
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o Use of monounsatur ated (up to 20% of the total energy intake) and polyunsaturated
fats (up to 10% of the total energy intake). Monounsaturated fats e.g. plant oils and
nuts lowers LDL cholesterol levels without decreasing HDL cholesterol or
triglycerides while polyunsaturated fats e.g. linoleic acid and omega ­3­fatty acids
reduce LDL cholesterol when used instead of saturated fats. However , they can also
bring about small reductions in HDL cholesterol when compared with
monounsaturated fats
o Intake of Omega­3 fatty acids improve the health of the blood vessels, as well as
reducing Hypertension, blood clotting, inflammation and decrease the synthesis of
VLDL. They are found in fish oil, flaxseed oil and walnuts or fish oil
supplementation
o Dietary cholesterol, less than 200 mg/day/. Flax seeds are one the richest source of
omega 3
o Antioxidants such as vitamin C and vitamin E protect the arteries from damage.
o Garlic may help reduce the level of fats in the blood, improve blood flow and reduce
blood clotting.
o Potassium, magnesium and calcium are minerals that help reduce blood pressure
(maintain cell fluid balance) and blood clotting. Magnesium and potassium also helps
in muscle contraction. Low potassium level is associated with high blood pressure.
Low magnesium level is also associated high blood pressure and angina while
magnesium intake is associated with decreased incidence of CHD
o Control diabetes
o Nutritional supplements may only be effective if dietary intake is inadequate.
o Avoid foods that cause choking or that are hard to manage e.g. peanut butter, raw
vegetables, dry or crisp foods
o If the patient has problem with saliva production , foods can be moistened with small
amount of liquid e.g. gravy
o Exercise – regular daily walks of about 1 hour (to expend at least 200 kcal/day) –
Exercise has been shown to increase the level of HDLs, the so called “good cholesterol”
with no notable changes in or plasma triglycerides. Thus it helps maintain the health of
the vessels leading to the heart.
o Weight reduction using diet low in saturated fats and cholesterol. Weight reduction
reduces LDL cholesterol levels
o Stop smoking ­smoking oxidizes cholesterol, causing it to deposit in your blood vessels
and contribute to atherosclerosis.
o Avoid Sedentary lifestyle and stress ­ being physically active
o Reduced alcohol intake

Sur ger y
o Arterial reconstruction surgery to bypass them­ to redirect the flow blood flow in the

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artery
o Removal of fatty deposits in inner lungs (endarterectomy)
o Balloon angioplasty to widen the vessels(using balloon –tipped catheter inserted
through the artery at the groin or wrist)
Dr ug Ther apy
oDrug therapy aims – to prevent blood clotting

 PERIPHERAL VASCULAR DISEASE

Peripheral vascular disease is characterized by narrowing blood vessels in the legs and
sometimes the arms. Blood flow is restricted and causes pain in the affected areas. Risk factors
include hypertension and diabetes mellitus. Major risk factor is cigarette smoking which
constrict blood vessels.
Symptoms
Aching of the leg muscles when walking. Resting the leg for few minutes relives pain, but it
recurs shortly when walking is resumed. The symptom is called intermittent claudication
Intermittent claudication­A symptomatic pattern of peripheral vascular disease, characterized by
the absence of pain or discomfort in a limb, usually the legs, when at rest, which is followed by
pain and weakness when walking, intensifying until walking becomes impossible, and then
disappearing again after a rest period

Management
 Stop smoking
 Surgery
o Arterial reconstruction surgery to bypass them­ to redirect the flow blood flow in the
artery
o Removal of fatty deposits in inner linings (endarterectomy)
o Balloon angioplasty to widen the vessels(using balloon –tipped catheter inserted
through the artery at the groin or wrist)
 Drug therapy­e.g. antiplatelet or anticoagulant agents to prevent blood clotting
 Nutrition therapy as described for cerebrovascular diseases
 Exercise­The person should walk every day gradually increasing to about 1 hour and
stopping whenever intermittent pain occurs and resuming when it stops.
 Lifestyle­Regular inspection of feet, daily washing of feet and stocking change, good
fitting shoes to avoid pressure

 CONGESTIVE HEART FAILURE

 Congestive Heart Failure (CHF) or severe heart disease is when the heart can no longer
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provide or pump enough blood to the rest of the body as it is needed.


 CHF can happen as a result of damage to the heart muscle, including coronary artery
disease (CAD), heart attack, cardiomyopathy, valve disease, heart defects present at birth,
diabetes mellitus and chronic renal disease. Patients with heart failure usually suffer from
shortness of breath and swelling of the legs.
 Because of the reduced circulation, tissues retain fluid that would normally be carries off
by the blood. Sodium builds up, and more fluid is retained, resulting in edema. In an
attempt to compensate for this pumping deficit, the heart beats faster and enlarges, this
adds to the heart’s burden. In advanced cases when edema affects the lungs, death occurs.
 With the inadequate circulation, body tissues do not receive sufficient amounts of
nutrients. This insufficiency can cause malnutrition ad underweight, although the edema
can mask these problems.
Increased cellular free potassium
As reduced blood circulation depresses cell metabolism, cell protein is broken down and
releases its bound potassium in the cell. As a result, the amount of free potassium inside
the cell is increased, which increases intracellular osmotic pressure. Sodium ions in fluid
surrounding the cell then also increase in number to balance increased osmotic pressure
within the cell and to prevent cell dehydration. In time, the increased sodium outside the
cell causes still more water retention
Symptoms
o Shortness of breath (dyspnea) when you lie down
o Fatigue and weakness
o Swelling (edema) in your legs, ankles and feet
o Rapid or irregular heartbeat
o Reduced ability to exercise
o Fainting and severe weakness.
o Persistent cough or wheezing with white or pink blood­tinged phlegm
o Increased need to urinate at night
o Swelling of your abdomen (ascites)
o Sudden weight gain from fluid retention
o Lack of appetite and nausea
o Difficulty concentrating or decreased alertness

Dr ug Ther apy
o Diuretics(Any substance that tends to increase the flow of urine, which causes the
body to get rid of excess water)to be used to aid in the excretion of water
o Digitalis to strengthen contraction of the heart muscles.
o Because diuretics can cause loss of potassium the client’s potassium should be
carefully monitored to prevent hypokalemia, which can upset the heartbeat.
o When necessary prescribe supplementary potassium.
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Diet Ther apy


o Reduce fluid intake to 11/2­2 liters per day.
o Sodium restricted diet 1 – 2 g/day.
o Salt should not be used in cooking or at table
o Fresh unprocessed foods such as meat, fish, eggs, milk and are moderate sources – use
in small units.
o Fruits especially oranges, bananas, kiwifruit, avocados, green beans, pumpkin,
pineapple, strawberries, spinach, tomatoes, broccoli, potatoes, sweet potatoes, yams
and prunes can be useful to restore potassium levels and unprocessed cereals contains
little sodium.
o Processed foods and cereals products are rich in sodium and should be avoided.
o Moderation of alcohol

N/B Two hormones are involved in fluid balance in normal circulation i.e Aldoster one and
Antidiur etic hor mone (ADH) also known as vasopressin. There mechanisms can result into
increased cardiac edema.
Aldoster one hor mone­As the heart fails to propel blood flow circulation forward, deficient
cardiac output effectively reduces blood flow through kidney nephrons. Decreased renal blood
flow pressure triggers the liver to produce a hormone to stimulate adrenal glands to produce
aldosterone that in turn effects a reabsorption of sodium in an ion exchange with potassium and
water reabsorption follows
Antidiur etic hor mone­Cardiac stress and reduced renal flow cause the release of antidiuretic
hormone from the pituitary gland. ADH then stimulates more water reabsorption in nephrons of
the kidney thus increasing the problem of edema

 RHEUMATIC HEART DISEASE

Rheumatic heart disease is caused by damage to the heart valves and heart muscle
from the inflammation and scarring caused by rheumatic fever.
 Rheumatic fever is an inflammatory disorder caused by a Group A streptococcus
bacteria that normally affects the throat. It affects the connective tissue of the body,
causing temporary, painful arthritis and other symptoms. In some cases, rheumatic
fever causes long­term damage to the heart and its valves. This is called rheumatic
heart disease.
 Rheumatic fever usually begins as a sore throat or tonsillitis in children.
 Rheumatic fever mostly affects children between 5­15 years in developing countries,
especially where poverty is widespread.
Symptoms of Rheumatic Hear t Disease
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o Shortness of breath
o Fatigue
o Irregular heart beat
o Chest pain and fainting

 MYOCARDIAL INFARCTION

 This is sudden tissue death caused by blockage of vessels that feed the heart muscle, also
called heart attack or cardiac arrest
 A heart attack occurs when the flow of blood to the heart is blocked, most often by a
build­up of fat, cholesterol (Atherosclerosis­it is the primary cause) which form a plaque
in the arteries that feed the heart (coronary arteries).Other contributing factors are
abnormal blood clotting, hypertension and infections caused by rheumatic fever(which
damages heart valves)
 The heart tissue is denied blood because of this blockage and dies

Symptoms.
o Pain, or a squeezing or aching sensation in your chest or arms that may spread to your
neck, jaw or back
o Nausea
o Pressure and tightness
o Indigestion
o Heartburn or abdominal pain
o Shortness of breath
o Cold sweat
o Fatigue
o Lightheadedness or sudden dizziness

Heart attack symptoms vary. Not all people who have heart attacks have the same symptoms or
have the same severity of symptoms. Some people have mild pain; others have more severe pain.
Some people have no symptoms, while for others, the first sign may be sudden cardiac arrest
(sudden, unexpected loss of heart function, breathing and consciousness. Cardiac arrest usually
results from an electrical disturbance "short circuits" in the heart that disrupts its pumping action,
stopping flow to the rest of the body. It differs with heart attack which occurs when blood flow
to a portion of the heat is blocked. Heart attack can result into cardiac arrest) However, the more
signs and symptoms you have, the greater the likelihood you're having a heart attack.

Some heart attacks strike suddenly, but many people have warning signs and symptoms hours,
days or weeks in advance. The earliest warning may be recurrent chest pain (angina) that's

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triggered by exertion and relieved by rest. Angina is caused by a temporary decrease in blood
flow to the heart.

Taking aspirin during a heart attack could reduce heart damage by helping to keep your blood
from clotting. Aspirin can interact with other medications, however, so don't take an aspirin
unless your doctor or emergency medical personnel recommend it.

If you encounter someone who is unconscious, first call for emergency medical help. Then begin
CPR to keep blood flowing. Push hard and fast on the person's chest — about 100 compressions
a minute. It's not necessary to check the person's airway or deliver rescue breaths unless you've
been trained in CPR.
Use of tobacco and of illicit drugs, such as cocaine, can cause a life­threatening spasm. A heart
attack can also occur due to a tear in the heart artery (spontaneous coronary artery dissection).

Risk Factor s
 Certain factors contribute to the unwanted buildup of fatty deposits (atherosclerosis) that
narrows arteries throughout your body.
Heart attack risk factors include:
 Age. Men age 45 or older and women age 55 or older are more likely to have a heart
attack than are younger men and women.
 Tobacco. Smoking and long­term exposure to secondhand smoke increase the risk of a
heart attack.
 High blood pressure. Over time, high blood pressure can damage arteries that feed your
heart by accelerating atherosclerosis.
 High blood pressure that occurs with obesity, smoking, high cholesterol or diabetes
increases your risk even more.
 High blood cholesterol or triglyceride levels. A high level of low­density lipoprotein
(LDL) cholesterol (the "bad" cholesterol) is most likely to narrow arteries.
 However, a high level of high­density lipoprotein (HDL) cholesterol (the "good"
cholesterol) lowers your risk of heart attack.
 Diabetes. Insulin, a hormone secreted by your pancreas, allows your body to use glucose,
a form of sugar. Having diabetes — not producing enough insulin or not responding to
insulin properly — causes your body's blood sugar levels to rise. Diabetes, especially
uncontrolled, increases your risk of a heart attack.
 Family history of heart attack. If your siblings, parents or grandparents have had early
heart attacks (by age 55 for male relatives and by age 65 for female relatives), you may
be at increased risk.
 Lack of physical activity. An inactive lifestyle contributes to high blood cholesterol
levels and obesity. Exercise is also beneficial in lowering high blood pressure.
 Obesity. Obesity is associated with high blood cholesterol levels, high triglyceride levels,
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high blood pressure and diabetes. Losing just 10 percent of your body weight can lower
this risk, however.
 Stress. You may respond to stress in ways that can increase your risk of a heart attack.
 Using stimulant drugs, such as cocaine or amphetamines
 A history of preeclampsia. This condition causes high blood pressure during pregnancy
and increases the lifetime risk of heart disease.
 A history of an autoimmune condition, such as rheumatoid arthritis or lupus. Conditions
such as rheumatoid arthritis, lupus and other autoimmune conditions can increase your
risk of having a heart attack.
Complications
Abnormal heart rhythms (arrhythmias), Heart failure, Heart and valve rupture

Dietar y Management
o The dual goal is to allow the heart to rest and its tissue to heal.
o After the attack, the client is in shock. This causes a fluid shift and the client may feel
thirsty. The client should be given nothing by mouth (NPO), however until after
evaluation/ if nausea remains after the period of shock, IV infusions are given to prevent
dehydration.
o After several hours, the client may begin to eat. A liquid diet may be recommended for
the first 24 hours.
o A low cholesterol diet – low sodium diet is usually given, regulating the amount eaten.
o Foods should not be extremely hot or extremely cold.
o Food should be easy to chew and digest and contain little roughage so that the work of
the heart is minimal. Both chewing and increased activity of the gastro intestinal tract that
follow ingestion of high fiber foods cause extra work for the heart.
o Limit types and amounts of fats.
o Sodium is limited to prevent fluid accumulation

 ANEURSYM

 Aneurysm occurs when part of a blood vessel (arteries) e.g. aorta or brain blood vessel or
cardiac arteries becomes weakened (thinning of the artery wall), swells and bulges
outwards (like a balloon).
 The swelling can be quite small or very large. The most common aneurysm affects the
brain. A brain aneurysm can leak or rupture, causing bleeding into the brain (hemorrhagic
stroke). This type of hemorrhagic stroke is called a subarachnoid hemorrhage.
 Most brain aneurysms, however, don't rupture, create health problems or cause
symptoms.

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Symptoms

Ruptur ed aneur ysm


A sudden, severe headache is the key symptom of a ruptured aneurysm. This headache is often
described as the "worst headache" ever experienced.
Common signs and symptoms of a ruptured aneurysm include:
 Sudden, extremely severe headache
 Nausea and vomiting
 Stiff neck
 Blurred or double vision
 Sensitivity to light
 Seizure
 A drooping eyelid
 Loss of consciousness
 Confusion
Unr uptur ed aneur ysm
An unruptured brain aneurysm may produce no symptoms, particularly if it's small. However, a
large unruptured aneurysm may press on brain tissues and nerves, possibly causing:
 Pain above and behind an eye
 A dilated pupil
 Change in vision or double vision
 Numbness, weakness or paralysis of one side of the face
 A drooping eyelid
Risk Factor s
A number of factors can contribute to weakness in an artery wall and increase the risk of a brain
aneurysm. Brain aneurysms are more common in adults than in children and more common in
women than in men.
Some of these risk factors develop over time; others are present at birth.
Risk factor s that develop over time
These include:
 Older age
 Smoking
 High blood pressure (hypertension)
 Hardening of the arteries (arteriosclerosis),
 High cholesterol level,
 Drug abuse, particularly the use of cocaine
 Head injury
 Heavy alcohol consumption
 Lower estrogen levels after menopause

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Risk factor s pr esent at bir th


These include:
 kidney disease
 Abnormally narrow aorta the large blood vessel
 Cerebral arteriovenous malformation (brain AVM)
 An abnormal connection between arteries and veins in the brain
 Family history of brain aneurysm, particularly a first­degree relative, such as a parent,
brother or sister
Complications
 When a brain aneurysm ruptures, the bleeding usually lasts only a few seconds. The
blood can cause direct damage to surrounding cells, and the bleeding can damage or kill
other cells.
 It also increases pressure inside the skull.
 If the pressure becomes too elevated, the blood and oxygen supply to the brain may be
disrupted to the point that loss of consciousness or even death may occur.

Management
 Keep your hypertension in check
 Maintain a healthy lifestyle
 Keep your blood cholesterol levels under control
 Stay away from stress
 Get some exercise
 Maintain a good diet
 Avoid excessive alcohol drinking
 Quit smoking

 HYPERTENSION

 Hypertension is also referred to as high blood pressure/elevated blood pressure.


 According to WHO, hypertension is defined as a condition in which the blood pressure is
greater than 160/95 mm Hg i.e. when systolic pressure exceeds 160 mm Hg and diastolic
pressure exceeds 95 mm Hg
 It is a condition in which the arteries have persistently elevated blood pressure(i.e. it is
where. the force of the blood against your artery walls is high enough that it may
eventually cause health problems, such as heart disease )
 Blood pressure is determined by the amount of blood your heart pumps and the amount
of resistance to blood flow in your arteries. The more blood your heart pumps and the

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narrower your arteries, the higher your blood pressure


Tests and Diagnosis
 A sphygmomanometer( a pressure­measuring gauge) is usually placed around the arm to
measure the blood pressure
 A blood pressure reading, given in millimeters of mercury (mm Hg), has two numbers.
 The first, or upper, number measures the pressure in your arteries when your heart beats
(systolic pressure).
 The second, or lower, number measures the pressure in your arteries between beats
(diastolic pressure).
 Blood pressure measurements fall into four general categories:
 Normal blood pressure. Your blood pressure is normal if it's between 90/60mmHg and
120/80 mm Hg.
 High blood pressure is considered to be 140/90mmHg or higher
 Low blood pressure is considered to be 90/60mmHg or lower
 Once blood pressure reaches 120/80mm Hg, the risk of cardiovascular disease begins to
increase.­Prehypertension.
 Pr ehyper tension is a systolic pressure ranging from 120 to 139 mm Hg or a diastolic
pressure ranging from 80 to 89 mm Hg.
 Prehypertension tends to get worse over time.
 Stage 1 hyper tension. Stage 1 hypertension is a systolic pressure ranging from 140 to
159 mm Hg or a diastolic pressure ranging from 90 to 99 mm Hg.
 Stage 2 hyper tension. More severe hypertension, stage 2 hypertension is a systolic
pressure of 160 mm Hg or higher or a diastolic pressure of 100 mm Hg or higher.
 Both numbers in a blood pressure reading are important. But after age 60, the systolic
reading is even more significant.
 Isolated systolic hypertension — when diastolic pressure is normal but systolic pressure
is high — is a common type of high blood pressure among people older than 60.
Summer y
Blood Systolic(mm Hg) Diastolic(mm Hg)
pr essur e(BP)
Classification
Normal < 120 And <80
Prehypertension 120­139 80­89
Stage 1 140­159 90­99
hypertension
Stage 2 More or equals More or equals
hypertension 160 100

Symptoms
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 Many people with hypertension have no symptoms.


 Headache, dizziness, impaired vision, failing memory, shortness of breath, pain over the
heart, gastrointestinal disturbances and unexplained tiredness are some of the symptoms
Causes
There are two types of high blood pressure.
 Primary (essential) hypertension
o For most adults, there's no identifiable cause of high blood pressure (the cause is
unknown). This type of high blood pressure, called essential hypertension or
primary hypertension, tends to develop gradually over many years.90% of
hypertension fall under this category
 Secondary hypertension
o Some people have high blood pressure caused by an underlying condition. This
type of high blood pressure, called secondary hypertension, tends to appear
suddenly and cause higher blood pressure than does primary hypertension.
o Various conditions and medications can lead to secondary hypertension,
including:
Kidney problems e.g glomerulonephritis, Adrenal gland tumors, Diseases of the
ovary, Thyroid problems, Certain defects in blood vessels you're born with
(congenital), Certain medications, such as birth control pills, decongestants, over­
the­counter pain relievers and some prescription drugs, , Illegal drugs, such as
cocaine and amphetamines, Alcohol abuse or chronic alcohol use, Obstructive
sleep apnea

Risk Factor s
 High blood pressure has many risk factors, including:
 Age. The risk of high blood pressure increases as you age. Through in early middle age,
or about age 45, high blood pressure is more common in men.
 Women are more likely to develop high blood pressure after age 65
 Race. High blood pressure is particularly common among blacks, often developing at an
earlier age than it does in whites. Serious complications, such as stroke, heart attack, and
kidney failure, also are more common in blacks.
 Family histor y. High blood pressure tends to run in families.
 Being over weight or obese. The more you weigh the more blood you need to supply
oxygen and nutrients to your tissues. As the volume of blood circulated through your
blood vessels increases, so does the pressure on your artery walls.
 Not being physically active. People who are inactive tend to have higher heart rates. The
higher your heart rate, the harder your heart must work with each contraction and the
stronger the force on your arteries. Lack of physical activity also increases the risk of
being overweight.
 Using tobacco. Not only does smoking or chewing tobacco immediately raise your
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blood pressure temporarily, but the chemicals in tobacco can damage the lining of your
artery walls. This can cause your arteries to narrow, increasing your blood pressure.
Secondhand smoke also can increase your blood pressure.
 Too much salt (sodium) in your diet. Too much sodium in your diet can cause your
body to retain fluid, which increases blood pressure.
 Too little potassium in your diet. Potassium helps balance the amount of sodium in
your cells. If you don't get enough potassium in your diet or retain enough potassium, you
may accumulate too much sodium in your blood.
 Too little vitamin D in your diet. It's uncertain if having too little vitamin D in your diet
can lead to high blood pressure. Vitamin D may affect an enzyme produced by your
kidneys that affects your blood pressure.
 Dr inking too much alcohol. Over time, heavy drinking can damage your heart. Having
more than two drinks a day for men and more than one drink a day for women may affect
your blood pressure. If you drink alcohol, do so in moderation.
 Str ess. High levels of stress can lead to a temporary increase in blood pressure. Certain
chronic conditions. Certain chronic conditions also may increase your risk of high blood
pressure, such as kidney disease and sleep apnea.
 Sometimes pr egnancy contributes to high blood pressure, as well.
 Although high blood pressure is most common in adults, childr en may be at risk, too.
For some children, high blood pressure is caused by problems with the kidneys or heart.
But for a growing number of kids, poor lifestyle habits, such as an unhealthy diet, obesity
and lack of exercise, contribute to high blood pressure.

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Other r isks factor s of high blood pr essur e

Complications
 Excessive pressure on your artery walls caused by high blood pressure can damage your
blood vessels, as well as organs in your body.
 The higher your blood pressure and the longer it goes uncontrolled, the greater the
damage
Uncontr olled high blood pr essur e can r esult into
 Hear t attack or str oke. High blood pressure can cause hardening and thickening of the
arteries (atherosclerosis), which can lead to a heart attack, stroke or other complications.
 Aneur ysm. Increased blood pressure can cause your blood vessels to weaken and bulge,
forming an aneurysm. If an aneurysm ruptures, it can be life­threatening.
 Hear t failur e. To pump blood against the higher pressure in your vessels, your heart
muscle thickens. Eventually, the thickened muscle may have a hard time pumping
enough blood to meet your body's needs, which can lead to heart failure.
 Weakened and nar r owed blood vessels in your kidneys. This can prevent these organs
from functioning normally.
 Thickened, nar r owed or tor n blood vessels in the eyes. This can result in vision loss.
 Metabolic syndr ome. This syndrome is a cluster of disorders of your body's metabolism,
including increased waist circumference; high triglycerides; low high­density lipoprotein
(HDL); or "good," cholesterol; high blood pressure; and high insulin levels.
 Tr ouble with memor y or under standing. Uncontrolled high blood pressure may also
affect your ability to think, remember and learn. Trouble with memory or understanding

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concepts is more common in people with high blood pressure


 Hyper tension can lead to damaged or gans, as well as several illnesses, such as renal
failure (kidney failure), aneurysm, heart failure, stroke, or heart attack

DASH DIET AND HIGH BLOOD PRESSURE

 DASH stands for ­Dietary Approaches to Stop Hypertension (DASH Diet)


 This a dietary pattern promoted to prevent and control hypertension.
 It is a diet rich in fruits, vegetables, and low­fat dairy foods/fat free dairy foods
 It also emphasizes on moderate amount of whole grains, fish, poultry and nuts
 But the diet should be low/limited in sodium, sweets, sugary or sugar sweetened foods,
red meat and fats
 The DASH diet is also recommended to prevent osteoporosis, cancer, heart diseases,
stroke and diabetes
DASH diet suggests
 Fr uits: 4­5 daily ser vings. Fruits are rich in potassium, magnesium, and fibre
 Vegetables: 4­5 daily ser vings e.g. tomatoes, broccoli, carrots, sweet potatoes, greens.
They are high in fibre
N/B. Increased intake of vegetables and fruits must be ensured for increase intake of potassium
i.e. 4.7grams or 4700mg per day.
 Whole gr ains: 6­8 daily ser vings e.g. brown bread, brown rice, cereals. They are reach
in fibre
 Low fat or fat fr ee dair y pr oducts: 2­3 daily ser vings e.g. yought, fresh milk. They are
rich in calcium, vitamin D, and proteins. Choose low fat dairy of fat free because dairy
products are reach in saturated fats
 Lean meat, poultr y and fish: 6 ser vings or fever daily. They are rich in protein, B
vitamins, iron and zinc. Remove the skin from poultry. Grill, bake, or boil your meat
 Fats and oils: 2­3 daily ser vings. Fats helps your body absorb essential vitamins and
helps the immune system. Too much fat increases the risk of heart diseases, diabetes and
obesity more so the saturated fats
 Nuts, seeds and legumes: 4­5 ser vings per week e.g. beans, kidney beans, peas,
sunflower seeds
 Sodium: Reduce the sodium intake to 1500 mg (2/3 teaspoon) daily. Begin by
reducing the amount of salt/sodium you eat to not more than 2 to 3g sodium or 6 g of
sodium chloride. Other measures to reduce sodium intake: never put salt at the table and
no salt should be used in severe hypertension, do not use salted foods such as biscuits,
cakes, pastries, bread, dry fish, salted butter, peanut butter, cheese, salted potato chips,
baking powder, sodium bicarbonate, sodium benzoate, salt preserved foods such as
pickles and canned foods

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 Increased intake of potassium to 4.7gr ams or 4700mg per day. This is ensured by
increased intake of fruits and vegetables
You can achieve this by ensuring that you add servings of vegetables at lunch and dinner; and
servings of fruits to your meals or s snacks
Other lifestyle changes can help prevent and lower high blood pressure:

 Cut back on alcohol if you drink too much


 Lose weight if you're overweight
 Exercise regularly
 Cut down on caffeine
 Stop smoking
 Try to get at least six hours of sleep a night
 Increase intake of foods rich in Omega 3 fatty acids
 Physical activity at least 30 minutes’ walk daily.
 Drug therapies for reducing blood pressure
 Fluid may be restricted to 1000ml­ 1500 ml per day if needed
N/B Nutrients that have effect on blood pressure are calcium, potassium and sodium

 HYPERLIPIDEMIA
 Hyperlipidemia is characterized by elevated concentrations of circulating lipids,
increasing the risk of atherosclerosis and other serious conditions. Specific classes of
hyperlipidemia include hyper lipopr oteinemia, elevated very low­density lipoprotein
(VLDL) and low­density lipoprotein (LDL) levels, hyper cholester olemia (elevated
cholesterol levels), and hyper tr iglycer idemia (elevated triglyceride levels).
 Hyperlipidemia is typically asymptomatic and is frequently detected during routine
screening.

Nutr itional Consider


Elevated ations of blood lipids, particularly LDL cholesterol, are a significant
concentrations
risk factor for atherosclerosis and coronary heart disease.
 Reducing saturated fat and cholesterol intake decreases these concentrations. Cholesterol
is present only in foods of animal origin, and these products are often the primary source
of saturated fat in a person’s diet. Thus, a diet that reduces or eliminates these products
lowers total and LDL cholesterol and triglycerides.

The key nutritional interventions are as follows:

Reduced Dietar y Fat and Cholester ol

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 Following a diet low in saturated fat and total fat and replacing saturated with
unsaturated fat lower cholesterol production and blood lipids. A diet deriving ≤ 7% of
calories from saturated fat and ≤ 200 mg/day of cholesterol.

Vegetarian (especially vegan) diets that are free of cholesterol and very low in
saturated fat reduce LDL cholesterol by 17% to 40%, with the strongest effects seen
when the diet is combined with exercise.

Reducing total fat, saturated fat, and cholesterol intake also lowers triglyceride levels
by approximately 20%.

Proteins should make up 12­20% of the diet.
 Consuming small amounts of fats in their naturally occurring form (eg, nuts) may be
preferable to using oils because of their potentially cardio­protective nutrients:
magnesium, fiber, vitamin E, and flavonoids.
 Soluble fiber (mostly fr om oats, bar ley, pectin r each fr uits and beans) reduces
cholesterol concentrations chiefly through binding of bile acids, leading to increased
cholesterol excretion.
 Soluble fiber appears to be most effective in the context of a diet low in saturated fats.
Soluble fiber lowers total cholesterol and lowers the LDL: HDL cholesterol ratio.
Common sources include oats, barley, legumes, and many fruits and vegetables.
 While diets high in refined carbohydrates (e.g. white flour) can increase plasma
triglyceride concentrations, the opposite is typically seen with diets high in unrefined,
low–glycemic–index carbohydrate sources, such as legumes and most whole grains.
Carbohydrates should make up 50­55% of the calories.
 Soy protein reduces hepatic cholesterol synthesis and may increase the hepatic LDL
receptor uptake of cholesterol. In clinical tests, soy protein decreased total cholesterol
by 9%, LDL by 13%, and triglycerides by 10%.
 Nuts (almonds, peanuts, pecans, and walnuts) appear to have hypolipidemic effects,
apparently due to their fiber, plant sterol, and unsaturated fat content. Walnuts, for
example, lowered total cholesterol by 12% and LDL cholesterol by 16%, and lowered
the LDL: HDL ratio by 12%.
 Plant sterols (often in the form of margarine) reduce LDL cholesterol concentrations
by roughly 10% by inhibiting cholesterol absorption.
 Avoiding alcohol may help reduce triglycerides. Alcohol appears to raise
triglycerides by 5 to 10 mg/dL. Restricting its consumption joins diet, exercise, and
weight loss as cornerstones of treatment for patients with elevated triglyceride levels.
 Use Fat free or low fat milk
 Nutrition consultation to advise patient in above diet and arrange follow–up.
 Smoking cessation.
 Alcohol restriction for hypertriglyceridemia.

Weight r eduction
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o Exercise prescription (patient–specific). Obese patients should be instructed to attain


ideal body weight by appropriate reduction in caloric intake and regular exercise.

N/B 1.Fats ar e divided into two categor ies.1. Satur ated. 2. Unsatur ated

Saturated fats raises LDL cholesterol level. Unsaturated fats are divided into two.
Monounsaturated and polyunsaturated fats. Both monounsaturated and polyunsaturated lowers
LDL cholesterol levels. Good sources of unsaturated fats are plant/vegetable oils and nuts.
Therefore to reduce cholesterol in the body: 1. Increase intake of polyunsaturated fats 2.Increase
intake of plant proteins as compared to animal proteins e.g. legumes, dry beans, nuts, whole
grains, and vegetables 3. Increase intake of soluble fiber (mostly fr om oats, bar ley, pectin
r each fr uits and beans)

N/B 2.Cholester al, Lipopr oteins and Lipids

Cholesterol and triglycerides (TG)­Cholester ol is a fatlike substance in all cell membranes and
blood that helps in cell membrane support; hormone production (such as estrogen, testosterone,
progesterone, aldosterone and cortisone); vitamin D and bile production. Cholesterol and
triglycerides (TG) cannot dissolve in blood and must be transported to and from cells by
individual components containing both lipids and proteins (lipoproteins).There are five types of
lipoproteins, classified according to the fat contentment and thus their density. Those with
highest fat content possesses the lowest density

Chylomicr ons. They have the highest lipid(They are the largest) and lowest density and are
composed mainly of dietary TG, with a small amount of carrier protein .They accumulate in
portal blood after meal and efficiently cleared from the blood by lipoprotein lipase enzyme/They
transport diet derived fat lipids mostly triglycerides from the intestinal cells into the blood. They
are synthesized in the intestinal wall

Inter mediate density lipopr otein. They continue the delivery of endogenous TG to cells and
carry about 40% cholesterol. They are synthesized in the liver

Ver y Low Density Lipopr otein (VLDL)

These lipoproteins contain about 9% protein and are made by the liver cells to transport
triglycerides that are produced within the body mainly in the liver and intestinal mucosa to
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various tissues in the body. They are synthesized in the liver

Low Density Lipopr otein (LDL)

These lipoproteins contain 21% proteins. They are derived from VLDL as cells remove
triglycerides from them. They are composed of cholesterol. They circulate throughout the body
making their contents available to all cells. As the cells take the triglycerides from them they
pick cholesterol and phospholipids to build new membranes, make hormones or to store for later
use. They are cleared from circulation by special low density lipoprotein receptors found on the
liver cells. This clearance by the low density receptors is crucial in the control of blood
cholesterol levels. They are synthesized in the liver

High Density Lipopr otein (HDL)

They are formed in the liver from endogenous sources. High density lipoproteins contain 50%
protein. They transport cholesterol back to the liver from peripheral cells for catabolism or
disposal (excretion). They are also thought to favour cholesterol excretion through the synthesis
of bile and are referred to as good lipoprotein. They are synthesized in the liver

 HYPERLIPOPROTEINEMIA

 Hyperlipoproteinemia is a common disorder. It results from an inability to break down


lipids or fats in your body, specifically cholesterol and triglycerides. There are several
types of hyperlipoproteinemia. The type depends on the concentration of lipids and which
are affected.
 High levels of cholesterol or triglycerides are serious because they’re associated with
heart problems.
Causes
Hyperlipoproteinemia can be a primary or secondary condition.
 Primary hyperlipoproteinemia is often genetic. It’s a result of a defect or mutation in
lipoproteins. These changes result in problems with accumulation of lipids in your body.

 Secondary hyperlipoproteinemia is the result of other health conditions that lead to high
levels of lipids in your body. These include:
o diabetes

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o hypothyroidism
o pancreatitis
o use of certain drugs, such as contraceptives and steroids
o certain lifestyle choices
 It is important to recognize that hyperlipoproteinemia may be secondary to diet, drugs,
disorders of metabolism and diseases. It is difficult to correct a secondary dyslipidemia
unless the primary problem is addressed. Thus, the first step in analysis is always a
detailed history including evaluation of diet, medications (prescription or over­the­
counter), family history, and personal history of thyroid disease, diabetes, or kidney
disease.  

Ther e ar e five
Type types
1 is of pr imar
an inherited y hyper lipopr
condition. oteinemia:
It causes the normal breakdown of fats in your body to
be disrupted. A large amount of fat builds up in your blood as a result.
 Type 2 runs in families. It’s characterized by an increase of circulating cholesterol, either
low­density lipoproteins (LDL) alone or with very­low­density lipoproteins (VLDL).
These are considered the “bad cholesterols.”
 Type 3 is a recessively inherited disorder in which intermediate­density lipoproteins
(IDL) accumulate in your blood. IDL has a cholesterol­to­triglycerides ratio that’s higher
than that for VLDL. This disorder results in high plasma levels of both cholesterol and
triglycerides.
 Type 4 is a dominantly inherited disorder. It’s characterized by high triglycerides
contained in VLDL. The levels of cholesterol and phospholipids in your blood usually
remain within normal limits.
 Type 5 runs in families. It involves high levels of LDL alone or together with VLDL.

Symptoms of hyper lipopr oteinemia


 Lipid deposits are the main symptom of hyperlipoproteinemia. The location of lipid
deposits can help to determine the type. Some lipid deposits, called xanthomas, are
yellow and crusty. They occur on your skin.
 Many people with this condition experience no symptoms. They may become aware of it
when they develop a heart condition.
Other signs and symptoms of hyperlipoproteinemia include:
o pancreatitis (type 1)
o abdominal pain (types 1 and 5)
o enlarged liver or spleen (type 1)
o lipid deposits or xanthomas (type 1)
o family history of heart disease (types 2 and 4)
o family history of diabetes (types 4 and 5)
o heart attack

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o stroke

 Physical examination should include careful inspection of the skin, tendons, and eyes
looking for xanthoma, xanthelasma, corneal arcus, and lipemia retinalis, which directly
suggest a lipid disorder.
 In addition, evaluation of the blood pressure and peripheral pulses may provide evidence
for existing atherosclerosis, raising the probability of finding a lipid disorder upon
laboratory testing.

Dietar y and Lifestyle changes


 Restrict total calories to maintain a desirable weight.
 Consume less than 200mg/day of cholesterol.
 Total fat consumption should be 25% to 30% of total calories.
 Saturated fat should be less than 7% of total calories.
 Polyunsaturated fat should be 10% or less of total calories.
 Monounsaturated fat should be 20% or less of total calories.
 Carbohydrate should be predominantly of the complex variety and provide 50%
to 60% of total calories
 Fibre should be 20 to 30g/day
 Protein should account for approximately 15% of total calories 
 In addition to dietary modification, a therapeutic lifestyle change must include
regular exercise

TOPIC: RENAL DISORDERS

RENAL DISEASES

Physiology and function of kidneys

 The kidneys are two bean­shaped organs, each about the size of a fist, each weighing
about 150g. They are located just below the rib cage, one on each side of the spine.
 Every day, the two kidneys filter about 120 to 150 quarts of blood to produce about 1 to 2
quarts of urine, composed of wastes and extra fluid. The urine flows from the kidneys to
the bladder through two thin tubes of muscle called ureters, one on each side of the
bladder. The bladder stores urine.
 In men the urethra is long, while in women it is short.

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Functions of the Kidney


The kidneys are essential to life through three functions: excretory, endocrine, and regulatory
1. Excr etor y function: Excretory functions serves to remove potentially toxic metabolic
substances such as urea (major end products of protein metabolism), uric acid, keto acid
creatinine, as well as hydrogen ions which arise from sulphur containing amino acids.
They also excrete surplus quantity of water, sodium, potassium, calcium, phosphate and
magnesium from the blood.
2. Regulator y functions­ Regulatory functions controls electrolytes, acid­ base and fluid
balance. The regulatory functions helps in the maintenance of serum concentrations of
sodium, potassium, chloride, bicarbonate and hydrogen ions
 Acid­base balance is maintained through a buffer system, which maintains blood at pH of
7.4
 Bicarbonate carries hydrogen ions to the kidneys where they are removed from extracellular
fluid in the tubules, returned to the bloodstream as needed
 Phosphate buffers intracellular fluid
 When fluid volume is low, anti­diuretic hormone (ADH) or vasopressin is released from the
anterior pituitary; increases absorption of water in the collecting duct. When extracellular
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volume (ECV) decreases, the renin­angiotensin­aldosterone system is activated  excretes


less sodium chloride

3. Endocr ine functions. Endocrine functions include conver sion of the inactive form of
vitamin D (25­hydr oxy­cholecalicifer ol) to active vitamin D (1, 25
dihydr oxycholecalcifer ol), synthesis of er ythr opoietin hormone (needed for the
production of red blood cells in the bone marrow), and for the synthesis and release of
renin, which regulates the blood pressure.
 Deficiency of erythropoietin is a factor in the severe anaemia present in chronic
renal disease.
 Active vitamin D promotes efficient absorption of calcium by the gut and is one
of the substances necessary for bone remodelling and maintenance; and also
promotes the metabolism of calcium and phosphorus

How do the kidneys wor k?


• These functions are accomplished by a filtering units called the nephron. Each kidney is
made up of about a million nephrons (The basic functional unit of the kidney). Each
nephron consists of a glomerulus (a filter) and a long tubule (the collecting duct)
• Each nephron filters a small amount of blood. The nephrons work through a two­step
process. The glomerulus lets fluid and waste pr oducts pass thr ough it; however, it
pr events blood cells and lar ge molecules, mostly pr oteins, fr om passing. The filtered
fluid then passes through the tubule, which sends needed minerals back to the
bloodstream and removes wastes. The final product becomes urine. The tubule helps in
the r eabsor ption of water , sodium, potassium, chlor ide.
• Kidney receives 20% of cardiac output, which allows the filtering of approximately 1600
litres/day of blood. As the filtrate passes through the nephrons, it is concentrated or diluted
to meet the body’s needs. In this way, the kidneys help maintain both the composition and
the volume of body fluids and, consequently, they maintain fluid balance, acid­base balance,
and electrolyte balance.

• The liquid waste is sent via two tubes called ureters from the kidneys to the urinary bladder,
from which they are excreted in approximately 1.5 liters of urine per day. These waste
materials include end products of protein metabolism (urea, uric acid, creatinine,
ammonia, and sulfates), excess water and nutrients, dead renal cells, and toxic
substances. When the urinary output is less than 500 ml/day, it is impossible for all the
daily wastes to be eliminated. This condition is called oliguria. When the kidneys are
unable to adequately eliminate nitrogenous waste (end products of protein metabolism),
renal failure can result. The recycled materials are reabsorbed (taken back) by the blood.
They include amino acids, glucose, minerals, vitamins, and water.
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Key ter ms
 Azotemia – accumulation in the blood of abnormal quantities of urea, uric acid, creatinine,
and other nitrogenous wastes
 Oliguria –Abnormally small production of urine(A condition of having urinary volumes of
less than 500ml/day)
 Anuria­Inability to urinate
 Uremia – Presence of an unacceptable level of nitrogenous wastes in blood. Also known as
azotemia
 Haematuria­Presence of blood in the urine
 Proteinuria­Presence of excessive protein, mostly albumin but also globulin in the urine
 Glomerular filtration rate (GFR) – the quantity of glomerular filtrate formed per unit in
all nephrons of both kidneys
 Nephritic syndrome – the syndrome of hematuria (presence of blood in urine),
hypertension, and mild loss of function that results from acute inflammation of the capillary
of the glomerulus
 Nephritisis­ a general term referring to the inflammatory diseases of the kidneys. Nephritis
can be caused by infection, degenerative processes, or vascular disease.
 Nephrolithiasis – a condition marked by the presences of renal calculi (stones)
Nephrolithiasisis a condition in which stones develop in the kidneys. The size of the stones
varies from that of a grain of sand to much larger
 Nephrotic syndrome – a condition resulting from loss of the glomerular barrier to protein
and characterized by massive edema and proteinuria, hypoalbuminemia,
hypercholestrolemia, hypercoagulability, and abnormal bone metabolism
 Nephrosclerosisis the hardening of renal arteries. It is caused by arte­riosclerosis and
hypertension. Although it usually occurs in older people, it sometimes develops in young
diabetic clients.
 Hemodialysis – a method of clearing waste products from the blood in which blood passes
by the semipermeable membrane of the artificial kidney and waste products are removed by
diffusion
 Renal failure – the inability of a kidney to excrete the daily load of end­stage renal disease
 End stage renal disease – a disease characterized by the kidney’s inability to excrete waste
products, maintain fluid and electrolyte balance, and produce hormones

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 DISEASES OF THE KIDNEY


The manifestations of renal disease are a direct consequence of the portion of the nephron and
the glomerular which are mostly affected. These manifestations include:
 Nephritic syndrome
 Nephrotic syndrome
 Acute renal failure (ARF)
 Chronic renal failure
 End­stage renal disease (ESRD)

Others Kidneys diseases are


 Diabetic Nephr opathy damage to the nephrons in the kidneys from unused sugar in
the blood, usually due to Diabetes.
 Polycystic Kidney Disease (PKD) is a hereditary kidney disease in which many
cysts grow in the kidneys.  These cysts may lead to kidney failure.
 Acute Kidney Injur y ­ Sudden kidney failure caused by blood loss, drugs or
poisons.  If the kidneys are not seriously damaged, acute renal failure may be
reversed.
 Chr onic Kidney Disease ­ Gradual loss of kidney function is called Chronic Renal
Failure or Chronic Renal Disease. It results from progressive and irreversible
destruction of nephrons, regardless of the cause It is also called chronic kidney
disease
 End­Stage Kidney Disease ­ The condition of total or nearly total and permanent
kidney failure.

N/B. The most common kidney diseases are acute renal failure, chronic renal failure, end stage
renal disease, polycystic kidney diseases and diabetic nephropathy
 NEPHRITIC SYNDROME /GLOMERULONEPHRITIS
Glomerulonephritis is a group of diseases that injure the part of the kidney that filters blood
(called glomeruli). It is a type of kidney disease characterized by inflammation of the filtering
mechanisms in your kidneys, called the glomeruli, the small blood vessels in the head of the
nephron. It is mostly common in its acute form in children 3 to 10 years of age although it can
occur in adults past age 50.

The onset is sudden and lasts a short time and proceed to either complete recovery or
development of chronic nephrotic syndrome.

Causes

It is mostly caused by
 streptococcal infection

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Other causes are metallic poisoning

 shock e.g. accident, injury


 scarlet fever,
 respiratory infections
 pneumonia,
 surgery on other parts of the body,
 drugs
 lupus and hereditary nephritis

Symptoms

Classical symptoms
 Haematuria(blood in the urine)­It is present mostly when nephritis is caused by an
infection or as result of accident or injury resulting into blood lost
 Proteinuria (loss of albumin and globulin. Low albumin levels in the blood leads to
oedema and also trigger cholesterol and lipoprotein synthesis in the liver, resulting in
hyperlipidemia)

Other symptoms
 Oedema and shortness of breath can occur as a result of sodium and water retention
 Tachycardia and elevated blood pressure/hypertension may be present due to reduced
blood flow
 Anorexia
 Anaemia­ May be present mostly when nephritis is caused by an infection or as result of
accident or injury resulting into blood loss
 Nausea and vomiting
 Increased blood urea nitrogen, due to the diminished out put
There may be oligur ia (decreased output of urine about <400 mls/day)
Or anur ia (lack of urine) and ur emia which may signal development of acute renal failure

Nutr itional implications


 Impaired protein metabolism and excretion.
 Fluid imbalance.
 PEM.

Aims of nutr itional management


 to spare the diseased kidneys
 to prevent uremia (presence of urea or other nitrogenous waste in the blood also called
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uraemic syndrome)
 To prevent oedema
 To maintain adequate nutrition.

Diet ther apy

Ener gy

 Provide high carbohydrate diet (60% of total kilocalorie) to cater for the increased energy
demand and protein sparing effect, prevent/reduce catabolism of protein, ketosis, as well
prevent starvation. For adults, provide (35 – 50Kcal/Kg/bwt).

For children 80kcal/kg body weight and 10% for infection.

 Sufficient calories is given without increasing the protein intake by means of e.g sugar,
honey, glucose, and starchy foods (cereals in all forms are recommended).Sufficient
carbohydrate helps in preventing protein catabolism (reduce catabolism of protein),
starvation and ketosis. Above mentioned foods are not only rich in calories but also poor
in sodium and potassium

Pr otein
 Adequate protein should be given unless there is oliguria, uremia(elevated blood urea in
the blood­i.e with normal BUN levels) or anuria.
 Limit protein at 0.6­0.8g/kg bwt/day for adults if there is uremia(when BUN levels are
high), oliguria and uremia. Animal proteins should be provided
 Usually, provide 0.5g of protein/ kg of ideal body weight for older children and 1­1.5
g/kg per day for younger children. Provide proteins from the animal sources.
 A low protein is recommended so as to give rest to the kidney
 High­protein diets are not recommended as they may encourage damage to the nephrons,
leading to a progression of renal insufficiency

Fluid
 Fluid should be restricted if there is oedema, hypertension, or oliguria. The fluid is
restricted for disposal of oedema fluid.
 Adjust fluid intake to fluid output, which occurs through urine, vomiting and diarrhoea.
Volume of fluid intake is calculated from volume of urine passed in previous 24hrs.
 If urine output is above 1000ml in 24 hours do not r estr ict, if output is below 1000ml in
24 hours r estr ict by giving output equivalent plus 500ml(in adults), if no ur ine output
give 500ml to 700ml.
 The equivalent plus 500ml is based on the volume of fluid excreted and allowance, 500
ml/day, is given for insensible water loss (urine, vomiting, diarrhoea and perspiration). It
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should be calculated based on the amount of water consumed with drugs, fluid from milk,
soups, tea etc.
 The equivalent plus 500ml normally happens in the later stage of the disease and this plus
500 is for adults

Sodium
 Sodium (Na) should be restricted to control hypertension and edema. Restriction depends
on the extent of symptoms present. Restriction varies with the degree of symptoms
present (oliguria, oedema and hypertension).
 If renal function is impaired, sodium is restricted to 500 to 1000 mg/day.
Calcium

 About 1g/day should be given


Potassium
 Monitor potassium intake as renal clearance of potassium is impaired when severe
oliguria is a complication, and this may lead to potassium intoxication and even require
dialysis as hyperkalemia can result in cardiac arrest.
 Should be restricted to 1mmol/kg /day. Too much potassium in the body results into
uneven heat beat and thus the heart may stop suddenly(cardiac arrest)

Phosphor us
 This is a mineral found in almost all foods. High phosphors in blood can cause calcium to
be pulled from the bones and thus make bones weak and break easily
 Restrict phosphorus intake to 8­12 mg /kg/day
Other s
 Provide small frequent meals as there is poor appetite
 Provide iron rich foods in case anaemia results from haematuria, iron supplement may be
necessary
 Ensure that the diet is of low fat(less than 30%). Include emulsified and easily digestible
fat to provide non­protein calories for energy needs.

Example

Patients particulars: Age­ 5 yrs., wt­15kgs, B.P­130/90, urine output­300 ml

Requirements: Energy 15 x 80=1200 + 120(10%) =1320 kcals

Protein: 1.25 x 15=20 to 25 g/day

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Sodium: 500 mg

Fluid: 300 + 25 ml/kg body weight=300 + (25 x 15) =675 ml

 NEPHROTIC SYNDROME
Nephrotic syndrome is caused by the failure of the glomerular capillary wall to act as an
impermeable barrier to plasma proteins, resulting in the loss of albumin and other plasma
proteins in the urine.

Causes
This can be caused by:
 progressive glomerulonephritis (glomerular disorders)
 Kidney damage from infection
 Some medications, illicit drugs and toxins which increase permeability
 Metabolic disorders e.g diabetes nephropathy as a result of diabetes mellitus
 Preeclampsia
 Reaction to toxic venom.
 immunological and hereditary diseases
 chemical damage (from some medications or illicit drugs) which increase permeability
 heavy metals
 Some cancers.
Clinical symptoms

 Heavy pr oteinur ia (large quantities of protein in the urine­at least 3.0g per day),
 Hypoalbuminemia (low albumin level in the blood/low serum albumin­due to large
protein losses in the urine)
 High cholester ol in the blood (Low albumin levels production of trigger cholesterol)
 Peripheral oedema.
 Ascites with fluid collecting in the peritoneal cavity causing distension of abdomen.
 Stretch marks often appear on the stretched skin.
 Elevated serum lipid and cholesterol levels over 300mg/100ml.
 Free fat bodies are found in the urine.
 Specialized binding proteins for thyroid and iron are lost in the urine which may
sometimes lead to hypothyroidism and anaemia.

Proteinuria develops when the leakage of protein from the glomeruli exceeds the absorptive
capacity of the renal tubules. Plasma albumin is in small molecules and escapes readily through a
leak in the glomerular membrane. Plasma globulin which have high molecular weight appear in

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urine in much smaller amounts. Unlike in nephr itis, haematur ia, anaemia and nitr ogen
r etention ar e always absent. At times anaemia be present mostly when nephrotis is caused by
an infection or as result of accident or injury resulting into blood loss

Nutr itional implications


 PEM
 Impaired protein and fat metabolism and excretion.
Aim of nutr itional management
 To control and correct protein deficiency.
 To correct and prevent edema.
 To maintain adequate nutrition.
 To afford better resistance to infection.
 To avoid unnecessarily harm to the kidney.
 Replacement of albumin and other protein lost from the plasma into the urine.

Diet ther apy/Nutr ition car e in nephr otic syndr ome

 The diet should provide sufficient protein and energy to maintain a positive nitrogen
balance and to produce an increase in plasma albumin concentration and disappearance of
edema.
Pr otein
 Provide 0.8 to 1.0 g/kg of ideal body weight.
 Although there is protein lose (heavy proteinuria) through the kidney, high protein
provision will cause deterioration of the renal function/high protein could cause further
renal damage in patients who have nephrotic syndrome.
 Some studies suggest 0.8 ­ 1g per kg of body weight/day
 The recommended protein intake for children who have nephrotic syndrome is the
Dietary Reference Intake for age plus the amount of urinary protein loss. Children who
have persistent proteinuria may require 2.0 to 2.5 g/kg of protein per day
 Some studies suggest that a low or very­low protein diet with essential amino acid
supplementation reduces proteinuria.
Ener gy
 Provide high energy intake of 35­50 kcal/kg/day for adults, and 100­150 kcal/kg/day for children

 An adequate energy intake sustains weight and spares protein for tissue synthesis. Complex
carbohydrates should be the primary source of energy intake.
 Weight loss may be recommended for obese patients, because they have an increased risk of
comorbid diseases and complications.
 Calculate according to individual needs. If the patient is obese, formulate a weight. reduction diet
regime

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 Weight loss may be recommended for obese patients, because they have an increased risk of
comorbid diseases and complications.

Fats
 The diet should be of low fats to control the elevated blood lipids (hypercholesterolemia
and hyperlipidemia i.e. to provide 20­25% of the total calories. Restrict intake of
saturated fats/animal fats

 The diet should be low in saturated fats/animal fats (saturated fat <7% of total fat), and
cholesterol <200 mg/dL per day.
 A diet low in saturated fat, trans­fats, cholesterol, and refined sugars helps to control
elevated LDL and VLDL. Dietary measures are usually inadequate for controlling blood
lipids, thus a combination of statin therapy (drugs that can lower cholesterol) and the
Therapeutic Lifestyle Changes diet lowers serum lipid levels. Fish oil supplementation
(12 g/day) may be beneficial for patients who have IgA nephropathy, which is a caused
by the deposition of immunoglobin A in the kidneys
Sodium
 The level of sodium prescribed is based on the severity of edema and hypertension.
Controlling sodium intake helps to control edema(since the body has tendency to retain
water), therefore, sodium is usually restricted to 1 to 2 g/day, depending on the severity
of the patient’s signs and symptoms.
Fluid
 Fluid should be restricted if there is oedema, hypertension, or oliguria. The fluid is
restricted for disposal of oedema fluid.
 Adjust fluid intake to fluid output, which occurs through urine, vomiting and diarrhoea.
Volume of fluid intake is calculated from volume of urine passed in previous 24hrs.
 If urine output is above 1000ml in 24 hours do not r estr ict, if output is below 1000ml in
24 hours r estr ict by giving output equivalent plus 500ml(in adults), if no ur ine output
give 500ml to 700ml.
 The equivalent plus 500ml is based on the volume of fluid excreted and allowance, 500
ml/day, is given for insensible water loss (urine, vomiting, diarrhoea and perspiration). It
should be calculated based on the amount of water consumed with drugs, fluid from milk,
soups, tea etc.
 The equivalent plus 500ml normally happens in the later stage of the disease and this plus
500 is for adults

Fluid restriction is often necessary and should be based on the patient’s symptoms. Diuretics can
help maintain fluid and sodium balance. If the diuretics prescribed for the edema cause
potassium losses, patients are encouraged to select food rich in potassium
Vitamins and miner als:

 Provide iron, based on the individual patient’s need


 Ensure patient is meeting Dietary Reference Intakes for B­complex vitamins (niacin,
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riboflavin, and thiamin) and vitamin C. Supplement as needed


 Supplement 1 to 1.5 g of calcium, not to exceed 2,000 mg
Limit phosphorus to <12 mg/kg per day

 In case of poor appetite provide small frequent meals.


Abnormalities in iron, copper, zinc, and calcium levels are directly related to the urinary loss of
proteins that are involved in their metabolism. E.g., the increased loss of transferrin causes
decreased plasma iron levels. Iron supplementation is important for patients who have nephrotic
syndrome. Copper is also bound to protein, and serum copper levels are often compromised.
However, clinical manifestations do not occur as a result of the low copper levels; therefore,
supplementation is not necessary. Supplemental zinc may be needed, as zinc is bound to
albumin. In addition, decreased levels of calcium and serum 1,25­dihydroxycholecalciferol may
occur as a result of being bound to albumin. Supplemental calcium (about 1000 to 1500
milligrams per day), vitamin D, and iron may be needed to normalize serum levels, and to help
prevent bone loss and rickets

*IgA nephropathy is a form of glomerulonephritis (inflammation of the glomeruli of the kidney).


It is a condition in which a protein (immunoglobulin A) causes damage to the kidneys.

 RENAL FAILURE
Classification of kidney failur e
1. Acute kidney Injury (AKI)
2. Chronic kidney disease (CKD)

Acute kidney injury has replaced acute kidney failure while chronic kidney disease has replaced
chronic renal failure

 ACUTE KIDNEY INJ URY (AKI)


 This refers to an abrupt/sudden decline of kidney function over a period of hours or
days following a traumatic injury or metabolic insult. It is characterized by a sudden
reduction in glomerular filtration rate (Normal filtration rate is 125 ml/1 min) and an
alteration in the ability of the kidney to excrete the daily production of metabolic
waste.
 There is high mortality and the condition needs a medical emergency in which and
nutrition support
 AKI has replaced the term acute r enal failur e, as the condition (AKI) does not
always result in chronic kidney disease (AKI can be reversed)
 The diagnostic criterion for AKI is an abrupt (within 48 hours) reduction in kidney
function defined as an absolute increase in the serum creatinine level of at least 0.3
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mg/dL(increase serum creatinine­increase creatinine in the blood because the kidney


cannot clear the creatinine. cr eatinine should be clear ed completely by glomer uli),
a 50% increase in the serum creatinine level, or a documented urine output of less
than 0.5 mL/kg per hour for more than 6 hours

The loss of kidney function r educes ur ine output and allows nitr ogenous waste to build up
in the blood. With prompt treatment, acute kidney injury is often reversible.

Classification/Staging System for AKI (as per Acute Kidney Injury Network )
Stage Creatinine Clearance Urine Output
1 Serum creatinine increase of at least 0.3 mg/dL, or a <0.5 mL/kg per hour for more
150% to 200% increase than 6 hours
2 Increase in serum creatinine level to greater than <0.5 mL/kg per hour for more
200% to 300% of baseline than 12 hours
3 Increase in serum creatinine level to greater than <0.3 mL/kg per hour for 24
300% of baseline, or serum creatinine level of 4.0 hours or anuria for 12 h
mg/dL with an acute increase of at least 0.5 mg/dL

Causes of Acute Kidney Injur y (AKI)


Causes of acute kidney injur y [AKI]) fall into one of the following categor ies:

 Pre­renal(Problems affecting the flow of blood before it reaches the kidneys)


 Post­renal(Problems affecting the movement of urine out of the kidneys)
 Renal(Problems with the kidney itself that prevent proper filtration of blood or
production of urine)

 Pre­renal(Problems affecting the flow of blood before it reaches the kidneys)

 Sudden loss of blood supply or reduced supply of blood to the kidneys(reduced renal
blood flow) as a consequence of
o severe illness
o sepsis( e.g. caused by bacteria)
o internal haemorrhage
o shock e.g. as a result of injury and accidents
o blood loos e.g. at the time of delivery
o heart failure and heart arrhythmias;
o burns
o ulcers
o sickle cell anaemia
o aneurysm
o acute haemolytic disorders (RBC are destroyed due to some diseases)

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Post­renal (Problems affecting the movement of urine out of the kidneys) e.g.
o blood clots
o Trauma
o transfusion reactions
o kidney inflammation, stones and tumours;
o loss of fluid from the gut as in severe diarrhoea or vomiting, acute intestinal
obstruction
o diabetic coma( excessive urination and excessive sweating)
o cervical and prostate cancer surgical complications
o Exposure to a nephrotoxic chemical or drug (e.g., radiologic dyes, cleaning
solvents, pesticides, and gentamicin). In haling tetra­chloromethane (CCl4) or
mercury (Hg)
o general anaesthesia and streptococcal infection e.g. E.coli food poisoning
Renal (Problems with the kidney itself that prevent proper filtration of blood or production of
urine) e.g.
o glomerular disease(nephritis)
o tubular necrosis ,
o nephrotoxins like paracetamol and some varieties of mushrooms
Symptoms

Oligur ic phase
 Follows precipitating event and may last for a few days to five weeks.
 Volume of urine may be as little as 20ml to 200ml a day (oliguria). Most patient produces
less than 400 ml of urine per day. This is because of decline in renal functions. Oliguria
leads to fluid retention. Anuria may be present
 Excretion of sodium, water, potassium and nitrogenous waste are all reduced

 There is risk of overloading patient with both fluid and electrolyte by both oral and
intravenous through the vein
 There is danger of hyperkalemia due to increased breakdown of damaged tissues leading
to increased release of intracellular potassium. Elevated potassium (hyperkalemia) can
alter heart rhythm and lead to heart failure.
 Nausea and vomiting
 Blood pressure elevated
 Signs of uremia may be present (Accumulation of waste product of protein metabolism in
blood. Serum urea nitrogen and creatinine levels are increased)

 Elevated serum phosphate levels (hyperphosphatemia) promote excessive secretion of


parathyroid hormone, leading to losses of bone calcium
 Oral intake is usually difficult during this phase because of anorexia, vomiting and

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nausea
 Neuromuscular disturbances: symptoms may include altered thought processes, sleep
disorders, muscle cramping, sensory deficits, tremor and seizures.
 Other effects: defects in platelet function and clotting factors prolong bleeding time and
contribute to bruising and gastrointestinal bleeding. Skin changes include increased
pigmentation and severe pruritus (itchiness). Patients with uremia typically have
suppressed immune responses.
 Death is caused not because of rise in blood urea but potassium intoxication or water
intoxication due to over treatment with fluids to stimulate urine excretion.

Diur etic phase


 The patient may start passing moderate amount of urine
 In the following day larger than normal amount of urine may be passed
 The urine volume may increase gradually to between 2 to 5litres per day and excretion of
sodium potassium and other solutes also increases
 Blood urea falls to normal in 7 to10 days indicating that gromerula filtration has
effectively improved.
Nutr ition implications
 Fluid imbalance.
 Electrolyte imbalance.
 Impaired food intake and excretion.
Aims of nutr itional management
 To support overall medical management
 Maintain adequate nutrition status in order to minimize endogenous protein catabolism
 Provide an optimal environment for wound healing
 Preventing infections
 Minimize uremia.
 Control edema and electrolyte imbalance

Tr eatment of Acute Kidney Injur y


 Treatment involves a combination of dr ug ther apy, dialysis and nutr ition ther apy to
restore fluid and electrolyte balances and minimize blood concentrations of toxic waste
products. Treatment is highly individualized to suit the patient’s needs. Correcting the
underlying illness is necessary to prevent further damage to the kidneys
Nutr ition ther apy/Dietar y management
 It has been shown that early attention to nutritional status often in the form of total
parenteral nutrition (TPN) and early dialysis, have a positive impact on patient survival.
TPN is important because of reduced oral intake
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Pr oteins
 During oliguric phase reduce proteins to a minimum amount required to compensate for
endogenous process
 Initially during acute phase no proteins should be given to the patient and as the condition
improves only 20gms proteins should be given. If not on dialysis allow 0.6 ­ 1g/kg
bwt/day. If on dialysis allow a more liberal amount of protein of 1.1 ­ 1.5g/kg bwt/day. A
40gm protein diet may be used where the weight of an adult patient is unknown
 60­75% of dietary protein should be of high biological value e.g. eggs, meat, fish,
poultry, milk
N/B. Protein should be restricted or stopped if the patient is under conservative treatment and
blood urea is rising and the patient is not on dialysis

Calor ies
 Sufficient calories from carbohydrates and fats are used to increase the caloric content of
the diet and spare the breakdown of body proteins
o 35KCal/kg/body weight (patients with normal weight).
o 20­30KCal/kg/body weight (obese patients)
o 40­50KCal/kg/body weight (underweight/catabolic patients)

Car bohydr ate.

 55­60% of energy should be provided by carbohydrate, a minimum of 100g/day


should be provided to minimise tissue protein breakdown e.g two litters of 5%
glucose meets this

Fluid intake
 Adjust fluid intake to fluid output, which occurs through urine, vomiting and diarrhoea.
Volume of fluid intake is calculated from volume of urine passed in previous 24hrs. If
urine output is above 1000ml in 24 hours do not restrict, if output is below 1000ml in 24
hours restrict by giving output equivalent plus 500ml, if no urine output give 500ml to
700ml. An individual with fever, vomiting or diarrhea r equir es additional fluid. Patients
undergoing dialysis can ingest fluids more freely.

Sodium
 Sodium is restricted to avoid fluid retention
 Control hypertension and prevent congestive cardiac failure
 Restriction of total sodium to 1000 ­ 2000mg daily is necessary during the oliguric phase.
Do not give salt if there is anuria, elevated high blood pressure and when the level of
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urine produced is too little


Other electr olytes
 Serum electrolyte levels are monitored closely to determine appropriate electrolyte
intakes. Depending on the results of laboratory tests and the clinical assessment,
restrictions may be necessary for potassium (2000­3000 mg/day) Potassium is controlled
to avoid hyperkalemia and hypokalemia, phosphor us (8­12 mg/day)
N/B. Potassium intoxication (hyperkalemia) has deleterious effect on heart. Potassium sources
like tomatoe juice, coffee, tea, cocoa and potassium rich vegetables can be avoided

Haemodialysis or peritoneal dialysis may be considered when blood urea level is over 200
mg/100ml.The energy and protein content of the diet may then be increased

Diur etic phase


In oliguric patients, recovery from kidney injury sometimes begins with period of diuresis in
which large amounts of fluid (up to 3 liters daily) are excreted.

 The stage indicates a return of renal function to normal


 The patient is passing a large amount of urine and so is at risk from excessive loss of
water, sodium, bicarbonate, phosphate and magnesium
 Prescribe a normal diet with free fluid intake
 May need to be supplemented with electrolytes
 Proteins intake restriction continues until BUN and serum creatinine returns back to
normal.
 The fluid and electrolyte status need to be monitored by daily weighing and blood and
urine analysis

N/B 30% of ICU patients develop acute renal injury

 CHRONIC KIDNEY DISEASE


 It is also known as uraemia as the level of urea in blood is very high.

 Chronic kidney disease (CKD) is where the kidneys don't work well for longer than 3
months as 90% of functioning renal tissue is destroyed. This is as a result of the progressive
deterioration of kidney tissue during several months or years as scar tissue is substituted
for viable kidney tissue.
Causes of chr onic Kidney disease
 Chronic Kidney disease can be attributed to several underlying causes, some of the most
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common being nephrotic syndrome, glomerularnephritis, acute renal failure, diabetes,


hypertension, and HIV
1. Nephr otic syndr ome: This is a loss of protein through the glomerular lumen, which can
lead to proteinuria, hypoalbuminemia, edema, increased cholesterol, poor bleeding times,
and alterations in bone metabolism
2. Glomer ular nephr itis (nephr itic syndr ome): This is an inflammatory response in the
glomerulus capillary loop. It normally occurs after streptococcal infections, and can cause
hypertension and blood in the urine along with decreased renal function. The main side
effect of this disease is hematuria.
3. Acute kidney injur y: This develops when filtration rate and urea production suddenly
drop, a process that can be reversed if caught in time
4. Diabetic nephr opathy: As blood sugars continue to rise, the damage to the small blood
vessels in the kidney increase with time. Diabetes mellitus especially type II
5. Ather oscler osis and hyper tension: Poor blood pressure control places continued high
pressure on the kidneys’ arteries and weakens them.
6. HIV: Patients with HIV may be taking nephrotoxic drugs to help combat the infection.
This can lead to lactic acidosis, crystal­induced obstruction, interstitial nephritis, and
electrolyte abnormalities. The HIV infection can affect the cells in the kidney and also
can attack the nephrons within the kidneys that help filter the by­products.
7. Abdominal surgical emergency, Gout, exposure toxic substances and polycystic kidneys

N/B. CKD is a risk factor of cardiovascular disease

Who is at r isk of CKD


 are at
Adults 60increased
years or older
risk of developing CKD if they:
 have diabetes
 have a family history of kidney disease
 have established cardiovascular disease
 have high blood pressure
 are obese (body mass index ≥30)
 are a smoker

Symptoms
 Decrease in renal blood flow and glomerular filtration because of damaged nephrons
 Low glomerula filtration rate
 Increased creatinine or urea in the blood, blood and/or protein in the urine
 Dehydration( Increased thirst at night leading to dehydration ) or water intoxication,
sodium depletion, high serum potassium, acidosis(chronic growth failure leads to acidosis
that increases calcium reabsorption from the bones leading to osteomalacia) and
increased susceptibility to infection as a result of impaired of immune function
 Oedema, high blood pressure (hypertension), irregular heartbeats and GFR of below 15
mL/min/1.73m2.

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 Gastrointestinal problems due to increased waste products­Loss of appetite, changes in


taste, nausea, vomiting and hiccups. Gastrointestinal can result into weight loss
 Weakness, poor sleeping habits, fatigue caused by an increased amount of waste products
in the blood
 Neurological problems­twitching, convulsions, and coma may occur
 Anaemia(due to impaired erythropoietin and loss of blood through nose bleeding,
haematuria and gastrointestinal bleeding) leading to tiredness, breathlessness and
tendency to bleed due to abnormal platelet function
 Uremic symptoms of anorexia and vomiting resulting from accumulation of urea and
creatinine.
 Hyperlipidemia
 Skin changes pigmentation, muscle cramping and itching, restless leg
 Osteodystrophy, dwarfism and ricket growth failure may occur

Diagnosis
Chronic kidney disease (CKD) is diagnosed as:
By the symptoms and GFR’s Role. The presence of kidney disease is measured through the
GFR, which gauges the patient’s level of kidney function.

 an estimated or measur ed glomer ular filtr ation r ate (GFR) < 60 mL/min/1.73m2 that is
present for ≥3 months with or without evidence of kidney damage; or
 evidence of kidney damage with or without decreased GFR that is present for ≥3 months
as evidenced by the following, irrespective of the underlying cause:
 albuminuria
 haematuria after exclusion of urological causes
NB: If the GFR is ≥60 mL/min/1.73m2, and there is no evidence of kidney
damage, then CKD is not present
CKD – is characterized by gradual, irreversible deterioration

Kidney failure is defined by a GFR below 15 mL/min/1.73m2.

CKD Stage GFR Level


1 (normal) ≥ 90 mL/min/1.73m2.
2 (mild decrease) 60­90 mL/min/1.73m2.
3 (moderate decrease) 30­60 mL/min/1.73m2.
4 (Severe decrease) 15­30 mL/min/1.73m2.
5 (kidney failure) <15 mL/min/1.73m2.

Consequences of CKD
In the early stages of CKD, the nephrons compensate by enlarging so that they can handle the
extra workload. However, as the nephrons deteriorate, there is additional work for the remaining
other nephrons which overburdens them, thus continue to degenerate until the kidneys are unable
to function adequately resulting in kidney failure. End­stage r enal disease (ESRD), results
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when the extent of kidney damage necessitates active treatment (dialysis/transplant).


Nutr ition implications /Consequences of CKD
 Altered electrolyte and hormones:
 Uremic syndrome.
 Cardiovascular complications.
 Bone disease.
 Gastro­intestinal disturbances.
 Growth failure and wasting syndrome.
 Anemia.
 Protein energy malnutrition – patients with CKD often develop PEM and wasting.
Anorexia is a contributor to poor food intake that may result from hormonal
disturbances, nausea & vomiting, restrictive diet, uremia and medications. Nutrient
losses also contribute to malnutrition and may result from vomiting, diarrhea,
gastrointestinal bleeding, and dialysis. Catabolic state resulting due to some illnesses
can also contribute to protein illness.

 END­STAGE RENAL DISEASE (ESRD)

It is where the kidneys cannot keep up with waste and fluid clearance on its own .It is where there is
severe renal failure. At this point, dialysis or a kidney transplant is needed.

Five stages of chronic kidney disease

There is no cure for CKD.

Stages 1 and 2: Kidney disease is relatively unrecognized in stages 1 and 2 because there
typically are no symptoms. Stages 1 and 2 generally are diagnosed when there is increased
creatinine or urea in the blood, blood and/or protein in the urine, a family history of polycystic
kidney disease, or evidence of kidney damage on radiologic exams.

Stage 3: As patient’s progress to stage 3, they will experience uremia, anemia, high blood
pressure, and slight metabolic bone disorders. These disturbances will lead to fatigue, fluid
accumulation, decreased urine output, sleep disturbances, and kidney pain.

Stage 4: As patient’s progress to stage 4, uremia, anemia, high blood pressure, and bone
disorders become more prominent. The disturbances seen in stage 3 worsen and lead to
additional complications of nausea, changes in taste, uremic breath, decreased appetite,
neuropathy problems, and mental concentration issues.

At this stage, patients develop uremia because of the endocrine and metabolic changes that
occur. Later, patients develop osteodystrophy(bone disorders due to renal disease as a result of
calcium and phosphorus imbalances),anemia, oxidative stress that leads to heart and vascular

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diseases, impaired immune function, and protein energy malnutrition as a result of inflammation
from oxidative and carbonyl stressors.

Patients in stage 4 might complain of weakness, malaise, poor sleeping habits, fatigue, and loss
of appetite caused by an increased amount of waste products in the blood. These waste products
can lead to gastrointestinal disturbances that can result in poor food consumption, which in turn
cause weight loss and the symptoms described above.

Patients at this stage will be referred to a nephrologist for quarterly medical appointments to
track disease progression. It is at this point that they start receiving information about dialysis or
transplant.

Stage 5: In stage 5, the patient has reached full kidney failure. Together with the metabolic and
endocrine disorders seen in stage 4, the patient will have little to no urine output and can
experience itching, muscle cramping, changes in skin color, and increased skin pigmentation.
Patients might have weakness, malaise, poor sleeping habits, fatigue, and loss of appetite
because of increased waste products in the blood, which can result in gastrointestinal problems,
weight loss, and symptoms seen in other stages. Unless patients undergo a kidney transplant,
they are given options for different types of dialysis treatment or hospice/palliative care.

The following clinical values should be monitored: Serum albumin and total protein, Urinary
protein, Glomerular filtration rate, Dietary protein, fat, and cholesterol, Daily weights, Serum
lipids)

Labor ator y Tests used to investigate CKD


 Ur ine tests ­ Albuminur ia
• Excessive amounts of proteins in the urine are a key marker of kidney damage and of
increased renal and cardiovascular disease risk.
Factors Other than CKD known to Increase Urine Albumin Excretion
• Urinary tract infection
• High dietary protein intake
• Congestive cardiac failure
• Acute febrile illness
• Heavy exercise within 24 hours
• Menstruation or vaginal discharge
• Drugs (especially NSAIDs
 Ur ine tests ­ Haematur ia
• In many people, haematuria is related to menstruation or urinary tract infection (UTI).
• Persistent haematuria, or haematuria found in conjunction with other indicators of kidney
damage necessitates investigation.
• Glomerular haematuria is due to kidney disease.
 Blood tests – glomerular filtration rate (GFR)*
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• GFR is accepted as the best measure of kidney function.


• GFR can be estimated (eGFR) from serum creatinine using prediction equations.
Clinical situations wher e eGFR r esults may be unr eliable and/ or misleading include:
• acute changes in kidney function (e.g. acute kidney failure)
• people on dialysis
• exceptional dietary intake (e.g. vegetarian diet, high protein diet, recent consumption of
cooked meat, creatine supplements)
• extremes of body size
• diseases of skeletal muscle, paraplegia, or amputees (may overestimate eGFR) or high
muscle mass (may underestimate eGFR)
• children under the age of 18 years
• severe liver disease present
• eGFR values above 90 mL/min/1.73m2
• drugs interacting with creatinine excretion (e.g, fenofibrate, trimethoprim)

Management/tr eatment of CKD

Objectives of tr eatment
 To prevent protein metabolism and minimize toxicity due uremia
 To avoid dehydration or over hydration
 To correct acidosis
 To correct electrolyte imbalances, from depletion, vomiting and diarrhoea
 To obtain optimal nutritional status by preventing PEM and weight loss
 To slow disease progression
 To prevent or alleviate symptoms

Tr eatment/r enal r eplacement ther apy


 Kidney transplantation
 Dietary management
 Dialysis
 Lifestyle modification
 Medical therapy

Lifestyle modification
 Lifestyle modification: cessation of smoking, weight reduction, low­salt diet, physical
activity, and moderate alcohol consumption are successful in reducing overall CVD risk.
Carbonated beverages; Soft­drink (especially cola) consumption has been associated with
diabetes, hypertension and kidney stones. The relationship between imbibing cola
beverages and the development of kidney stones has been attributed to urinary
acidification by phosphoric acid.

Dr ug ther apy:
 Hypertension, and hypertension can contribute to the progression of CKD. Reducing
blood pressure to below threshold levels is one of the most important goals in
management of CKD

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 Antihypertensive drugs are usually prescribed, which can also reduce proteinuria and
help prevent additional kidney damage.
 Erythropoietin administration (to treat anemia)
Glycaemic control: For people with diabetes, blood glucose control significantly reduces the
risk of developing CKD, and in those with CKD reduces the rate of progression
Dietar y management
Dietar y management can be divided as pr e­dialysis dietar y management and dialysis
dietar y management

Pr e­ESRD (pr e­dialysis) dietar y management


Pr oteins
 In patients with a GFR <25 ml/min a low protein diet of about 0.5 –
0.8g/kg(0.6gm/kg/bwt) body weight helps to reduce azotemia (uremia) and
hyperkalemia and control acidosis (35­40gms of protein is adequate to maintain nitrogen
equilibrium) where patients have a GFR<25 ml/min
 When BUN rises protein intake need to be restricted to 20gms per day.
 A 40gm protein diet may be used where the weight of an adult patient is unknown
 60­75% of dietary protein should be of high biological value e.g. eggs, meat, fish,
poultry, milk
N/B. Protein should be restricted or stopped if the patient is under conservative treatment and
blood urea is rising and the patient is not on dialysis

Ener gy
 Recommended Allowance

o 30­35KCal/kg/body weight (patients with nor mal weight)­wt maintenance


o 20­30KCal/kg/body weight (obese patients)­wt r eduction
o 40­50KCal/kg/body weight (under weight/catabolic patients)­wt gain

Fluid
 Volume of fluid intake is calculated from volume of urine passed in previous 24hrs. If
urine output is above 1000ml in 24 hours do not restrict, if output is below 1000ml in 24
hours restrict by giving output equivalent plus 500ml, if no urine output give 500ml to
700ml.
 Intake to be increased in the event of fever, vomiting or diarrhea.
Sodium
 The need for sodium varies and both severe and excesses have to be avoided
 The restriction varies between 1000 – 2000 grams per day.
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 Do not give salt if there is anuria, elevated high blood pressure and when the level of
urine produced is too little
All renal patients advised on a No Added Salt (NAS) diet:
o Avoid adding salt at the table
o Use small amount in cooking or none at all
o Reduce intake of salty foods (e.g., cheese, smoked food, savoury snacks)
o Limit intake of packet, processed & convenience foods
o Encourage use of pepper, herbs and spices as alternative flavourings
Potassium
 The potassium level has to be adjusted to maintain normal levels in the blood. In severe
vomiting significant losses of potassium may occur and these may need careful potassium
supplementation
 The dietary intake is kept at about 1500mg/day.
 If overnight urine output is above 1000ml do not restrict potassium intake.

Calcium ir on, and phosphor us


 Chronic renal failure with uremia causes secondary hyperthyroidism which in turn results
in hyperphosphatemia and hypocalcemia leading to osteodystrophy
 Phosphate intakes need to be restricted to 8­12 mg/day Start restriction early before
symptoms of bone deformity develops
 Calcium supplementation helps to prevent hypocalcemia. Recommended Calcium
supplementation is1000­1500mg/day
 Parenteral supplementation of iron is essential because of deficient production of
erythropoietin.
 Vitamin supplementation to help correct osteodystrophy or activated form of vitamin D
and water soluble vitamins.

Dialysis
 In kidney failure, there is need for nitrogenous wastes to be removed from the body; to
slow down progression to End Stage Renal Disease (ESRD).
 This waste removal is called dialysis.
 Dialysis is a procedure that replaces some of the kidney’s functions. Active dialysis is
perfumed when there is more than 95% kidney failure. It keeps the body in balance by
removing waste products including salts and excess fluids, maintaining a safe level of
blood chemicals such as potassium, sodium and chloride in the body and controlling
blood pressure
 There are two basic kinds of dialysis­
o Hemodialysis ­In this, an artificial kidney, hemodialyzer is used to remove the
waste products from the blood. This is done by circulating the blood through the

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machine (hemodialyzer) that contains tubing of semipermeable membranes


o Per itoneal dialysis ­removal of waste products from the blood by injecting the
flushing solution into the abdomen and using the client’s peritoneum as the
semipermeable membrane.
 The most common is hemodialysis.

Haemodialysis
 Hemodialysis requires permanent access to the bloodstream through a fistula. Fistulas are
unusual openings between two organs.
 This permanent access (fistula) are often created near the wrist and connect an artery and
a vein. .
 Large needles are inserted into the fistula .Prior to each dialysis and are removed when
dialysis is complete.
 Waste products and electrolytes move by osmosis from the blood into the dialysate and
are removed.
 Hemodialysis is done three times a week for approximately 3 to 5 hours each visit.
Dialysis replaces kidney function by removing excess fluid and wastes from the blood. In
hemodialys the blood is circulated through a dialyzer (artificial kidney), where it is
bathed by a dialysate (a solution that selectively removes fluid and wastes).
 The circulation consist of a pump (the heart), and blood vessels. Artery carry blood away
from the heat to the tissues at high pressure. Veins return blood to the heart at a low
pressure. The machine then pumps the cleansed blood back into your body

Types of hemodialysis

i. Intermittent hemodialysis
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ii. Continuous hemodialysis. The difference between the two is the speed.
Continuous is the slow method

Per itoneal dialysis


 Peritoneal dialysis is a treatment for kidney failure that uses the lining of your abdomen
or belly, (peritoneum or peritoneal cavity) to filter your blood inside your body.
 The process uses the peritoneal cavity as a semipermeable membrane. A catheter is
surgically implanted in the abdomen and into the peritoneal cavity.
 When you start peritoneal dialysis, dialysis solution –water with salt and other additives­
flows from a bag through the catheter into your belly. When the bag is empty, you can
disconnect your catheter from the bag and go on with the normal activities.
 While the dialysis solution is inside your belly, it soaks up wastes and extra fluid from
your body. After a few hours, you drain the used dialysis solution into a drain bag.
 The process of first draining the used dialysis solution and then replacing it with fresh
solution is called an exchange .Most people do four to six exchanges every day that lasts
about 10 to 12 hours a day, three times a week.
 It is less efficient than hemodialysis
 Patients with peritoneal dialysis have higher protein needs (about 1.2­1.5g/kg of protein)
because of greater protein losses.
 The advantage of peritoneal dialysis is that is usually performed in the home(it is mostly
performed by patients themselves)
Per itoneal dialysis

Types of per itoneal dialysis


1) Continuous ambulatory peritoneal dialysis (CAPD)
2) Automated peritoneal dialysis (APD)
Continuous ambulator y per itoneal dialysis (CAPD)
 It does not require a machine. It takes 4­5 hours.The dialysis fluid is exchanged 4­5 times
daily, making this a 24­hour treatment. Protein losses are somewhat higher than those

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from hemodialysis and other peritoneal dialysis.


 Clients on CAPD have a more normal lifestyle than do clients on either hemodialysis or
other peritoneal dialysis as they can read, watch television, or sleep.
 Some complications associated with CAPD include peritonitis, hypotension (therefore
require additional fluid and sodium replacement), and weight gain (as a result of
absorbing 600­800 calories/day from the glucose dialysate). This may be desirable in
patients who are underweight, but eventually dietary intake may have to be modified to
account for energy absorbed from dialysate.
 It is associated with hypotension because sodium and potassium are removed during this
process. The loss of sodium can be as much as 6g/day, thus these patients may need
higher sodium intakes.
Automated per itoneal dialysis (APD)
 Uses a machine
Dietar y management

Aim of nutr itional management in dialysis


The pur pose of diet in dialysis is to:
 Maintain optimal nutrition to preserve normal body weight.
 Control abnormal body biochemistry and symptoms of uremia.
 Provide sufficient protein for tissue building.
 Allow adequate [moderate] amount of calories for energy and protein sparing.
 Prevent or retard the development of bone disease.
 Slow down disease progression.

Hemodialysis­dietar y management

Pr otein

 Dialysis is a drain on body protein, and the daily intake should be increased to
compensate for the loses but the amount must be carefully controlled to prevent the
accumulation of protein waste between treatments
Pr oteins
Recommended allowance
1.0gm/kg IBW (1.0gm­ 1.2gm 1kg/kg/day for maintenance)
1.0­1.2 gm/kg Bwt – weight maintenance
1.5 kg Bwt /day – weight increase
1.2 kg Bwt /day – weight reduction

65­75% to be of HBV

Calor ies

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Recommended allowance
 30­35 kcals /kg Bwt /day –for wt maintance(patient with nor mal weight)
 40­50 kcals /kg Bwt /day­wt incr ease(for under weight/wt gain)
 25­30 kcals /kg Bwt/day­wt r eduction(obese patients)

Potassium:

 1.5­3g/day
No restriction with urine output of 1000ml/day.

 Potassium is restricted to prevent hyperkalemia.


 Hypokalemia may lead to cardiac arrest.
 In case of Hypokalemia, potassium supplementation is required.
Sodium:
 2­3g/day
 Dietary sodium is restricted to help control fluid retention and hypertension.
 The state of blood pressure and the amount of fluid gained between dialysis determine
sodium needs on hemodialysis.
 Hypotension due to salt depletion require increased sodium intake.
All renal patients advised on a No Added Salt (NAS) diet:
o Avoid adding salt at the table
o Use small amount in cooking or none at all
o Reduce intake of salty foods (e.g., cheese, smoked food, savoury snacks)
o Limit intake of packet, processed & convenience foods
o Encourage use of pepper, herbs and spices as alternative flavourings

Phosphor us:
 1200 mg/day.
 Dietary phosphates are restricted in the Hemodialysis as they may cause constipation.
Calcium:
 500­1000mg/day.
 Supplementation of calcium and vitamin D is necessary due to reduced intestinal
absorption of calcium resulting from lack of active form of vitimin. D [1,25 dihydroxy­
D3]
Fluids:
 24hrs urine output + 500 mls / day.
 Calculated fluid intake prevents severe fluid overloading.
 Fluid intake should be increased in the event of hot weather or severe and persistent
pyrexia [fever], diarrhoea or vomiting
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Ir on:
 10 mg men/ women
 18 mg women of reproductive age.
 Although the main cause of anaemia is deficient production of erythropoietin due to
kidney failure:
 Iron depletion is common in uremic patients due to bleeding tendency.
 Some is also lost in hemodialysis and blood tests.
 Iron supplementation is therefore necessary parenterally.

B­vitamins

B ­vitamins:  Water­soluble vitamins are dialyzable.


 Require supplementation.
Thiamine 1.5mg/day
Riboflavin 1.8 mg/day
Niacin 20 mg/day
Pyridoxine 5­10 mg/ day
Folic Acid 1 mg/day
Vitamin C 100 mg/day
Vit. B12 , pantothenic Acid
5mg/day

Per itoneal dialysis­dietar y management


 Ensure increased protein intake due to higher albumin protein losses during peritoneal
dialysis (1.3­1.4g/kg/day). .Losses of 20­30 g protein can occur during a 24 hour
peritoneal dialysis, with an average of 1 g/hour.
 Calorie intake is decreased because of the glucose absorbed from the dialysate (25­30
Kcal/kg/day).
 Account for calories absorbed from dialysis fluid.
 The dialyser used in peritoneal dialysis contains glucose, in order to draw fluid from
blood to the peritoneal cavity by osmosis; about 60% of this glucose is absorbed. The
kcals from glucose (as many as 800 kcal /day) must be included in estimates of energy
intake.
 Weight gain is sometimes a problem when peritoneal dialysis continues for a long period.

 Restriction of sodium and potassium is not necessary as they are filtered from the blood
daily. Sodium intake therefore should be 3­4g daily (Individualize to blood pressure).

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 Potassium intake at 2­3g daily.


 Vitamins and iron supplements are still required.
 Allow adequate intake of fluids as excess fluid can easily be removed.

DIET PLAN

Pr e­ESRD (pr e­dialysis) dietar y management

Example 1

John is a 50 year old man weighing 70 kgs. He is on a conservative dietary management. He


needs to maintain his body weight
Calculate
 Calorie requirements
 Protein requirement, also show the amount of protein from High
biological value(HBV)
 CHO requirements
 Fat requirements
 Show the prescribed diet
Calculations
a) Calories=35 x 70=2450 kcals/day
b) Protein=0.6 x 70=42gm/day
42 x 4=168 kcals
HBV=65 + 75=140/2
70/100 X 42
=29.4 gm
HBV Protein=29gm
Diet=1 egg 7gm
1 cup of milk 8gm
2 oz(60g) meat 14gm
TOTAL= 29gm
42­29=23gm
Therefore 13gm should be from plants sources (Bread, starchy foods, vegetables and
fruits)
NB…Grains and legumes are not used as source of proteins because they are low
biological value proteins and also high in potassium
c) Carbohydrates= 50 + 60=110/2
=55%
=55/100 x2450=336.86
=337gm/day

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d) Fat: Should come from the remaining calories after protein and CHO
=2450­(163 +1347.57)
=2450­1515.5=934.5 Kcals
=943.5 Kcals
=943.5/9
=104gm/day
e) Diet prescribed
Calories=2450/day
Protein=42gm/day
CHO=337gm/day
Fat=104 gm/day

Example 2
A 70kg patient will take 42gms of protein per day. (70x0.6=42), HBV­65­75%. Thus 70/100
x42=29.4%. His diet could include
1egg ­7gms
1cup milk ­8gms
2oz (60gms) meat­14gms
=29gms protein
This allows only 13gms of protein to be obtained from other protein containing foods in the diet
e.g. bread, starch foods cereals and vegetables.
Example 3
If the patient passed 700mls, urine his fluid allowance will be 1200mls in 24hrs
The fluid intake will be 700 ml Urine +500 ml= 1200mls/24hrs. Patients should weigh
themselves daily and measure urine output, each 1000ml of retained fluid will add a kg of Bwt.

Diet plan

Hemodialysis­dietar y management

Example 1 ­ A 60­kg female receiving hemodialysis three times per week should be eating
60g/day of protein. If 75% of this protein is to be HBV protein, then 46grams of protein should
be in the form of eggs, meat, fish, poultry, milk or cheese. A possible combination of these foods
that would contribute 46gms of HBV protein would be:
Food Protein
1 egg 7
2oz chicken 14
3oz beef 21
1/2cup milk 4
Total 46

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The remaining 14gms is obtained from LBV protein. Sources: breads and cereals, vegetables,
potatoes, pasta, and milk­free desserts. A combination of foods that would provide 14gms of
LBV protein is:
Food Protein (g)
3 slices bread 6
3/4cup cereal 3
1/2cup mashed potato 2
½ cup carrots 1
1/2 cup peas 1
1/2cup orange juice 0.5
1 small apple 0.5
Total 14

Example 2­ A 30 yrs old Female on hemodialysis IBW­ 60 kgs, Ht 162.5 cm (5’5), Light
worker. To calculate her dietary requirements;

Protein should be high, hence allow 1gm per kg of body weight.


60kgs x1 gm =60 gms, 70% should be HBV. 70/100 x 60 = 42gms

Calories Allowance­ 30­35 kcals /kg, Allow 35cals= 35x60=2100cals


CHO allowance is normal 50­60 % of total calories, Allow 60%= 60/100x2100 =1260cals divide
by 4 =315gms
Fat allowance is normal 20 ­30% of total calories, allow 30%= 30/100 x2100 =630/9 =70gms

The diet prescription


Calories ­2100
Protein ­ 60gms
CHO ­ 315gms
Fat ­ 70gms
Meal patterns
Breakfast
Milk ½exchange
Fruit 1 exchange
Bread 3 exchange
Meat 1 exchange
Fat 3 exchange
Lunch
Meat 1 exchange
Bread 1 ½ exchange
Veggies 1 exchange
Fruit 2 exchanges
Fat 3 exchange
Sugar 2 exchanges
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Supper
Meat 2 exchanges
Bread 1 ½ exchanges
Veggies 1 exchange
Fruit 1 exchange
Fat 2 exchange
Snacks
10.00 am
Fruit 1 exchange
Bread 2 exchange
Milk ¼ exchange
Fat 1 exchange
Sugar 4 exchanges
4.00 pm
Fruit 1 exchange
Bread 2 exchange
Milk ¼ exchange
Fat 1 exchange
Sugar 4 exchanges

Sample Menu
1 boiled egg
1 cup uji ½ cup milk +3 tsps sugar
1 small fruit
2 slices bread 2 tsps margarine +2 tsps jam
Lunch
1 ½ cup Ugali/rice/potatoes or equivalent
1 oz (30gms) meat/fish/poultry
½ cup veggies
1 cup fruit salad 2 tsps sugar
3 tsps cooking fat
Supper
1 ½ cup Ugali/Rice/potatoes or other equivalent
2 oz (60gms) meat
½ cup veggies
1 small fruit
2 tsps cooking fat

Snacks
10.00am
A fruit
Tea ¼ cup milk +2 tsps sugar
2 slices bread 1 tsps margarine +2 tsps jam
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4.00 pm
1 fruit
2 slices bread 1 tsp margarine + 2 tsps jam
1 cup Tea (¼ cup milk) + 2 tsp sugar

 KIDNEY STONES(NEPHROLITHIASIS)

 Kidney stones (renal lithiasis, nephrolithiasis) are hard deposits made of minerals and
salts that form inside the urinary tack and the kidney, their passage can cause severe pain
or block the urinary tract.
 Kidney stones are formed when the concentration of components in the urine reaches a
level in which crystallization is possible. They are generally composed of calcium salts
(calcium oxalate and calcium phosphate), uric acid, cysteine, or struvite (triple salt of
ammonium, magnesium, and phosphate).
 In general, however, large amounts of fluid—at least half of it water (1.5­2
liters/day)—are helpful in diluting the urine (to produce at least 2 litres/day of urine), as
is a well­balanced diet. The goal of rigorous hydration is to keep the urine dilute,
preventing the crystallization of stone­forming minerals. Once the stones have been
analyzed, specific diet modifications may be indicated.

Types of kidney stones

Calcium Oxalate Stones


 About 70­80% of the renal stones formed contain calcium oxalate, and are most
common in middle­aged men. Oxalate is a normal product of metabolism that readily
binds to calcium.
 Recent studies provide no support for the theory that a diet low in calcium can reduce
the risk of calcium oxalate renal stones. In fact, higher dietary calcium intake may
decrease the incidence of renal stones for most people. Dietary intake of excessive
animal protein has been shown to be a risk factor for stone formation in some clients.
 Stones containing oxalate are thought to be partially caused by a diet especially rich
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in oxalate, which is found in beets, wheat bran, chocolate, tea, strawberries, and
spinach.
 Evidence also indicates that deficiencies of pyridoxine, thiamine, and magnesium
may contribute to the formation of oxalate renal stones. People who form calcium
oxalate stones are advised to reduce their dietary intake of oxalate and to avoid
supplementation with vitamin C, which grades to oxalate in the body.

Examples of foods high in oxalates:


Vegetables Fruits Others
­ Beets ­ Oranges, orange peel ­ Barley
­ Collard greens ­ Strawberries* ­ Cocoa
­ Leeks ­ Kiwi ­ Nuts
­ Green beans ­ Grapes ­ Tea*
­ Eggplant ­ Figs ­ Soybean products
­ Parsley ­ Lemmon peels ­ Wheat bran*
­ Spinach* ­ Whole wheat flour
­ Sweet potatoes

Ur ic acid stones. 

 Uric acid stones can form in people who don't drink enough fluids or who lose too
much fluid, those who eat a high­protein ( Diet high in purines)
 Purines are the end products of nucleoprotein metabolism and are found in all meats,
fish, and poultry. Organ meats, anchovies, sardines, meat extracts, and broths are
especially rich sources of them. Uric acid stones are usually associated with gout

Cystine stones. 
 These stones form in people with a hereditary disorder that causes the kidneys to
excrete too much of certain amino acids (cystinuria).

Str uvite Stones.


 Struvite stones are composed of magnesium, ammonium and phosphate, are usually
seen in women.
 They are sometimes called infection stones because they develop following urinary
tract infections caused by certain microorganisms.
 Treatment consists of long­term effective antibiotics as well as surgical or ultrasonic
removal of stones. A low­phosphorus diet is often prescribed.

 POLYCYSTIC KIDNEY DISEASE

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 Polycystic kidney disease (PKD) is an inherited disorder in which clusters of cysts


develop primarily within your kidneys.
 Cysts are noncancerous round sacs containing water­like fluid. The cysts vary in size
and, as they accumulate more fluid, they can grow very large.

Symptoms
Polycystic kidney disease symptoms may include:
 High blood pressure
 Back or side pain
 Headache
 Increase in the size of your abdomen
 Blood in your urine
 Frequent urination
 Kidney stones
 Kidney failure
 Urinary tract or kidney infections

Causes
 Abnormal genes cause polycystic kidney disease, and the genetic defects mean the
disease runs in families. Rarely, a genetic mutation can be the cause of polycystic kidney
disease.

Dietar y Management
 Eliminate toxins, especially kidney toxins, Exercise and rest sufficiently.
 A low sodium, 1200 mg sodium diet helps to keep blood pressure low which in turn can
help keep cystic organs smaller.
 A neutral protein is neither low protein nor high protein. It is neutral. What goes in,
comes out. A neutral plant based protein diet that is individually calculated to 0.6 grams
of protein per kilogram of body weight is something to try for maintaining healthy cystic
kidneys.
 Drinking enough water to shut down vasopressin or about 3 litres of water per day, might
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help assure the health of polycystic kidneys.


 An alkaline vegan diet that avoids all animal proteins (ground meats, dairy, egg whites,
milk, cheese, beef, pork, chicken), soy proteins, yeast, alcohol, concentrated sugars seems
to make us feel better.

Kidney tr ansplant. 

 A kidney transplant involves surgically placing a healthy kidney from a donor into your
body. Transplanted kidneys can come from deceased or living donors. You'll need to take
medications for the rest of your life to keep your body from rejecting the new organ. You
don't need to be on dialysis to have a kidney transplant.
Aim of nutr itional management
 Promoting nutritional repletion during the early post­operative period.
 Maintaining good nutrition in the ensuing period.
 Maintaining normal body weight.
 Counteracting the side effects caused by immuno­suppressive therapy.

Dietar y management

 The diet prescription is based on the kidney functions as indicated by: urine output,
serum creatinine, blood urea nitrogen (BUN), potassium and phosphorus.
 Initially clear liquids are given to the patient during the early post­ operative period, and
then progresses to solid foods as tolerated. Finally the patient is placed on an essentially
normal diet.
Pr otein
 Initially a low protein diet.
 Once graft function is established give 1 to 2g /KgBWT. This is because immuno­
suppressive therapy used increases the body’s protein requirements. After first month the
requirements drop to 1g/KgBWT.

Calor ies
 Calorie requirements are such that; first month following transplant and during treatment
of acute rejection, 30 – 35KCal/kg bwt. After the first month sufficient calories to
achieve optimal weight for height. At all times, no more than 50% of calories while
encouraging complex carbohydrates and avoiding simple sugars.
 A low carbohydrates diet is prescribed due to excessive weight gain after transplant,
which is partly due to increased appetite and steroid therapy.

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Fats
 Increase intake of polyunsaturated fats and reduce intake of saturated fats.
Sodium
 Ensure low intake as steroids cause sodium retention (250 – 2000mg/day).
Potassium
 May be restricted if hyperkalemia occurs.
Phosphor us
 Serum phosphorus levels decrease after transplant, and patients may require
supplementation (1,200mg/day).
 Encourage intake of high phosphorus foods e.g. dairy products, eggs and meat.
Calcium
 Give 1,200 mg/day.
Ir on
 May require supplementation after the operation.
Fluids
 Add liberal amounts unless fluid retention and hypertension worsens.

TOPIC: METABOLIC AND ENDOCRINE DISORDERS­GOUT

GOUT

 A gout is a disorder of purine metabolism in which abnormal levels of uric acid


accumulate in the blood and result to deposition and crystallization of uric acid at the
joints.
 The deposition and crystallization of uric acid results in inflammation and sharp joint
pain.

Purines
 The name "purines" refers to a specific type of molecule made up of carbon and nitrogen
atoms, and these molecules are found in cells' DNA and RNA.
 They are typically found in the nucleus of any plant or animal cell and therefore purines
are part of normal diet as they are found in food and drinks from plants and animals.
.Essentially, purines are the building blocks of all living things. In the human body,
purines can be divided into two categories:

o Endogenous purines that are manufactured by the body


o Exogenous purines that enter the body via food

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Exogenous purines, the purines that a person eats, are metabolized by the body. Specifically, the
liver breaks down the purines and produces a waste product called uric acid. The uric acid is
released into the bloodstream and is eventually filtered by the kidneys and excreted in the urine.

If too much uric acid builds up in the bloodstream it is called hyperuricemia. In some people,
hyperuricemia can cause kidney stones or lead to an inflammatory joint condition called gout.

Main Risk factor s/ causes


 Excessive intake of red meat and fish which result to elevated uric acid in the blood
 Excessive intake of alcohol, as it blocks the elimination of uric acid from the body
 Excessive consumption of stimulant beverages as caffeine if part of the chemical
family of purine. It transforms into uric acid in the body
 Hormonal factor
 Obesity

Sym ptom
 s/Inflammation
im plication s and pain of the joints especially the meta tarsal pharyngeal ( the base
of big toe)
 A risk factor to chronic arthritis

Aim of n utrPrevent
ition al m an agem accumulation
excessive en t of uric acid

Man agem
 en t of low purine diet by restricting consumption red meat, fish, alcohol, stimulants,
Use
and high protein foods to avoid exogenous addition of purines to the existing high
uric acid load is recommended
 Encourage consumption of alkalizing foods e.g. lemons, tomatoes, green beans,
fruits milk and milk products
 Intake of fluids about 3lts/day to enhance excretion of uric acid based on assessment
is recommended
 Moderate protein intake ( 0.8g/kg/day)
 Maintain adequate CHO intake to prevent ketosis
 Limit fat intake
 Avoid large and heavy meals late in the evening
 Encourage consumption of whole grains

N/B. People with hyperuricemia are encouraged to eat foods with low purine concentrations and
avoid foods with high purine concentrations. In addition, foods and drinks that inhibit the body's
ability to metabolize purines, such as alcohol and saturated fats, should be limited or avoided
altogether
A summar y of the r isk factor s/ foods that have r elatively high concentr ations of pur ines
with other foods with moder ate and low concentr ations of pur ines.

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High Pur ine Foods/r isk factor s/causes Moder ate Pur ine Foods: Eat Low Pur ine Foods
Limited Quantities
Any vegetables that
Meats, especially organ meats or Certain vegetables, including are not listed as
"sweetmeats," such as liver, brains, and asparagus, spinach, mushrooms, moderately high in
beef kidneys, as well game meats, such as green peas and cauliflower (no purines, such as leafy
venison, which are typically fatty more than ½ cup per day) greens, carrots and
tomatoes

Condiments that
Foods containing saturated fats: these tend
Beef, pork, lamb, fish and poultry contain oils, spices,
to inhibit the body's ability to metabolize
(no more than 4­6 oz daily) and vinegars are
purines
generally acceptable

Seafood, particularly scallops and other Rice, enriched pastas


Wine* (1­2 glasses, when gout
shellfish, anchovies, sardines, herring, and and breads, potatoes,
symptoms are absent)
mackerel and popcorn

Foods and drinks made with high fructose Wheat bran and wheat germ (1/4 Nuts and nut products,
corn syrup, such as sodas1 cup dry daily) such as peanut butter

Dairy products
Supplements containing yeast or yeast Dried beans, lentils and peas (1 cup
(preferably low­ or no­
extract cooked)
fat)
Eggs, particularly egg
Gravy Oatmeal (2/3 cup dry daily)
whites
Alcoholic beverages, especially ­Beer* Fruit juice (no corn syrup) Coffee and tea
Meat­based soup stocks Fruits

Meat­based soup stocks Fruits

*Alcoholic drinks can inhibit the body's ability to eliminate uric acid, so people with gout are
advised to avoid alcohol or drink in moderation. Beer is notorious for bringing on gout attacks
because it contains both alcohol and brewer’s yeast, which is high in purines.

People on a low­purine diet should drink plenty of water to aid with digestion and lower uric
acid concentrations in the blood.

HYPERTHYROIDISM
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This is a condition due to overactive thyroid gland. (It is where the thyroid gland overproduces
the thyroxine hormone). Thyroxine hormone controls the rate of energy metabolism in the cells.

Iodine is needed for the production of thyroxine hormone. The body contains about 15 to 20 mg
of iodine, and most of this (70% to 80%) is in the thyroid gland.

Hyperthyroidism may be initiated by hormonal imbalances or tumors.

Causes
 Hormonal imbalances
 Tumors

Sym ptom
 s Increased
an d im plication s of rate
metabolic hyper thyr oidism
 Increased basal metabolic rate by increasing oxygen uptake and reaction rates of
enzyme systems handling glucose
 Excessive production of the thyroid hormones
 Increased energy expenditure and weight loss
 Nervous excitation due to excessive hormone product
 Tachycardia ( high heart rate)
 Increased perspiration and heat sensitivity

Aim s ofm an
Toagem en t
prevent/control weight loss‑through provision of high calorie diet.
 Reduce workload

Man agem
 en t
Treat the underlying cause
 Use of high calorie diet to meet the extra energy needs is recommended
 Refer to high calorie diet

HYPOTHYROIDISM
This is state resulting from reduced activity of the thyroid gland. The gland does not produce
sufficient levels of thyroxine hormone.

Causes
 Inadequate iodine intake and selenium deficiency

Sym ptom
 s/Enlargement
im plication sof thyroid gland as the cells enlarge to trap as much iodine as possible
 Sluggishness and weight gain
 In pregnancy it can result to impaired fetal development

Aim of m
 anTo
agem en t iodine deficiency
control

Man agem
 en t
Recommend iodine rich foods e.g. sea foods or iodine fortified foods
 Recommend suitable exercise program

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TOPIC: RESPIRATORY DISEASES


THE RESPIRATORY SYSTEM

The respiratory conducting passages are divided into the upper respiratory tract and the lower
respiratory tract. The upper respiratory tract includes the nose, pharynx, and larynx. The lower
respiratory tract consists of the trachea, bronchial tree, and lungs. These tracts open to the outside
and are lined with mucous membranes. In some regions, the membrane has hairs that help filter
the air. Other regions may have cilia to propel mucus.

INFECTIONS OF THE RESPIRATORY SYSTEM

UPPER RESPIRATORY TRACT INFECTIONS


 The upper respiratory tract includes the nose (sinuses, nasal passages), pharynx, and
larynx. Upper respiratory tract infection is any infection of any of the components of the
upper airway.
 Upper respiratory tract infection include Common Cold, Sinusitis, Phar yngitis,
Epiglottitis and Lar yngotr acheitis)

 Respiratory tract infections (Upper and lower tract infections) are communicable, in the
sense that they are spread from one person to another, the contraction occurs basically
when exposed to an infected person. By inhaling the air which contains the germs, by
contact with an infected person's body fluids (when one touches the eyes, mouth, or nose
with the infected body fluids).
 Increased amount of oxygen, fluid intake, and humidified air can help fight the symptoms
of a mild to moderate infections.

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COMMON COLD (NASOPHARYNGIS/ RHINOPHARYNGIS)


 A cold is a mild viral infection of the nose, throat, sinuses and upper airways. It's very
common and usually clears up on its own within a week or two.

Causes

It is caused by a virus that inflames the membranes in the lining of the nose and throat. Colds are
caused by more than 200 different viruses.
After the virus enters the body, it causes a reaction — the body's immune system begins to react
to the foreign virus. This, in turn, causes:
 An increase in mucus production (a runny nose).
 Swelling of the lining of the nose (making it hard to breathe and causing congestion).
 Sneezing (from the irritation in the nose).
 Cough (from the increased mucus dripping down the throat).

Tr ansmission

 Person to person (When one is in contact with an infected person's body fluids e.g. through
coughs and sneeze.)
Risk Factor s
 Cold weather
 Low resistance due to fatigue, exhaustion, loss of sleep, stress, depression.
 Unhygienic family practices.
Symptoms of a cold 

The symptoms of a cold usually develop within a few days of becoming infected.
The main symptoms include:
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 a sore throat
 a blocked or runny nose
 sneezing
 a cough
 a hoarse voice
 generally feeling unwell
Less common symptoms of a cold include:
 a high temperature (fever) – this is usually about 37­39C (98.6­102.2F)

 a headache
 muscle pain
 loss of taste and smell
 mild irritation of the eyes
 a feeling of pressure in your ears and face  
 The symptoms are usually at their worst during the first two to three days, before they
gradually start to improve. In adults and older children, they usually last about 7 to 10
days, but can last longer. A cough in particular can last for two or three weeks.
 Colds tend to last longer in younger children who are under five, typically lasting around
10 to 14 days.

Complications of colds 
Colds usually clear up without causing any further problems. However, the infection can
sometimes spread to your chest, ears or sinuses.
MANAGEMENT
Diet ther apy
 Energy: High energy diets because of increased metabolic needs as cold comes with fever,
thus increased BMR.
 Fluid: In case of profuse nasal discharge, fluid intake (water) should be increased.
 Drink plenty of water, can add a pinch of turmeric and ginger powder to it.
 Incr eased vitamin C because of low immunity­ Consume citrus, lemon, orange fruits
etc. as they are have high vitamin C
 Food and soups should be served hot.
 Incr ease intake of vitamin A in your diet ­ all yellow fruits and vegetables contain
Vitamin A. Meat, fish, kidney and liver, liver oils of fish like cod, shark, and halibut are
richest source of vitamin A. If you are a vegetarian you can have fish liver oil
supplements but over dose can be toxic.
 Small frequent meals because of loss of appetite and smell
 Avoid milk and milk products ­ cottage cheese as they result into increased production of
mucus

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Functional foods
 Include garlic, ginger and onions in your food.
 Boil a mixture of Bishops weed (Ajwain), tea leaves and water and inhale the steam,
helps to decongest the nose block due to cold. Should do at least three times a day.
 Drink boiled mixture of ­ half cup water, little ginger, 2­3 leaves of sweet basil (tulsi) and
mint leaves, or you can eat the raw leaves, this will boost up your immunity and control
your cough and cold.
 Gargle with warm water, a pinch of salt and turmeric to sooth your throat.
 Take raw fruits and vegetables. Apple is good for cold, should consume at least one apple
a day.
 Avoid milk and milk products ­ cottage cheese as they result into increased production of
mucus
 Avoid spicy food, eggs, sweets and cold refrigerated drinks.
 Avoid cold drinks, cold water, ice creams and aerated drinks.
 Avoid all food with preservatives and additives.

SINUSITIS
Sinusitis is an infection/inflammation of the small air­filled cavities inside the cheekbones and
forehead. It develops in up to 1 in every 50 adults and older children who have a cold.

The sinuses are small, air­filled cavities behind your cheekbones and forehead.
The mucus produced by your sinuses usually drains into your nose through small channels. In
sinusitis, these channels become blocked because the sinus linings are inflamed (swollen).

Causes
Conditions that can cause sinus blockage include:

 The common cold
 Allergic rhinitis, which is swelling of the lining of the nose
 Small growths in the lining of the nose called nasal polyps
 A deviated septum, which is a shift in the nasal cavity
 A weakened immune system

Types

 Acute sinusitis usually starts with cold like symptoms such as a runny, stuffy nose and facial
pain. It may start suddenly and last 2­4 weeks.
 Sub­acute sinus inflammation usually lasts 4 to 12 weeks.
 Chronic inflammation symptoms last 12 weeks or longer.
 Recurrent sinusitis happens several times a year.

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Signs and symptoms


Sinusitis usually occurs after an upper respiratory tract infection, such as a cold. If you have
a persistent cold and develop the symptoms below, you may have sinusitis.
Symptoms of sinusitis include:
 a green or yellow discharge from your nose

 a blocked and runny nose


 pain and tenderness around your cheeks, eyes or forehead
 a sinus headache
 a high temperature (fever) of 38C (100.4F) or more
 toothache
 a reduced sense of smell
 bad breath (halitosis)
Children with sinusitis may be irritable, breathe through their mouth, and have difficulty feeding.
Their speech may also sound nasal (as though they have a stuffy cold).
The symptoms of sinusitis often clear up without treatment within a few weeks (acute sinusitis),
although occasionally they can last three months or more (chronic sinusitis).

Dietar y Management

As in common cold

Functional foods
Foods that r educe and pr event inflammation
 Fish such as wild salmon, cod, and sardines are high in omega 3 fatty acids.
 Tur mer ic spice, contains curcumin, which actively reduces inflammation.
 Avocados are high in omega 3 fatty acids and can reduce immune dysfunction.
 Beans, such as mung, pinto, and kidney, are also high in omega 3 fatty acids.
 Red bell pepper s are rich in Vitamin C and acts as an antioxidant.
 Gr een vegetables such as broccoli, asparagus, leafy greens, and bean sprouts contain
high levels of vitamin C and calcium, helping to counteract histamine, “the substance that
can contribute to inflammation, runny nose, sneezing, and other related symptoms.”
 Vitamin A is considered a ‘membrane conditioner’ that helps build healthy mucus
membranes in the head, chest, and throat and is great for skin and eye health. Vitamin A
is plentiful in sweet potato, carrots, dark leafy greens, squash, apricots, rockmelon, paw
paw, and red and yellow capsicum. Infact paw paw is rich in vitamins A, C and E.
 Citr us fr uits such as oranges, grapefruit, and berries are also high in vitamin C.
 Other fr uits such as tomatoes, apples and pears are rich in Quercetin, a natural
antihistamine.
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 Gr een tea and drinking more fluids can help to alleviate any headaches that can result
from dehydration caused by constant sneezing and blowing your nose.
 Spices like ginger

PHARNGITIS (SORE THROAT)


 Pharyngitis (sore throat) is an inflammation of the pharynx or throat – the area between
the tonsils and the larynx (voice box). A sore throat is characterised by redness, swelling
and pain in this area, which can make swallowing or speech difficult.
 The pharynx is connected to the mouth, nose, oesophagus, larynx and ears. It is also close
to the tonsils (at the back of the pharynx) and the adenoids (higher up in the nasal portion
of the pharynx).
 A sore throat is usually the first symptom of a mild illness such as a cold or the flu.
However, it can also be an indication of a more serious condition, such as strep throat or
scarlet fever.

Causes

Sore throat can be caused by viruses or bacteria.


Vir al causes
Viruses cause most sore throats:

 Most commonly, the viruses that cause the common cold are responsible for viral
pharyngitis.

o In young children, the condition is usually mild, and can be mistaken for a
common cold or flu.

 Other viral infections that can result in pharyngitis include influenza (flu), measles,
chickenpox and herpes.

Bacter ial causes


Bacteria can also cause a sore throat:

 The most common bacterial cause of a sore throat is the streptococcus bacterium, which
causes the serious condition strep throat.

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Other causes

 Smoking cigarettes, consuming excessive alcohol, breathing in chemical fumes or air


pollution, or swallowing substances that irritate or damage the lining of the throat can
also cause pharyngitis.

Sym p t om s
Inflammation of the pharynx causes it to redden and swell. The condition is characterised by a
raw, scratchy or burning sensation in the back of the throat, and pain, especially when
swallowing.
Other symptoms may include:
 Tenderness or swollen glands at the front of the neck
 Sneezing and coughing
 Hoarseness
 Runny nose
 Mild fever
 General fatigue
 Painful breathing and speaking
 Pus in the throat
 Ear infection
 Sinusitis
 Abscess near the tonsils

T r ea t m en t
 Usually no specific treatment is required if you have viral pharyngitis (such as mono),
which usually clears up within a week.
 Bacterial infections such as strep throat can be effectively treated with antibiotics.
Antibiotics do not help with viral infections.
 For chronic pharyngitis (persistent pain due to a respiratory, sinus, or mouth infection
spreading to the throat), your doctor should treat the primary source of infection.
Home r emedies
Most sore throats will go away by themselves after a few days and can be effectively treated at
home.
To relieve the pain and discomfort of a sore throat, you could try the following:

 Get a lot of rest.


 Drink plenty of fluids.
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 Gargle with warm salt water or some other home­made gargle to wash away mucus and
irritants.
 Avoid smoking cigarettes.
 Eat largely soft foods for a couple of days to avoid irritating your throat.
 Suck non­prescription lozenges containing a mild anaesthetic. Zinc lozenges can relieve
sore throats and other cold symptoms. Mildly anaesthetic sprays and mouthwashes are
also available over the counter.
 If mouth breathing or dry air causes your sore throat, try using a humidifier in your home.
 If your nose is blocked, use a nasal spray to prevent mouth breathing. (Caution: using
these products for more than a couple of days may result in dependency. If you have
heart disease or high blood pressure, check with a doctor before using any decongestant
products.)
 Apply a warm heating pad, compress or salt plaster to your throat.
 Try steam inhalations.

Management

Nutr ition ther apy: As in common cold

Functional foods

 Lemon and water ­ Mix 1 teaspoon lemon juice in 1 cup water for this home remedy for
sore throats; the astringent juice will help shrink swollen throat tissue and create a hostile
(acidic) environment for viruses and bacteria
 Ginger , lemon and honey ­ This sore throat home remedy mixes 1 teaspoon each of
powdered ginger and honey, 1∕2 cup of hot water, and the juice of 1∕2 squeezed lemon. Pour
the water over the ginger, then add the lemon juice and honey, and gargle. Honey coats the
throat and also has mild antibacterial properties.
 Hot sauce and water ­ The capsicum in hot peppers helps alleviate pain and fights
inflammation. Add five shakes of ground cayenne pepper (or a few shakes of hot sauce) to a
cup of hot water for sore throat relief. It'll burn, but try this gargle every 15 minutes and see
if it helps.
 Tur mer ic and water ­ This yellow spice is a powerful antioxidant, and scientists think it has
the strength to fight many serious diseases. For a sore throat remedy, mix 1/2 teaspoon of
turmeric and 1/2 teaspoon of salt into 1 cup of hot water and gargle.
 Clove tea ­ Add 1 to 3 teaspoons of powdered or ground cloves to water, then mix and
gargle. Cloves have antibacterial and anti­inflammatory properties that can help soothe and
heal a sore throat.
 Tomato juice ­ For temporary relief of sore throat symptoms, gargle with a mixture of 1/2
cup tomato juice and 1/2 cup hot water, plus about 10 drops hot pepper sauce. The
antioxidant properties of lycopene may help remedy a sore throat faster.

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P r even t ion

 If you are prone to sore throats, try changing your toothbrush every month – the bristles
can harbour bacteria. Also throw away your old toothbrush after recovery from a sore
throat so as not to re­infect yourself.
 Try not to share eating and drinking utensils with other people.
 When you use public telephones or water faucets, try to avoid touching them with your
nose or mouth.
 Do not have close contact with someone who has a sore throat.
 If you live in a polluted environment, try to stay indoors as much as possible on days
when the pollution is very bad.
 Don't consume large amounts of alcohol.
 Avoid areas where there is a lot of cigarette smoke.
 If the air is very dry, try humidifying your home.
 Build up your body's natural defences: reduce stress levels and get plenty of rest. This
can help you to avoid infections such as strep throat.

EPIGLOTTITIS

 Epiglottitis is a medical emergency that may result in death if not treated quickly. The
epiglottis is a flap of tissue at the base of the tongue that keeps food from going into
the trachea, or windpipe, during swallowing.
 When it gets infected and inflamed, it can obstruct, or close off, the windpipe, which may
be fatal unless promptly treated.
 Respiratory infection, environmental exposure, or trauma may result in inflammation and
infection of other structures around the throat. This infection and inflammation may
spread to the epiglottis as well as other upper airway structures.
 With continued inflammation and swelling of the epiglottis, complete blockage of the
airway may occur, leading to suffocation and death. Even a little narrowing of the
windpipe can dramatically increase the resistance of an airway, making breathing much
more difficult.

Causes

Causes of epiglottitis include bacteria, viruses, and fungi, especially among adults.

 Various organisms that can cause epiglottitis e.g Streptococcus pneumoniae, herpes simplex


virus type 1, and Staphylococcus aureus, 
 Other types of epiglottitis are caused by heat damage. Thermal epiglottitis occurs from
drinking hot liquids; eating very hot solid foods; or using illicit drugs

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Symptoms
When epiglottitis strikes, it usually occurs quickly, from just a few hours to a few days. The most
common symptoms include sore throat, muffling or changes in the voice, difficulty speaking, fever,
difficulty swallowing, fast heart rate, and difficulties in breathing.
Fever is usually high in children but may be lower in adults or in cases of thermal epiglottitis.

CAUTION:

Epiglottitis is a medical emergency. Someone who is suspected of having epiglottitis should be taken
to the hospital immediately. Try to keep the person as calm and comfortable as possible. Make no
attempt at home to inspect the throat of a person suspected of having epiglottitis. This can cause the
windpipe and surrounding tissues to close and an irregular heartbeat, which can lead to respiratory
and/or cardiac arrest (stopping of breathing and/or heart) and death.

Complications
Epiglottitis can cause a number of complications, including:

 Respir ator y failur e. This is when the airway narrows and become completely
blocked. This can lead to respiratory failure — a life­threatening condition in which
the level of oxygen in the blood drops dangerously low or the level of carbon dioxide
becomes excessively high.

Pr evention
Epiglottitis can often be prevented with proper vaccination against H influenza type b (Hib). Adult
vaccination is not routinely recommended, except for people with immune problems such as sickle
cell anaemia, splenectomy (removal of the spleen), cancers, or other diseases affecting the immune
system.
Common sense pr ecautions
Of course, the Hib vaccine doesn't offer guarantees. Immunized children have been known to
develop epiglottitis — and other germs can cause epiglottitis, too. That's where common sense
precautions come in:

 Don't share personal items.


 Wash your hands frequently.
 Use an alcohol­based hand sanitizer if soap and water aren't available.

LARYNGOTRACHEITIS (CROUP)

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 Croup is the common name for laryngotracheitis. This is when the voice box (larynx),
trachea (windpipe) and airways from the lungs (bronchi) become infected. It's a common
condition and only rarely has serious consequences.

 Croup mainly affects children under the age of six. Croup is a condition in which parts of
your child's respiratory (breathing) system become infected, leading to inflammation.
Thick mucus is also produced. The airways from the lungs are likely to be swollen and
this makes it difficult for air to move into and out of the lungs.

Symptoms
Acute laryngotracheitis in children and adults
 sore throat that triggers a cough;
 Changed and rough voice.
 headaches;
 a feeling of a lump in the throat;
 Coughing fits that occur mostly at night. They are accompanied by wheezing, dyspnea.
 The child is very restless and scared, crying constantly. He sits or stands. This is due to
the fact that he just cannot take a horizontal position, as the cough in this position is
reinforced (due to edema).
Causes
It is caused by a virus. Very occasionally croup may be caused by bacteria or an allergic
reaction.

Pr evention
Croup is spread by droplets in the air which are released when someone with the infection
coughs or sneezes. The disease can also be passed on by touching a surface that has been
contaminated. You can reduce the risk of croup by making sure your child washes his/her hands
regularly. If possible, keep your child away from people who have a respiratory infection.

Tr eatment
.Drug therapy:
Nutrition therapy: As in common cold

Middle ear infection (otitis media)


A middle ear infection (otitis media) develops in an estimated one in every five children under
the age of five with a cold.
Symptoms of a middle ear infection include:
 severe earache
 a high temperature of 38C (100.4F) or above
 flu­like symptoms, such as vomiting and a lack of energy

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 some loss of hearing


Most middle ear infections will resolve without treatment within a few days. Treatment is
usually only required if your child has repeated middle ear infections.

Chest infection
A chest infection such as bronchitis and pneumonia can occur after a cold, as your immune
system is temporarily weakened.
Symptoms of a chest infection include a persistent cough, bringing up phlegm (mucus),
and shortness of breath.
Minor chest infections will resolve in a few weeks without specific treatmen

LOWER TRACT INFECTIONS


 The lower respiratory tract begins from the trachea and ends in the lungs. The tract enters
the lungs and divides into the bronchi. Then each of the bronchi divides further into
smaller air pipes that are bronchioles.
 These bronchioles end in small air sacs which are known as alveoli. Many alveoli bunch
up together and form the alveolar sac. From these alveoli the blood capillaries go out.
 The common illnesses are bronchiolitis, pneumonia, bronchitis and flu.
 Lower respiratory tract infection cause greater harm to the human body than the upper
respiratory infections.

LOWER RESPIRATORY TRACT INFECTIONS


BRONCHITIS

 Bronchitis or Bronchial Infection refers to the swelling and inflammation of the


membranes lining the bronchial tubes. The swelling of the tubes reduces the airway
passage resulting in coughing spells. These coughing spells are usually accompanied
by breathlessness. At times phlegm is also there.
 It is mostly caused by a virus one gets from the flu or the common cold but can also

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be caused by bacteria and fungi


Risk factor s
 Heavy smoking as long­term cigarette smoking affects the bronchial tubes and
this leads to excess mucus production that eventually leads to the inflammation of
the tubes.
 The inflammation is also high among those who work in quarries, mining field
and also grain handlers. They are continually exposed to dust particles and
poisonous fumes.

Symptoms

 Shortness of breath
 Rapid breathing
 Chest constriction
 Coughing and wheezing
 Blood in cough at times
 Nose block
 Fever

Types of Br onchitis or Br onchial Infection

Bronchitis or Bronchial Infection generally affects people in two forms–Acute Bronchitis (which


lasts for one to three weeks) and chronic Bronchitis (which lasts for minimum 3 months to two
years in a continuum).
o Acute Br onchitis or Acute Br onchial Infection: In acute bronchitis, there are symptoms of
hacking cough and it also produces phlegm that at times is accompanied by an upper
respiratory tract infection. In most cases, it is a viral infection, but sometimes bacterial
infection is also found. Acute bronchitis goes away with good hygiene.

 Chr onic Br onchitis or Chr onic Br onchial Infection: Chronic bronchitis, however, is a

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serious ailment and a long term disorder which requires medical attention

Symptoms of chr onic br onchial infection


 Coughing up yellow or grey mucus
 Wheezing
 Sore Throat
 Nose Block.
 Cough with blood
 High fever
 Trouble breathing
 Chest pain

Management and pr evention: 

Antibiotics: Since bronchitis usually results from a viral infection, hence antibiotics aren't
usually effective in treating bronchial infection. However, a doctor might still prescribe an
antibiotic if he or she suspects that the infection is caused by a bacterial invasion.

o Cough Medicine: It is always considered best not to suppress a cough that brings up the
mucus, since coughing also helps in removing the irritants from your lungs and clears the
air passages. Still, if your cough keeps you miles away from sleeping, one might also try
using cough suppressants or cough medicines at bedtime.

Avoid Cigar ette and Smoke: Cigarette smoke usually increases the risk of chronic bronchitis.
Hence it has to be avoided at all cost. People who smoke, particularly long­time smokers, and
also those who experience second­hand smoking, have an increased risk of not just bronchial
infection but also lung cancer.

Get Vaccinated: Many cases of acute bronchitis might result from influenza, which again
caused by an influenza virus. Thus, getting a yearly flu vaccine can help and protect you from
getting flu. Considering the option of vaccination that protects against some types of pneumonia
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is also recommended.

Wash Your Hands: To avoid and cure communicable diseases and also to reduce the risk of
catching a viral or bacterial infection, consider washing your hands frequently and also get in the
habit of using hand sanitizers.

Wear a Sur gical Mask: If anyone you know is suffering from bronchitis or COPD, considering
the idea of wearing a face mask at work and in crowds is worth giving a thought and at times it
becomes a necessity since prevention is better than a cure.

Dietar y management: As in common cold

Other r emedies

 If you do suffer from shortness of breath or tightness in the chest, rubbing turpentine over
the chest can offer some much needed relief.
 Warm salt water gargles can also help to loosen the phlegm and reduce constriction that
you may feel in your chest.
 The best way to treat bronchitis is by getting adequate rest. 

PNEUMONIA

 The term pneumonia comes from the Greek word pneuma meaning “ breath”

 Pneumonia refers to an acute inflammation of the lung caused by an infectious


agent that primarily affects the microscopic air sacs known as alveoli.
 The air sacs may fill with fluid or pus (purulent material), causing cough with
phlegm or pus, fever, chills, and difficulty breathing.
Causes/Infectious agents
 Infection by organisms.  A variety of organisms, including bacteria, viruses and
fungi, can cause pneumonia but is mostly caused by
viruses and bacteria. The organisms (bacteria and fungi) can be as a result of
aspiration of normal bacterial flora and/ or gastric contents secretions and through
inhalation of the virus and bacteria. Aspiration and gastric secretion delivers
bacteria straight to the lungs
 Medications 
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 Conditions such as autoimmune diseases


It is most serious for infants and young children, people older than age 65, and people with
health problems or weakened immune systems.

Symptoms

The signs and symptoms of pneumonia are nonspecific and vary from mild to severe, depending
on factors such as the type of germ causing the infection, and your age and overall health. Mild
signs and symptoms often are similar to those of a cold or flu, but they last longer
 Fever
 Sweating and shaking chills
 Cough, with or without phlegm (sputum). The sputum may be rusty or green or tinged
with blood. Coughing is the immune response by the body
 Sneezing(pulmonary defense mechanism to guard against pneumonia)
 Chest pain when you breathe or cough
 Fast breathing and feeling short of breath.
 Fast heartbeat.
 Shaking and "teeth­chattering" chills.

 Fatigue
 Nausea, vomiting or diarrhea
 Purulent sputum( containing pus)
Newborns and infants may not show any sign of the infection. Or they may vomit, have a fever
(and cough, appear restless or tired and without energy, or have difficulty breathing and eating.

People older than age 65 and people in poor health or with a weakened immune system may
have a lower than normal body temperature. Older people who have pneumonia sometimes have
sudden changes in mental awareneness

For some older adults and people with heart failure or chronic lung problems, pneumonia can
quickly become a life­threatening condition.

Classification of pneumonia

Pneumonia is classified according to the types of germs that cause it and where you got the
infection.

1. Community­acquir ed pneumonia
Community­acquired pneumonia is the most common type of pneumonia. It occurs outside of
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hospitals or other health care facilities. It may be caused by:

Bacter ia. The most common cause of bacterial pneumonia in the Streptococcus pneumonia This
type of pneumonia can occur on its own or after you've had a cold or the flu.
Mycoplasma pneumoniae also can cause pneumonia. It typically produces milder symptoms than
do other types of pneumonia.
Walking pneumonia, a term used to describe pneumonia that isn't severe enough to require bed
rest, may be caused by M. pneumoniae.

Vir uses. Some of the viruses that cause colds and the flu can cause pneumonia. Viruses are the
most common cause of pneumonia in children younger than 5 years. Viral pneumonia is usually
mild. But in some cases it can become very serious.

Fungi. This type of pneumonia is most common in people with chronic health problems or
weakened immune systems, and in people who have inhaled large doses of the organisms. The
fungi that cause it can be found in soil or bird droppings.

2. Hospital­acquir ed pneumonia. Some people catch pneumonia during a hospital stay for
another illness. This type of pneumonia can be serious because the bacteria causing it may be
more resistant to antibiotics. People who are on breathing machines (ventilators), often used in
intensive care units, are at higher risk of this type of pneumonia.

3. Health car e­acquir ed pneumonia. Health care­acquired pneumonia is a bacterial infection


that occurs in people who are living in long­term care facilities or have been treated in outpatient
clinics, including kidney dialysis centers. Like hospital­acquired pneumonia, health care­
acquired pneumonia can be caused by bacteria that are more resistant to antibiotics.

3. Aspir ation pneumonia. Aspiration pneumonia occurs when you inhale food, drink, vomit or
saliva into your lungs. Aspiration is more likely if something disturbs your normal reflex, such as
a brain injury or swallowing problem, or excessive use of alcohol or drugs.

Risk Factor s.

Pneumonia can affect anyone. But the two age groups at highest risk are:
 Children who are 2 years old or younger
 People who are age 65 or older
Other risk factors include:
 Chronic disease. You're more likely to get pneumonia if you have asthma, lung diseases
such as cystic fibrosis, diabetes, heart failure, stroke
 Malnutrition­Weakened or suppressed immune system.

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People who have HIV/AIDS, who've had an organ transplant, or who receive
chemotherapy or long­term steroids are at risk.
 Smoking. Smoking damages your body's natural defenses against the bacteria and viruses
that cause pneumonia.
 Being hospitalized. You're at greater risk of pneumonia if you're in a hospital intensive
care unit, especially if you're on a machine that helps you breathe (a ventilator).
 Those with swallowing disorders
 Chest or upper abdominal surgery
 Preexisting lung disease
Complications
 Pneumonia can be treated successfully with medication. However, some people,
especially those in high­risk groups, may experience complications, including:
 Bacteria in the bloodstream (bacteremia). Bacteria that enter the bloodstream from your
lungs can spread the infection to other organs, potentially causing organ failure.
 Lung abscess. An abscess occurs if pus forms in a cavity in the lung. An abscess is
usually treated with antibiotics. Sometimes, surgery or drainage with a long needle or
tube placed into the abscess is needed to remove the pus.
 Fluid accumulation around your lungs (pleural effusion). Pneumonia may cause fluid to
build up in the thin space between layers of tissue that line the lungs and chest cavity
(pleura). If the fluid becomes infected, you may need to have it drained through a chest
tube or removed with surgery.
 Difficulty breathing. If your pneumonia is severe or you have chronic underlying lung
diseases, you may have trouble breathing in enough oxygen. You may need to be
hospitalized and use a breathing machine (ventilator) while your lung heals.

Management
Medical therapy
 Use of antibiotics
Dietary management
 Sufficient fluids (3 to 3.5 liters) if not contraindicated as much water is lost through sweat,
vomiting and diarrhea
 High energy diets because of increased metabolic needs as pneumonia comes with fever, thus
increased BMR. Eat high dense energy diet.You can also try to drink beverages that are
calorie­rich, such juices. Adding peanut butter or ice­cream to your fruits and cream
cheese, butter or olive oil to your vegetables adds calories.

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 Small frequent meals because of nausea, vomiting and diarrhea


 Adequate proteins for building new tissues and fixing damaged tissues. Protein­rich foods
can come from both animal and plant sources. Animal sources of protein include red
meat, pork, poultry or fish. Plant­based protein comes from nuts and seeds, and beans,
soybeans
 High vitamin and mineral intake. Multivitamin and mineral supplementation may be
beneficial
 Adequate fruits and minerals to supply necessary potassium

TOPIC: FEBRILE DISEASES

FEBRIBLE CONDITIONS

This refers to conditions that results into fever


Definition of ter ms
 
Hyper pyr exia

Hyperpyrexia is an extreme elevation of body temperature greater than or equal to 40.0 or 41.5 °C (104.0 or
106.7 °F). Such a high temperature is considered a medical emergency, as it may indicate a serious
underlying condition or lead to problems including permanent brain damage, or death. Infections commonly
associated with hyperpyrexia include roseola, measles

Hyper ther mia

Hyperthermia is an example of a high temperature that is not a fever. It occurs from a number of causes
including heatstroke, cocaine and drug reactions

Fever

Fever also known as pyrexia is an increase of more than 1 degree Celsius or any rise above the maximal
normal temperature.

Temper atur e classification

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Core (rectal, esophageal, etc.)

Hypothermia <35.0 °C (95.0 °F)


Normal 36.5–37.5 °C (97.7–99.5 °F)
Fever >37.5 or 38.3 °C (99.5 or 100.9 °F)
Hyperthermia >37.5 or 38.3 °C (99.5 or 100.9 °F)
Hyperpyrexia >40.0 or 41.0 °C (104.0 or 105.8 °F)

Measur ement of temper atur e can be done

 In the anus (rectum/rectal).It is the most accurate


 In the mouth (oral)
 Under the arm (axillary) or in the ear

 
FEVER
 
 It is an elevation of temperature above the normal and results from an imbalance (difference)
between the heat produce in the body and the heat eliminated from the body.

 The heat is produced as a natural response of the body, to destroy virus or pathogens in the
blood, by raising the body’s natural metabolic.
 Fever is a common symptom of many infections and chronic conditions(diseases)
 The normal body temperature varies from 36.5 degree Celsius – 37.5 degree Celsius (average
37°C) and is regulated by hypothalamus
 There is normally a diurnal variation of 1 degree Celsius, the lowest temperature being
between 2­4 am and highest in the afternoon.

Therefore fever also known as pyrexia is an increase of more than 1 degree Celsius or any rise above
the maximal normal temperature.

Fever increases BMR approximately 7% for each 0.83°C(1°F)

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Causes
A fever might be caused by
 Exogenous factors( infection): Any infection whether bacterial, viral, fungal or parasitic can
give rise to fever­a fever is a symptom of a disease
Other causes
 Certain inflammatory conditions such as rheumatoid arthritis— inflammation of the lining of
your joints (synovium)
 Some medications, such as antibiotics and drugs used to treat high blood pressure or seizures.
 Some immunizations, such as the diphtheria ,tetanus
 Endogenous factors: Antigen­antibody reaction can also result into fever
 Trauma; A massive crush injury may lead to pyrexia.

Types of fever s: Typhoid Fever, Rheumatic Fever, Meningitis, Small pox, viral hepatitis Influenza,
Malaria, Measles, Chicken Pox, etc.

Classification of fever

It must be noted that following types of fever association are generally noted as classic associations
and overlap might occur.

Acute fever (shor t fever )


 They are of short duration but the temperature may rise to even 39.5.°C.Fevers accompanying
infections like chicken pox, Cold, tonsillitis, typhoid, influenza, pneumonia, malaria, Chicken
pox, scarlet fever
Chr onic fever (Long fever )­ last fr om sever al days to months
 These are of long duration. Temperatures may remain low but fever continues for a long period
of time, even several months e.g. T.B

Continuous Fever

 The temperature remains above normal throughout the day and does not fluctuate more than 1
degree Celsius in 24 hours. This type of fever occurs in pneumonia, typhoid, urinary tract
infection, brucellosis, etc.

Remittent Fever

 The temperature remains above normal throughout the day and fluctuates more than 2 degree
Celsius in 24 hours. This type of fever is usually seen patients of typhoid infection. This type
of fever is most common in practice.

Inter mittent Fever

 There is alternation of temperature. There is high temperature for a few some hours in a day
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and then remains normal for the remaining hours e.g. malaria

Septic Fever

 The temperature variation between the highest temperature and lowest temperature is very
large and exceeds 5 degree Celsius. This type of fever occur in septicemia.

Symptoms of fever

 Rise in temperature of body heat

 Sweating, Perspiration or Shivering. Sweating results into loss of fluids and electrolytes

 Restlessness and agitated temper

 Pain and soreness all over the body but some limbs may be extra painful and sore

 Thirst

 Loss of Appetite

 Catabolism

Benefits of Fever

Fever is associated with release of endogenous pyrogens, which activate the T cells and thus enhance
the host defense mechanism.

Complications of Fever

It induces a state of catabolism which is detrimental to body. It may also lead to fluid and electrolyte
imbalance­due to sweating and loss of minerals. High grade fevers can lead to convulsions, brain
damage, circulatory overload and arrhythmia.

Management

Medical: Medications such as ibuprofen or paracetamol (acetaminophen) to lower the temperature

Dietar y modification in fever s

Ener gy: Increased by 50% if the temperature is high and tissue damage is high can be able to ingest
600­1200 kcal daily.
Car bohydr ates: Glycogen stores are replenished by readily absorbable glucose

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Pr otein: A high protein diet supplying 1.25­1.5g protein/kg body wt. should be fed. Protein
supplements can be incorporated in the beverages. A high protein is required because of increased
protein catabolism. Protein catabolism is especially marked in fevers such as typhoid, malaria and TB.
This depends on the severity and duration of the infection. Increased protein catabolism leads to
increased nitrogen wastes and places an additional burden on the kidneys.
Fats: Avoid fried foods. These foods are difficult to digest and also they may be associated with
excessive strain on the already poor gastro­intestinal system
Vitamins: All vitamins may be given as supplements to the patient. More so vitamin C which helps
enhance immunity and natural ability of the body to fight infection. Orange juice is a great source of
energy and is also loaded with Vitamin C. Avoid tinned or canned fruit juices as they are loaded with
preservatives and can delay the recovery process. 

Increase intake of vitamin E

Miner als: Sufficient intake Of: Sodium, potassium should be given liberally.
Fluids: Since loss of body fluids through sweat, vomiting & excretory wastes is high (urine), plenty of
water and other fluids is important especially during fever. Water also helps to flush the toxins out of
the body system and hastens recovery.
Fr equency. These feeding should be small & as frequent as possible. Generally, 6­8 feedings should
be sufficient
Foods to avoid: There are various foods to avoid when affected by fever.

 Do not consume red meat, as it is difficult to digest.


 Junk foods should be strictly avoided.
 You should also stay away from oily and high cholesterol foods
 Avoid cold foods like ice­creams.
 Carbonated drinks are a no­no.
 Alcohol and smoking should be completely avoided.

Conser vative measur es

 Some limited evidence supports sponging or bathing feverish children with tepid water The use
of a fan or air conditioning may somewhat reduce the temperature and increase comfort.
 If the temperature reaches the extremely high level of hyperpyrexia, aggressive cooling is
required (generally produced mechanically via conduction by applying numerous ice packs
across most of the body or direct submersion in ice water)

CONDITIONS LEADING TO FEVER

Malar ia

Malaria is a vector­ borne disease specifically caused by the female anopheles mosquito that caries the
plasmodium. Malaria is the most significant parasitic disease of human beings and remains a major
cause of morbidity and mortality worldwide

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It can cause growth failure, particularly young children and is a contributory factor to malnutrition

Complications/ metabolic changes

 Fever­Both acute and chronic fever is high leading to increased BMR


 Anorexia­ leading to vomiting
 Glycogen breakdown­ leading to weakness, fatigue
 Red cell destruction­leading to anemia
 Tissue protein catabolism­leading to wasting , muse wasting
Headache

Nutr itional Management

 High ener gy diet­Energy may be increased up to 50% based on the extent of fever, its duration
and associated weight loss
 High pr otein diet­Protein requirement increases by 25­505 above normal based on weight
loss. The protein should of high biological value. High protein beverages are preferred to the
regular solid meals
 Fat­Fat is needed to meet the increased energy needs. However, fat intake should be cautiously
planned considering palatability of diet and the patient’s tolerance. Fats in the form of fried
food should food should be avoided during malaria fever
 Vitamins and miner als­ increased B­complex vitamins in relation to increased energy needs.
Increased iron due to malaria induced anemia and increased vitamin A and C for immunity
 Fluid­Adequate amount to compensate for the loss of fluid through sweating
 Fr equency­ small frequent meals at an interval of about 2 hours (initially)

Medical ther apy to kill the micr oor ganism

Rheumatic Fever

 Rheumatic fever is caused by a reaction to the bacteria that causes strep throat, group
A streptococcus (a bacteria that causes strep throat). Although not all cases of strep throat
result in rheumatic fever, this serious complication may be prevented with diagnosis and
treatment of strep throat.
 Rheumatic fever causes your body to attack its own tissues after it’s been infected with the
bacteria that causes strep throat. It is an inflammatory disorder as this reaction causes
widespread inflammation throughout your body, which is the basis for all of the symptoms of
 rheumatic
The fever.
condition usually appears in children between the ages of 5 and 15, even though older

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children and adults have been known to contract the fever as well. It’s still common in places
like sub­Saharan Africa, south central Asia, and certain populations in Australia and New
Zealand.

Symptoms

Symptoms usually appear two to four weeks after your child has been diagnosed with strep throat. If
your child has any of the following symptoms, they should get a strep test: Common symptoms of
strep throat include:

 a sore throat
 a sore throat with tender and swollen lymph nodes
 a red rash
 difficulty swallowing
 thick, bloody discharge from nose
 a temperature of 101°F or above
 tonsils that are red and swollen
 tonsils with white patches or pus
 small, red spots on the roof of their mouth
 a headache/fever
 nausea
 vomiting
 sweating
 nosebleeds outbursts of crying or inappropriate laughter
 chest pain
 rapid fluttering or pounding chest palpitations

If your child has a fever, they might require immediate care. You should seek immediate medical care
for your child in the following situations:

 a temperature over 100°F in newborns to 6­week­old infants


 a temperature of 102°F or higher in babies 6 weeks to 2 years old
 a temperature of 103°F or higher in children age 2 years or older
 a fever that lasts more than three days in a child of any age

Risk Factor s for Rheumatic Fever

Factors that increase your child’s chances of developing rheumatic fever include:

 a family history because certain genes make you more likely to develop rheumatic fever
 the type of strep bacteria present because certain strains are more likely to lead to rheumatic
fever than others
 environmental factors present in developing countries, such as poor sanitation, overcrowding,
and a lack of clean water

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How to Pr event Rheumatic Fever

The most effective way to make sure that your child doesn’t develop rheumatic fever is to treat their
strep throat infection quickly and thoroughly. This means making sure your child completes all
prescribed doses of medication.

Practicing proper hygiene methods can help prevent strep throat. These include:

 covering your mouth when coughing or sneezing


 washing your hands
 avoiding contact with people who are sick
 avoiding sharing personal items with people who are sick

Effective Tr eatments for Rheumatic Fever

Treatment will involve getting rid of all of the residual group A strep bacteria and treating and
controlling the symptoms. This can include any of the following:

 Antibiotics
 Anti­Inflammatory
Bed Rest Treatment

Complications Associated with Rheumatic Fever

Rheumatic fever is relatively a serious illness that can cause long term complications such as stroke,
permanent damage to the heart and death if it is left untreated. One of the most prevalent
complications is rheumatic heart disease. Other heart conditions include:

 valve stenosis, which is a narrowing of a valve


 valve regurgitation, which is a leak in the valve that causes blood to flow in the wrong
direction
 heart muscle damage, which is an inflammation that can weaken the heart muscle and decrease
the heart’s ability to pump blood effectively
 atrial fibrillation, which is an irregular heart beat in the upper chambers of the heart
 heart failure, which happens when the heart can no longer pump blood to all parts of the body

Tuberculosis
 Etiology (cause)­It is an infection of the lungs caused by mycobacterium tuberculosis (bacillus
mycobacterium). It is an air bone disease characterized by the growth of nodules (tubercles) and
spread mostly in overcrowded area. It is one of the world’s more wide spread and deadly diseases
 It mostly occurs in the lungs, however it may occur in other organs like bones, kidney, spine, brain
etc. When it primarily affects the lungs, it is referred to as pulmonary tuberculosis. Pulmonary
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tuberculosis is the most common form of tuberculosis in Kenya


 Tuberculosis is an infectious disease and it is more contagious than pneumonia and is spread from
one person to another through tiny droplets released into air via coughs, spits, laughs, sings and
sneeze( It is an airborne disease)
 It occurs mostly among the disadvantaged populations such as the malnourished and those living in
overcrowded area and substandard housing
 It is on the increase in developing countries partly because of the HIV, the virus that causes
AIDS.HIV weakens a person’s immune system so it cannot fight the TB germs. As a result, people
with HIV are many times more likely to get TB and to progress from latent to active disease than
are people who are not HIV positive.
 Another reason why TB remains a major killer is the increase in drug resistant strains of the
bacterium. Some germs have developed the ability to survive and that ability is passed to their
descendants.
 Drug resistant strains of tuberculosis emerge when antibiotic e.g rifampin, isoniazid and injectable
medications including amikacin, kanamycin, and capreomyacin fails to kill all of the bacteria it
targets

Stages of TB.
There are two stages of TB
1. Latent TB/Inactive TB: In this condition, you have a TB, but the bacteria remain in your body in an
inactive state and cause no symptoms. It is not contagious in this stage. It can turn into active TB if
untreated. An estimated 2 billion people have latent TB
2. Active TB: This condition makes you sick and can spread to others. It can occur in the first few
weeks after infection with TB bacteria or it might occur years later. The acute phase resembles
pneumonia with high fever and increased circulation and respiration
Symptoms
Symptoms differs depending on the stage of TB infection
o Anorexia
o Fever and night sweat which increases calorie requirement(10% extra calorie per every 10 rise in
body temperature)­ i.e. if febrile, patients will be hypermetabolic
o Malaise( a feeling of weakness , illness, pain , uneasiness or simply not feeling well)
o Night sweats
o Weight loss( patients appear chronically ill and malnourished)
o Chronic cough lasting 2 weeks or more (Chronic cough is the most universal pulmonary
symptom). It may be dry at first but becomes productive of sputum as the disease progresses. More
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often than not , the sputum is blood steaked


o Chest pain
o Fatigue
o Enlarged lymph nodes which increases protein and micronutrients requirements for tissue repair
o Blood in the urine as a result of TB of the kidney or blood in the sputum resulting into loss of blood
that may predispose clients to anemia

Risk factors
 A healthy immune system often successfully fights TB bacteria. A number of diseases and
medications can weaken your immune system , including
 HIV/AIDS
 Diabetes
 Certain cancers
 Cancer treatment such as chemotherapy
 Malnutrition
 Very young or advanced age
 Tobacco use

Complications: Without treatment, tuberculosis can be fatal. Untreated active disease typically
affects your lungs, but it can spread to other parts of the body through the blood stream. Examples of
complications are
 Spinal injury
 Joint damage (Tuberculosis arthritis that usually affects the hips and the knees)
 Meningitis (Swelling of the membranes that cover your brain)­this my result into mental
impairment
 Kidney/ liver problems
 Heart disorders

Tests and diagnosis


 Physical exam test using stethoscope to check for the swelling of lymph nodes
 Skin test­It is not very accurate
 Blood test­.Requires sophisticated technology
 Imaging test­chest x­ray or a CT scan that may show white sports in your lungs where immune
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system has walled off TB bacteria. CT scan is more accurate


 Sputum test( mucus that comes with the cough).Sputum test is also used to test for drug resistant
strains of bacteria
Nutrition implications of TB

 Reduced protein synthesis and metabolism


 Reduced immunity
 Reduced food and nutrient intake
 Increased nutrient requirements
Objectives of Nutrition care and management of TB

 Achieve and maintain good nutrition status i.e. Maintain weight and prevent weight loss
 Prevent and control body wasting and weakness
 Correct nutritional deficiencies
 Accelerate healing process
 Control symptoms and prevent associated complications
Management
Dietary management
 Energy. Most patients with chronic tuberculosis are undernourished and underweight. Energy
needs are increased to minimize weight loss and achieve a desirable weight, to facilitate tissue
regeneration and to spare the protein. An additional 300­500kcals (35­40kcals/kg of ideal body
weight above normal intake) is recommended. High energy diet is also needed when the patient is
hypermetabollic to meet high metabolic demands and to minimize weight loos
 Adequate protein (2­3.5 kg per body weight) of high biological value to regenerate serum albumin
levels. serum albumin level is often very low due to tissue wasting and repair of worn out tissues

 Adequate amounts of calcium e.g. from milk and milk products (to promote healing of tuberculin
lesions), iron, and B­complex. Patients on isoniazid should be supplemented with B6 since the drug
inhibit its absorption complex are obtained mostly from whole grain cereals, pulses, nuts, seeds,
eggs, fish and chicken
 Vitamin A. Patient should be supplemented with vitamin A as conversion of beta carotene to
retinal is affected in the intestinal mucosa of TB patients
 Vitamin C for wound healing

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 Antioxidants( vitamin A, C, E, folic acid, zinc and selenium) to neutralize free radicals (ROS) and
prevent the production of peroxides from lipids
 A liberal amount of Ca should be included in the diet to promote the healing of TB lesions. Some
amount of milk should be included in the diet daily.
 Iron supplement may be necessary if the patient suffers from hemorrhages
 Carbohydrates­60 to 65% energy requirements should be from the carbohydrates
 Fats­25 to 30% energy requirements should be from fats
 Water. At least 8 glasses of water( 250 ml) or more of safe drinking water per day to reduce
dehydration rate
N/B Patients who have TB have low circulating concentrations of micronutrients such as vitamin
A, E, and D and the minerals iron, zinc and selenium
N/B 2. Undernutrition in TB patients lowers the immunity
Medical therapy
 Use of drugs
 Medication side effects. Nausea, vomiting, loss of appetite, a yellow colour to your skin(jaundice),
abdominal discomfort, interferes with B6 utilization, dark urine and fever, taste changes
 Most of the drugs used interact with some nutrients
Vaccination
Vaccinating children with BCG (Bacille Calmette –Guerin) vaccine. It is not effective in adults
Other remedies
 Adequate ventilation,
 Cover your mouth when sneezing o coughing when infected with the disease
 Wear a mask when attending to TB patients

Typhoid

 Typhoid fever is caused by Salmonella typhi


 Most cases of typhoid fever are seen in those aged 3–19 years and humans are the only
natural host and reservoir.
 The infection is transmitted by ingestion of faecally contaminated food or water. The
highest incidence occurs where water supplies serving a large population are faecally
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contaminated.
 The incubation period is usually 8–14 days, but may range from 3 days up to 2 months.
 Some 2–5% of infected people become chronic carriers who harbour S.typhi in the gall
bladder.
 Patients infected with HIV are at a significantly increased risk of severe disease due to S.
typhi and S. paratyphi.

Susceptibility is gener al.


 Susceptibility is increased in individuals with gastric achlorhydia (deficiency of HCL in
the stomach e.g. patient with anemia and cancer of the stomach) and HIV positive people.

Mode(s) of Tr ansmission
 Mode of transmission is person­to­person, usually via the faecal­oral route. Faecally
contaminated drinking water is a commonly identified vehicle.
 S. typhi may also be found in urine and vomitus and, in some situations, these could
contaminate food or water.
 Flies can mechanically transfer the organism to food, where the bacteria then multiply to
achieve an infective dose.
Body changes in typhoid
 Loss of tissue protein which may amount to as much as 250­500g of muscle tissue a day
 Body stores of glycogen are quickly depleted and the water and electrolyte balance is
disturbed
 Inflammation of the intestinal tract and diarrhea is a frequent complication
 Ulceration in the intestine may be so severe that hemorrhage and eve perforation of the
intestine may occur

Management
 Medical­Antibiotics
 Keeping the patient warm
 Rest in bed
 A modified diet
A modified diet: Objective
 To maintain adequate nutrition
 To restore positive nitrogen balance
 To provide positive relief from symptoms
 To correct and maintain water and electrolyte balance
 To avoid irritation of intestinal tract

Nutr ition ther apy


 High energy diet­initially during acute phase stage, a patient may be able to consume
only 600­1200 kcal/day but the energy intake should be gradually increased with
recovery and improved tolerance

 High protein diet­The protein should be increased to 1.5­2 g protein/kg body weight/day
 .It should be of high protein value to minimize tissue loss.
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 Carbohydrate­A liberal intake is required. Well cooked, easily digestible carbohydrate


like simple starches, glucose, honey, cane sugar etc. should be included because they
require les digestion and well assimilated

 Dietary fiber­All hash irritating fiber should be eliminated


 Fats­Fats are needed mainly to increase the energy intake. However due to diarrhea, fats
only in the emulsified form like cream, butter, whole milk, egg, yolk should be included
in the diet because they are easily digested and well tolerated by patients
 In the early stages intake of fat may aggregate nausea and so its intake should be
restricted
 Fried foods which are difficult to digest should be avoided

 Minerals­There is excessive loos of electrolytes like sodium ion, potassium and chloride
due to increased perspiration. Salty soups, broths, fruit juices, milk etc. should be
compensate for the loss of electrolytes
 Increased vitamin A and C for immunity and formation of collagen

 Increase vitamin B complex because of increased need for energy

 Fluid­increased fluid for rehydration of the body. A daily intake of 2.5 ­5 liters is
desirable. They may be included in the form of beverages, soups, juices, plain etc.

Smallpox

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 Smallpox was an infectious/contagious deadly disease caused by either of two virus ,


Variola major and Variola minor . There is no cure for small pox and the last naturally
occurring case of smallpox (Variola minor ) was diagnosed on 26 October 1977 in
Somalia and in 1949 in United States. Due to worldwide vaccination programs, this
disease has been completely eradicated.
 By 1980, the WHO declared that smallpox had been completely eradicated, although
government and health agencies still have stashes of smallpox virus for research
purposes.
 People no longer receive routine smallpox vaccinations. The smallpox vaccine can have
potentially fatal side effects, so only the people who are at high risk of exposure get the
vaccine.

Signs and symptoms

Historical accounts show that when someone was infected with the smallpox virus (inhale the
virus), they had no symptoms for between seven and 17 days. However, once the incubation
period (or virus development phase) was over, the following flu­like symptoms occurred:

 high fever
 chills
 headache
 severe back pain
 abdominal pain
 vomiting

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These symptoms would go away within two to three days. Then the patient would feel better.
However, just as the patient started to feel better, a rash/characteristic pimples would appear. The
rash started on the face and then spread to the hands, forearms, and the main part of the body.
The person would be highly contagious until the rash disappeared.

Within two days of appearance, the rash would develop into abscesses that filled with fluid and
pus (blisters will develop). The abscesses would break open and scab over. The scabs would
eventually fall off, leaving pit mark scars. Until the scabs fell off, the person remained
contagious.

Tr ansmission

 Coughing, sneezing, or direct contact with any bodily fluids could spread the smallpox
virus,
 Sharing of contaminated clothing or bedding
 It is also transmitted from one person to another primarily through prolonged face­to­face
contact with an infected person, usually within a distance of 6 feet (1.8 m),
 The virus can cross the placenta, but the incidence of congenital smallpox is relatively
low.

Tr eatment and pr evention for Smallpox


 There is no cure for the smallpox virus. As a result of worldwide, repeated vaccination
programs, the variola virus (smallpox) has been completely eradicated. The only people
considered to be at risk for smallpox are researchers who work with it in a laboratory
setting.

Chickenpox
 Chickenpox, also called varicella, is a viral disease characterized by itchy red blisters that
appear all over the body. It often affects children, and was so common it was considered
a childhood rite of passage.
 It’s very rare to have the chickenpox infection more than once. And since the chickenpox
vaccine was introduced in the mid­1990s, cases have declined.

Causes
 It is caused by varicella­zoster virus (VZV).

Symptoms

It begins with the non­rash symptoms that may last a few days and include:

 fever
 headache
 loss of appetite

One or two days after you experience these symptoms, an itchy r ush will begin to develop. The
rash goes through three phases before you recover. These include:
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 You develop red or pink bumps all over your body.


 The bumps become blisters filled with fluid that leaks.
 The bumps become crusty, scab over, and begin to heal.

­The bumps on your body will not all be in the same phase at the same time. New bumps will
continuously appear throughout your infection. The rash may be very itchy, especially before it
scabs over with a crust.

N/B. You are still contagious until all the blisters on your body have scabbed over. The crusty
scabbed areas eventually fall off. It takes seven to 14 days to disappear completely.

An itchy rash is the most common symptom of chickenpox.

Tr ansmission

Most cases occur through contact with an infected person. The virus is very contagious and can
spread through:

 Direct contact with saliva


 Through air by coughing and sneezing.
 Direct contact with fluid from the blisters

Pr evention

 Vaccination
 A child with chickenpox should stay home and rest until the rash is gone and all blisters
have dried, usually about 1 week.
 Pregnant women, newborns, or anyone with a weakened immune system (for instance,
from cancer treatments like chemotherapy or steroids) who gets chickenpox should see a
doctor right away.

Differ ence between small pox and chicken pox

Chickenpox was commonly confused with smallpox in the immediate post­eradication era.

 Unlike smallpox, chickenpox does not usually affect the palms and soles.
 Additionally, chickenpox pustules are of varying size due to variations in the timing of
pustule eruption: smallpox pustules are all very nearly the same size since the viral effect
progresses more uniformly.
 In contrast to the rash in smallpox, the rash in chickenpox occurs mostly on the torso,
spreading less to the limbs.
 A variety of laboratory methods are available for detecting chickenpox in evaluation of
suspected smallpox cases

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Meningitis

 Meningitis is an acute inflammation (swelling) of the protective membranes (meninges)


covering the brain and spinal cord. A bacterial or viral infection of the fluid surrounding
the brain and spinal cord usually causes the swelling.

Cause
 The infection by viruses, bacteria, or other microorganisms, and less commonly by
certain drugs. However, injuries and cancer can also cause meningitis.

Symptoms

The most common symptoms are


 Sudden high fever
 headache
 Inability to tolerate light or loud noises.
 Stiff neck
 Severe headache that seems different than normal
 Headache with nausea or vomiting
 Confusion or difficulty concentrating
 Seizure
 Sleepiness or difficulty waking
 No appetite or thirst

Signs in newbor ns

Newborns and infants may show these signs:

 High fever
 Constant crying
 Excessive sleepiness or irritability
 Inactivity or sluggishness
 Poor feeding
 A bulge in the soft spot on top of a baby's head (fontanel)
 Stiffness in a baby's body and neck

Infants with meningitis may be difficult to comfort, and may even cry harder when held

Meningitis can be life­threatening because of the inflammation's proximity to the brain and
spinal cord; therefore, the condition is classified as a medical emergency.

Pr evention and tr eatment

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 Immunization­Some forms of meningitis are preventable by immunization


 Giving antibiotics to people with significant exposure to certain types of meningitis may
also be useful
 The first treatment in acute meningitis consists of promptly giving antibiotics and
sometimes antiviral drugs

Complications
 Meningitis can lead to serious long­term consequences such as deafness, inflammation or
swelling of brain which may result into seizures/epilepsy, internal bleeding of the blood
vessels, hydrocephalus, or cognitive deficits, especially if not treated quickly.

Measles

 Measles, also called r ubeola, is a highly contagious respiratory infection that is caused
by a measles virus.
 It causes a total­body skin rash and flu­like symptoms, including a fever, cough, and
runny nose.
 Since measles is caused by a virus, there is no specific medical treatment for it and the
virus has to run its course. But a child who is sick should drink plenty of fluids, get lots
of rest, and be kept from spreading the infection to others.

Signs and Symptoms

 Fever
 Cough
 Runny nose
 Conjunctivitis (pink eye)
 Children who get the disease may develop tiny white spots inside the mouth or small red
sports with blue­white centers in the mouth
 Eventually full body rash

The measles rash breaks out 3­5 days after symptoms start, and can coincide with high fevers up
to 104°F (40°C). The red or reddish­brown rash usually first shows up as flat red spots on the
forehead. It spreads to the rest of the face, then down the neck and torso to the arms, legs, and
feet. The fever and rash gradually go away after a few days.

Contagiousness

 Measles is highly contagious — 90% of people who haven't been vaccinated for measles
will get it if they are near an infected person.
 Measles spreads when people breathe in or have direct contact with virus­infected fluid,
such as the droplets sprayed into the air when someone with measles sneezes or coughs.
A person who is exposed to the virus might not show symptoms until 8­10 days later.
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 Those with weakened immune systems due to other conditions (like HIV and AIDS) may
be contagious until they recover from measles.

Pr evention

There is no treatment for measles, but the measles­mumps­rubella (MMR) vaccine can prevent
it.

TOPIC: CONDITIONS LEADING TO SEVERE STRESS­STARVATION, BURNS,


SURGERY, LOW BIRTH WEIGHT AND ICU

CONDITIONS LEADING TO METABOLIC STRESS: SEPSIS, STARVATION,


TRAUMA, BURNS AND SURGERY

INTRODUCTION

Definition of ter ms

Glutamine – A major fuel source for rapidly dividing cells such as lymphocytes. It is the
preferential fuel in the gut mucosa (for gut metabaolism), especially during stress;

Gr owth hor mone –Realized from the anterior pituitary gland. It is thought to accelerate growth
in children and improve protein synthesis in injured patients. Oppose the actions of insulin

Cytokines – pro­inflammatory proteins released by cells of the immune system that serves to
regulate the immune system e.g. macrophages that act as mediators of shock and in sepsis;
examples include tumor necrosis factor, interleukin­ 1, and interleukin­6

Multiple or gan dysfunction syndr ome (MODS) ­ organ dysfunction that results from direct
injury trauma, or disease or as a response to inflammation;

Sepsis(infection) – the systemic response to an infectious agent. Sepsis occurs when chemicals
released into the blood stream to fight the infection trigger inflammatory responses throughout
the body. This changes can damage multiple organ systems, causing them to fail. If sepsis
progress to septic shock, blood pressure drops dramatically which may lead to death. It is more
common in older people and or those with week immunity

Shock – sudden disturbance of mental equilibrium; characterized by failure of the circulatory


system to maintain adequate perfusion of vital organs. It is critical (life threatening) condition as
the circulatory system fails to maintain the adequate blood flow to vital organs, sharply curtailing
the delivery of oxygen and nutrients to vital organs

Str ess

 Stress refers to a reaction or a response by an organism to stimulus events that disturb its

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equilibrium (homeostasis). Normally, the human body operates in a state of homeostasis


(metabolic equilibrium) and the balance is upset when the body is under stress.
 Some of the stimulus events (stress factors) that upset homeostasis are critical illness,
traumatic injury, sepsis, burns, starvation, accidents, gunshots or major surgery. The
metabolic response to stress is complex and involves most metabolic pathways. This state
is characterized by an accelerated catabolism of lean body or skeletal mass that clinically
results in negative nitrogen balance and muscle wasting. Starvation also results into
increased catabolism of lean body tissues
 The body constantly responds to these changes to maintain homeostasis

Tr auma­ trauma refers to a massive crush, injury or damage to the body e.g. accident, burns,
sepsis, surgery, starvation, critical illness etc. These conditions (traumas) can lead to mild or
severe metabolic stress

Types of str ess


Physical or physiological

They normally originate from disease or physical injury

Physiological stress Occurs in many hospitalized patients as a consequence of infection, fever,


surgery, burns or other trauma. Many patients are unable to meet the increased needs imposed by
stress. Compromised nutritional status has been shown increase susceptibility to infections,
prolonged hospital stay and increased mortality rate.

Psychological or sociological str ess

 Normally represented by emotional threshold or economic burden


 The metabolism effects during stress differs with that during starvation or fasting.

N/B. Some stress result into hypometabolisn e.g starvation while others result into
hypermetabolism e.g. surgery, burns, accidents, gunshots, critical illness, sepsis e.tc

METABOLIC RESPONSE TO STARVATION


Starvation­ Starvation is the period one involuntarily goes without food or the period when the
nutrients in the body are below the metabolic needs while fasting or dieting is where people
withhold food from themselves, such as when they try to lose weight.

Whatever the cause of inadequate food intake and nourishment (starvation or fasting), results are
the same.

The body extracts stored carbohydrate, fat, and protein (from muscles and organs) to meet
energy demands.
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 Liver glycogen is used to maintain normal blood glucose levels to provide energy for
cells. Although readily available, this source of energy is limited, and glycogen stores are
usually depleted after 8 to 12 hours of fasting.
 As the glucose stores (glycogen) decreases, lipid (triglyceride) stores may be substantial,
and the body begins to mobilize free fatty acids from adipose tissue to provide needed
energy to the body. After approximately 24 hours without energy intake (especially
carbohydrates), the prime source of glucose is from gluconeogenesis substrates.

Gluconeogenesis ­ is a metabolic pathway that results in the generation of glucose


from certain non­carbohydrate carbon).Energy from fat > 90%, energy from protein
< 10 %

 Some body cells, brain cells in particular, use mainly glucose for energy. During early
starvation (about 2 to 3 days of starvation), the brain uses glucose produced from muscle
protein. As muscle protein is broken down for energy, the level of br anched­chain
amino acids (BCAA ­. leucine, isoleucine, and valine) in circulation increases although
they are primarily metabolized directly inside muscle.
The body does not store any amino acids as it does glucose and triglycerides; therefore,
the only sources of amino acids are lean body mass (muscle tissue), vital organs
including heart muscle, or other protein­based body constituents such as enzymes,
hormones, immune system components, or blood proteins. By the second or third day of
starvation, approximately 75 g of muscle protein can be catabolized daily, a level
inadequate to supply full energy needs of the brain.
At this point, other sources of energy become more available. Fatty acids are hydrolyzed
from the glycerol backbone and both free fatty acids and glycerol are released into the
bloodstream. Free fatty acids are used, while glycerol can be used by the liver to generate
glucose via the process of gluconeogenesis.
 As starvation is prolonged, the body preserves proteins by mobilizing more and more fat
for energy. Ketone body production from fatty acids is accelerated, and the body’s
requirement for glucose decreases. Although some glucose is still vital for brain cells and
red blood corpuscles, these and other body tissues obtain the major proportion of their
energy from ketone bodies. Muscle protein is still being catabolized but at a much lower
rate, which prolongs survival. During this period of starvation, approximately 60% of the
body’s energy is provided by metabolism of fat to carbon dioxide, 10% from metabolism
of free fatty acids to ketone bodies, and 25% from metabolism of ketone bodies
 An additional defense mechanism of the body to conserve energy is to slow its metabolic
r ate (metabolic rate decreases by 20­25kcals/kg/day) thereby decreasing energy needs.
As a result of declining metabolic rate, body temper atur e dr ops, activity level
decr eases, and sleep per iods incr ease—all to allow the body to preserve energy
sources.
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If starvation continues, intercostal muscles necessary for respiration are lost, which may
lead to pneumonia and respiratory failure. Starvation will continue until adipose stores
are exhausted

N/B 1: The response therefore in chronic starvation is conservatory aimed at adopting to preserve
the lean body mass.
N/B 2. During starvation there is decrease in metabolic rate while in severe stress e.g. in burns,
gunshot, surgery, critical illness and sepsis there is increase in metabolic rate

METABOLIC RESPONSE TO SERVERE STRESS (BURNS,


SURGERY, CRITICAL ILLNESS, ACCIDENTS, SEPSIS)
 Whether stress is accidental (e.g., from broken bones or burns) or necessary (e.g., from
surgery), or as a result of an infection(sepsis) or due to critical illness, the body reacts to
these stresses much as it does to the stress of starvation— with a major difference.
 During starvation, the body’s metabolic rate slows, becoming hypometabolic. During
severe stress, the body’s metabolic rate rises profoundly, thus becoming hyper metabolic.

The response to critical illness, injury (burns), major surgery and sepsis characteristically
involves:
i. Ebb
ii. Flow phases

Ebb phase

The ebb phase, or early phase begins immediately after the injury. The aim of the ebb phase is to
conserve energy. Char acter istics of the ebb phase/ear ly phase.
 Decreased Oxygen Consumption
 Hypothermia (Lowered Body Temperature)
 Hypovolemia (A Decreased Volume Of Circulating Blood In The Body)
 Shock (Low Blood Perfusion To Tissues)
 Decreased Cardiac Output
 Vascular constriction
 Decrease in production of digestive enzyme
 Decrease urine production
 Insulin levels drop because glucagon is elevated (increased), most likely as a signal to
increase hepatic glucose production.
 Decrease in metabolic needs

The major medical concern during this time is to maintain cardiovascular effectiveness and
tissue perfusion

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Flow phase: “It brings hyper­metabolism”

Char acter istics of the flow phase

 Increased cardiac output­ Increased cardiac work immediately after a burn, because of
low amount of blood in the body
 Increase myocardial oxygen consumption,
 Increase body temperature (hyperthermia ),
 Increase energy expenditure(increased metabolic rate)
 Increase protein breakdown­ Muscle protein degradation (breakdown) becomes a
necessary and large source of energy­(protein is degraded much faster than it is
synthesized).This leads to loss of lean body mass and increased immune dysfunction
(Increased risk for infection)
 Increase nitrogen excretion/loss
 Liver dysfunction (the liver increases in size to help in removing the increased nitrogen
rates)
 Increased catabolism­ causing the rapid breakdown of energy reserves to provide glucose.
This is because of increased energy need due to hypermetabolism and increased catabolic
hormones(glucagon and cortisol)
 Changes in glucose metabolism­Elevated circulating levels of catecholamine, glucagon,
cortisol and gluconeogenic hormones in response to severe thermal injury propagate
(results into) inefficient glucose production in the liver.
 Sex hormones and growth levels decrease around 3 weeks post burn. This results in
growth retardation
 Decrease in protein synthesis
 Increase in gluconeogesis­increase in glucose production
 Increase in cytokines
 Increase in basal metabolic rate(increase in energy expenditure)

The flow stage lasts for days, weeks, or months until the injury is healed

Hor monal changes and Cell Mediated Response towar ds str ess
 Metabolic stress is associated with an altered hormonal state that results in an increased
flow of substrate but poor use of carbohydrate, protein, fat, and oxygen
 Counter­regulatory hormones, which are elevated after injury and sepsis, play a role in
the accelerated proteolysis that characteristically is seen.

Glucagon promotes gluconeogenesis, amino acid uptake, ureagenesis and protein catabolism.
Cor tisol, which is released from the adrenal cortex in response to stimulation by
adrenocorticotropic hormone secreted by the anterior pituitary gland, enhances skeletal muscle
catabolism and promotes hepatic use of amino acids for gluconeogenesis, glycogenolysis, and

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acute­phase protein synthesis.

 After injury or sepsis, energy production becomes increasingly protein­dependent.


Branched­chain amino acids (leucine, isoleucine, and valine) are oxidized from skeletal
muscle as a source of nitrogen, energy for the muscle, and carbon skeletons for the
glucose­alanine cycle and muscle glutamine synthesis.
 Lipid metabolism is also altered in stress and sepsis. Increased circulation of free fatty
acids is thought to result from increased lipolysis caused by elevated catecholamines and
cortisol, as well as a marked elevation in the ratio of glucagon to insulin. The free fatty
acids can be oxidized and used to form ketones, which provide energy to non­glucose
dependent tissues, or to resynthesize triglycerides.
 There is notable hyperglycemia observed during stress. This initially results from a
marked increase in glucose production and uptake secondary to gluconeogenesis and
elevated levels of hormones, including epinephrine, that diminish insulin release. Stress
also initiates the release of aldosterone, a corticosteroid that causes renal sodium
retention, and vasopressin (antidiuretic hormone), which stimulates renal tubular water
resorption. The action of these hormones results in conservation of water and salt and
support of the circulating blood volume (See table below)

N/B. During starvation we burn more fat and during severe stress, we burn more protein

Summar y of the affected or gan and the metabolic Response


Or gan Response

Liver ↑Glucose production

↑Amino acid uptake

↑Acute­phase protein synthesis

↑Trace metal sequestration

Central Nervous System Anorexia

Fever

↑Glucose

↑Triglycerides

↑Amino acids

↑Urea

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↓Iron

↓Zinc

Skeletal muscle ↑amino acid uptake from both luminal and circulating sources,
leading to gut mucosal atrophy (wasted away­degeneration of
cells)

Endocrine ↑Adrenocorticotropic hormone

↑Corticosol

↑Growth hormone

↑Epinephrine

↑Norepinephrine

↑Glucagon

↑Insulin

Effects of the hor mones dur ing Str ess*

Target Organ Hormonal Physiologic Response Signs/Symptoms


Response
Sympathetic Norepinephri Vasoconstriction Pallor, decreased glomerular
nervous system ne filtration rate, nausea,
and adrenal elevated blood pressure
medulla
Adrenal medulla Epinephrine Vasoconstriction Pallor, decreased glomerular
filtration rate, nausea,
elevated blood pressure
Increased heart rate Elevated blood pressure

Vasodilation Increased skeletal muscle


function
Central nervous system More alert, increased muscle
(CNS) stimulation tone
Bronchodilation Increased O2
Glycogenolysis, Increased blood glucose
lipolysis,
gluconeogenesis
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Adrenal pituitary Cortisol CNS stimulation Increased blood glucose,


and cortex (glucocorticoi increased serum
ds)
Protein catabolism, amino acids, delayed wound
gluconeogenesis healing
Stabilize cardiovascular Enhance catecholamine action
system
Gastric secretion Ulcers

Inflammatory response Decreased white blood cells


decreased (WBCs)
Allergic response
decreased
Immune response
decreased
Aldosterone Retain sodium and water,
(mineralocor increased blood volume,
ticoid) increased blood pressure
Posterior Antidiuretic Water reabsorbed,
pituitary hormone increased blood volume,
increased blood pressure
*Possible complications include hypertension, tension headaches, insomnia, diabetes mellitus,
infection, heart failure, peptic ulcer, and fatigue

Effects of Str ess on Nutr ient Metabolism


i. Pr otein Metabolism

Even if adequate carbohydrate and fat are available, protein (skeletal muscle) is mobilized for
energy (amino acids are converted to glucose in the liver). There is decreased uptake of amino
acids by muscle tissue, and increased urinary excretion of nitrogen.

Some non­ essential amino acids may become conditionally essential during episodes of
metabolic stress. During stress, glutamine is mobilized in large quantities from skeletal muscle
and lung to be used directly as a fuel source by intestinal cells. Glutamine also plays a significant
role in maintaining intestinal immune function and enhancing wound repair by supporting
lymphocyte and macrophage proliferation, hepatic gluconeogenesis, and fibroblast function
ii. Car bohydr ate Metabolism

Hepatic glucose production is increased and disseminated to peripheral tissues although proteins
and fats are being used for energy. Insulin levels and glucose use are in fact increased, but

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hyperglycemia that is not necessarily resolved by the use of exogenous insulin is present. This
appears, to some extent, to be driven by an elevated glucagon­to­ insulin ratio.

iii. Fat metabolism

To support hypermetabolism and increased gluconeogenesis, fat is mobilized from adipose stores
to provide energy (lipolysis) as the result of elevated levels of catecholamines along with
concurrent decrease in insulin production.

If hypermetabolic patients are not fed during this period, fat stores and proteins are rapidly
depleted. This malnutrition increases susceptibility to infection and may contribute to multiple
organ dysfunction syndrome (MODS), sepsis, and death.
iv. Hydr ation/Fluid Status

Increased fluid losses can result from fever (increased perspiration), increased urine output,
diarrhea, draining wounds, or diuretic therapy.
v. Vitamins and Miner als

Just as kcal needs increase during hypermetabolic conditions, so, too, do needs for most vitamins
and minerals. And if kcal needs are met, the patient will most likely receive adequate amounts of
most vitamins and minerals.

Special attention, however, should be given to vitamin C (ascorbic acid), vitamin A or beta­
carotene, and zinc.
 Vitamin C is crucial for the collagen formation necessary for optimal wound healing.
Supplements of 500 to 1000 mg/day are recommended.
 Vitamin A and beta­ carotene (vitamin A’s precursor) play an important role in the
healing process in addition to their role as anti­ oxidants.
 Zinc increases the tensile strength (force required to separate the edges) of a healing
wound. Supplements of 220 mg/day zinc sulfate (orally) when stable are commonly used.
Additional zinc may be necessary if there are unusually large intestinal losses (small
bowel drainage or ileostomy drainage).
These metabolic changes can result into malnutrition that eventually affects the immune system
and thus prolong the healing process

Immune System

 One of the first body functions affected by impaired nutritional status is the immune
system. When metabolic stress develops, hormonal and metabolic changes subdue the
immune system’s ability to protect the body. This activity is further depressed if impaired
nutritional status accompanies the metabolic stress. A deadly cycle often develops:

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 Impaired immunity leads to increased risk of disease,


 Disease impairs nutritional status, and
 Compromised nutritional status further impairs immunity.

Recovery requires that this cycle be broken by good nutrition

Role of Nutr ition


 For the immune system to function optimally, adequate nutrients must be available. A
well­nourished body will not be ravaged by infections the way a poorly nourished body.

Immune system components affected by malnutr ition include:


 Mucous membrane­ microvilli flattened which reduces nutrient absorption and decreases
antibody secretions
 Skin – thinned with less connective tissue. Integrity of the skin may be compromised as it
loses density and wound healing is slowed
 Gastrointestinal tract ­ Injury to the gastrointestinal tract because of malnutrition may
increase risk of infection­causing bacteria spreading from inside the tract to outside the
intestinal system.
 T­lymphocytes ­ are affected as the distribution of T cells is depressed
 Macrophages, granulocytes ­ the effect on macrophages and granulocytes requires that
more time be needed for phagocytosis kill time and lymphocyte activation to occur
 and antibodies – may be less available because of damage to the antibody response

Role of Nutr ients and Nutr itional Status on Immune System Components

Immune System Effects of Malnutr ition Vital Nutr ients


Component

Mucus Decreased antibody Vitamin B12, biotin, vitamins


secretions B6 and C

Gastrointestinal tract Flat microvilli, increased risk Arginine, omega­3 fatty acids
of bacterial spread to outside
GI tract

Skin Integrity compromised, Protein, vitamins A and C,


density reduced, wound niacin, zinc, copper, linoleic
healing slowed acid, vitamin B12

T­lymphocytes Depressed T­cell distribution Protein, arginine, omega­3


fatty acids, vitamins A, B12,
B6, folic acid, thiamine,
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riboflavin, niacin,
pantothenic acid, zinc, iron

Macrophages and Longer time for phagocytosis Protein, vitamins A, C, B12,


Granulocytes kill time and lymphocyte B6, folic acid, thiamine,
activation riboflavin, niacin, zinc, iron

Antibodies Reduced antibody response Protein, vitamins A, C, B12,


B6, folic acid, thiamine,
biotin, riboflavin, niacin

MedicalNutr ition Therapyfor MetabolicallyStr essed Patients

Energy requirements are highly individual and may vary widely from person to person. Total kcal
requirements are dependent on the basal energy expenditure (BEE) plus the presence of trauma,surgery,
infection, sepsis, and other factors. Additionally, age, height, and weight are often taken into consideration.

Harris­Benedict Formula
The Harris­Benedict formula is one of the most useful and accurate for calculating basal energy
requirements, although it generally overestimates BEE by 5% to 15%. It is important to remember this
formula uses current (actual) weight in the calculation.

Wtinpounds÷2.2 kg=Wtin kg

Ht in inches ÷ 2.54 cm = Ht in cm

Men = 66.5 + (13.8 × Wt in kg) + (5 × Ht in cm) ­ (6.8×Age)

Women = 655.1 + (9.6×Wt in kg) + (1.8×Ht in cm)­(4.7×Age)

Once BEE has been calculated, additional kcal for activity and injury are added:

BEE × Activity factor (AF) × Injury factor (IF)

Protein Requirements
Additional protein is required to synthesize the proteins necessary for defense and recovery, to spare lean
body mass, and to reduce the amount of endogenous protein catabolism for gluconeogenesis.

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Vitamin/MineralNeeds
Needs for most vitamins and minerals increase in metabolic stress; however,no specific guidelines exist for
provision of vitamins, minerals, and trace elements. It is usually believed that if the increased kcal
requirements are met, adequate amounts of most vitamins and minerals are usually provided. In spite of this,
vitamin C, vitamin A or beta carotene, and zinc may need special attention.

Fluid Needs
Fluid status can affect interpretation of biochemical measurements as well as anthropometry and physical
examination. Fluid requirements can be estimated using several different methods

Micronutrient Supplementation
Vitamin C: 500 to 1000 mg/daily in divided dose

Vitamin A: one multivitamin tablet containing vitaminA,one to four times daily


Zinc sulfate: 220 mg,one to three times daily

Activity Activity Factors Clinical Ener gy G,


status str ess pr otein/kg
factor BW/day

Bed rest 1.2 Elective surgery 1 – 1.2 1 – 1.5

Ambulatory­ 1.3 Multiple trauma 1.2 – 1.6 1.3 – 1.7


able to walk

Severe infection 1.2 – 1.6

Peritonitis 1.05 – 1.25

Multiple/long 1.1 – 1.3


bone fracture

Infection with 1.3 – 1.5


trauma

Sepsis 1.2 – 1.4 1.2 – 1.5

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Closed head 1.3


injury

Cancer 1.1 – 1.45

Burns (% BSA) 1.8­ 2.5

0­20% 1 – 1.5

20­40% 1.5 – 1.85

40­100% 1.85 – 2.05

Fever 1.2 per 10C


>370C

Fluid r equir ement based on: Water (ml)

Weight 100ml/kg/day for first 10 kg

50 ml/kg/day for the next 10 kg

20 ml/kg/ day for each kg above 20


kg

Age & weight 16­30 yrs (active) 40 ml/kg/day

20­55 35 ml/kg/day

55­75 30 ml/kg/day

>75 25 ml/kg/day

Energy 1ml/kcal

Fluid balance Urine output + 500 ml/day

Hydr ation/Fluid Status

Increased fluid losses can result from fever (increased perspiration), increased urine output,
diarrhea, draining wounds, or diuretic therapy.10
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Vitamins and Miner als

Just as kcal needs increase during hypermetabolic conditions, so, too, do needs for most vitamins
and minerals. And if kcal needs are met, the patient will most likely receive adequate amounts of
most vitamins and minerals. Special attention, however, should be given to vitamin C (ascorbic
acid), vitamin A or beta­carotene, and zinc. Vitamin C is crucial for the collagen formation
necessary for optimal wound healing. Supplements of 500 to 1000 mg/day are recommended.12
Vitamin A and beta­ carotene (vitamin A’s precursor) play an important role in the healing
process in addition to their role as anti­ oxidants. Zinc increases the tensile strength (force
required to separate the edges) of a healing wound. Supplements of 220 mg/day zinc sulfate
(orally) when stable are commonly used. Additional zinc may be necessary if there are unusually
large intestinal losses (small bowel drainage or ileostomy drainage).

NUTRITION IN BURNS
‐ A bur n is defined as an injury to the skin or other organic tissue caused by thermal
trauma.
‐ Trauma refers to a massive crush injury or damage to the body
‐ A burn occurs when some or all of the cells in the skin or other tissues are destroyed by
hot liquids (scalds), hot solids (contact burns), or flames (flame burns), radiation,
radioactivity, electricity, friction or contact with chemicals e.tc.
‐ Major burns result in severe trauma. When a patient suffer from burn injuries the energy
requirements can sometimes increase to as much as 100% above resting energy
expenditure, depending on the extent of the burn (Total Burnt Surface Area ­ TBSA) and
depth of the injury (degree of burns).
‐ Most burns heal without any problems but complete healing in terms of cosmetic
outcome is often dependent on appropriate care, especially within the first few days after
the burn. Most simple burns can be managed in primary care but complex burns and all
major burns warrant a specialist and skilled multidisciplinary approach for a successful
clinical outcome.
‐ Burns(burn wounds) may be distinguished and classified by their:
o Mechanism or cause
o The degree or depth of the burn
o The area of body surface that is burned,
o The region or part of the body affected
o The extent
I. Classification by mechanism or cause

Causally, burns may be classified as thermal or inhalational.


a) Ther mal bur ns involve the skin and may present as:
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‐ scalds – caused by hot liquid or steam;


‐ contact burns – caused by hot solids or items such as hot pressing irons and cooking
utensils, as well as lighted cigarettes;
‐ flame burns – caused by flames or incandescent fi res, such as those started by lighted
cigarettes, candles, lamps or stoves;
‐ flash burns of short duration but intense heat
‐ chemical burns – caused by exposure to reactive chemical substances such as strong acids
or alkalis;
‐ Electrical burns – caused by an electrical current passing from an electrical outlet, cord or
appliance through the body.

Mechanisms of ther mal injur y


 Scalds—spilling hot drinks or liquids or being exposed to hot bathing water. Cause
superficial to superficial dermal burns.
 Flame—they are often associated with inhalational injury and other concomitant trauma.
Flame burns tend to be deep dermal or full thickness.
 Contact—the object touched must either have been extremely hot or the contact was
abnormally long. Burns from brief contact with very hot substances are usually due to
industrial accidents. Contact burns tend to be deep dermal or full thickness.
b) Inhalational bur ns are the result of breathing in superheated gases, steam, hot liquids or
noxious products of incomplete combustion. They cause thermal or chemical injury to the
airways and lungs and accompany a skin burn in approximately 20% to 35% of cases.

Inhalational burns are the most common cause of death among people suffering fire­related burn
as they cause injury to the internal organs, upper highway edema and difficulty in breathing
II. Classification by the degr ee and depth of a bur n

Burns may also be classified by depth or thickness.

• It is important to estimate the depth of the burn to assess its severity and to plan future wound
care. Burns can be divided into three types, as shown below.

Depth of bur n Char acter istics Cause

Fir st degr ee bur n • Erythema Sunburn

• Pain •

Absence of blisters

Second degr ee (Par tial • Red or mottled • Contact with hot liquids
thickness)
Flash burns

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Thir d degr ee (Full • Dark and leathery • Fire


Thickness)
• Dry • Electricity or lightning

• Prolonged exposure to hot


liquids/ objects

a) Fir st­degr ee or super ficial bur ns are defined as burns to the epidermis that result in a
simple inflammatory response.
Char acter istics
 They affect only the outer/top layer of the skin (epidermis)
 They are caused by ultraviolet light e.g. solar radiation (sun burn), short heat
exposure/ brief contact with hot substances, liquids, short flames or flash flames
(scalds) on an unprotected skin
 They are painful
 Characterized by redness.
 They heal within a week (5­10 days)
 They heal with no permanent changes in skin colour, texture, or thickness(No
scaring)
 No blisters

b) Second­degr ee or par tial­thickness bur ns result when damage to the skin extends
beneath the epidermis into the dermis. The damage does not, however, lead to the
destruction of all elements of the skin.

Char acter istics


 They affect both the epidermis and the layer below it (the dermis).
 They are characterized by blisters, pain and redness
 They heal within 10–14 days (for milder burns) or 25–35 days (when the depth of burn is
greater).
 Scaring not very common
 They require hospitalization
o Super ficial second­degr ee bur ns are those that take less than three weeks to
heal.
o Deep second­degr ee bur ns take more than three weeks to close and are likely to
form hypertrophic scars.
c) Thir d­degr ee or full­thickness bur ns are those where there is damage to all epidermal
elements – including epidermis, dermis, subcutaneous tissue layer and deep hair follicles.
Char acter istics

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Epidermis, dermis, subcutaneous tissue(fat) and deep hair follicle are affected
Third­degree burn wounds cannot regenerate themselves without grafting. i.e.
they require surgery This because of extensive destruction of the skin layers
 They are wet or waxy
 Risk of scaring
 Require more than 21 days to heal
 They are characterized by a white burn site
 Lack of sensation due to the destruction of the nerve endings, disturbed
temperature control and a higher danger of infections.
 They require immediate hospitalization
 Can be caused by flame, oil, hot water etc.
In adults, a full­thickness burn will occur within 60 seconds if the skin is exposed to hot
water at a temperature of 53° C. If, though, the temperature is increased to 61° C, then
only 5 seconds are needed for such a burn.

Thir d­degr ee bur ns: They may also destroy the underlying bones, muscles and
tendons.

 Four th degr ee bur ns.


Char acter istics
 They destroy all layers of the skin
 They damage the underlying bones, muscles, and tendons.
 There is no sensation in the area since the nerve endings are destroyed.
 Definite scaring
 Waxy and coloured ( gray to charred and black)
 They are caused by e.g. high voltage electricity, grease, oil, steam, chemicals

In children, burns occur in around a quarter to a half of the time needed for an adult to burn.
 It is common to find all three types within the same burn wound and the depth may change
with time, especially if infection occurs. Any full thickness burn is considered serious.

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III. Classification by extent of bur n


The extent of burn, clinically referred to as the total body surface area burned (TBSA), is
defined as the proportion of the body burned.
Several methods are used to determine this measurement, the most common being the so­
called “r ule of nines”. This method assigns:
 9% to the head and neck region
 9% to each arm (including the hand)
 18% to each leg (including the foot) and
 18% to each side of the trunk (back, chest and abdomen).

The body is divided into anatomical regions that represent 9% (or multiples of 9%) of the total
body surface (Figure below). The outstretched palm and fingers approximates to 1% of the body
surface area.

NB: The “rule of nines” is used for adults and children older than 10 years, while the Lund and
Browder Chart is used for children younger than 10 years. The calculation assumes that the size
of a child’s palm is roughly 1% of the total body surface area

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Summar y: estimating the (TBSA) in r elation to the Body sur face ar ea: Rule of Nines:
1. The adult body is divided into anatomical regions that represent 9%, or multiples
of 9%, of the total body surface. Therefore 9% each for the head and each upper
limb. 18% each for each lower limb, front of trunk and back of trunk.
2. The palmar surface of the patient's hand, including the fingers, represents
approximately 1% of the patient's body surface.
3. Children:
 For children <1 year: head = 18%, leg = 14%
 For children >1 year: add 0.5% to leg, subtract 1% from head, for each
additional year until adult values are attained
Depth of bur ns
 Depth of burn (described as first­degree, second­degree and third­degree burns). Burn
wounds are dynamic and need reassessment in the first 24­72 hours because depth can
increase as a result of inadequate treatment or superadded infection.
 Burns can be superficial in some areas but deeper in other areas:
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1. Epidermal (superficial partial­thickness): red, glistening, pain, absence of blisters


and brisk capillary refill. Not life­threatening and normally heal within a week
without scarring.
2. Superficial dermal: pale pink or mottled appearance with associated swelling and
small blisters. The surface may have a weeping, wet appearance and is extremely
hypersensitive. Brisk capillary refill. Heal in 2­3 weeks with minimal scarring and
full functional recovery.
3. Deep dermal: blistering, dry, blotchy cherry red, doesn't blanch no capillary refill
and reduced or absent sensation. 3­8 weeks to heal with scarring, may require
surgical treatment for best functional recovery.
4. Full­thickness (third­degree): dry, white or black, no blisters, absent capillary
refill and absent sensation. Requires surgical repair and grafting.
5. Fourth­degree: includes subcutaneous fat, muscle, and perhaps bone. Requires
reconstruction and, often, amputation.
 Circumferential extremity burns: assess status of distal circulation, checking for cyanosis,
impaired capillary refilling or progressive neurological signs. Assessment of peripheral
pulses in burn patients is best performed with a Doppler ultrasound.
Bur n car e in the fir st 24 hour s
 Assessment of patient airway and ventilation status
 Fluid /electrolyte resuscitation of major importance
 Maintain vital organ function
 Restoration of blood flow to the heart, injured tissues and vessels

Ser ious bur n r equir ing hospitalization

 Greater than 15% burns in an adult


 Greater than 10% burns in a child
 Any burn in the very young, the elderly or the infirm
 Any full thickness burn
 Burns of special regions: face, hands, feet, perineum
 Circumferential burns
 Inhalation injury
 Associated trauma or significant pre­burn illness: e.g. diabetes

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The body’s metabolic r esponse to bur n

 The body’s metabolic response to burn is divided into 2 phases


1. The ebb phase/early phase
2. The flow phase.
 The ebb phase occurs immediately after a burn. If the patient survives, the ebb phase
evolves into the flow phase. The ebb phase is focused in maintaining heart action and
blood circulation and this is the major medical concern.

Char acter istics of the ebb phase/ear ly phase


 Decreased Oxygen Consumption
 Hypothermia (Lowered Body Temperature)
 Hypovolemia (A Decreased Volume Of Circulating Blood In The Body)
 Shock ((Low Blood Perfusion To Tissues)
 Decreased Cardiac Output
 Vascular constriction
 Decrease in production of digestive enzyme
 Decrease urine production
 Insulin levels drop because glucagon is elevated (increased), most likely as a signal to
increase hepatic glucose production.
 Decrease in metabolic needs

Flow phase:

“It brings hyper­metabolism”

Char acter istics of the flow phase


 Increased cardiac output­ Increased cardiac work immediately after a burn, because of
low amount of blood in the body
 Increase myocardial oxygen consumption,
 Increase body temperature (hyperthermia ),
 Increase energy expenditure(increased metabolic rate)
 Increase protein breakdown­ Muscle protein degradation (breakdown) becomes a
necessary and large source of energy­(protein is degraded much faster than it is
synthesized).This leads to loss of lean body mass and increased immune dysfunction
(Increased risk for infection)
 Increase nitrogen excretion/loss
 Liver dysfunction (the liver increases in size to help in removing the increased nitrogen
rates)
 Increased catabolism­ causing the rapid breakdown of energy reserves to provide glucose.
This is because of increased energy need due to hypermetabolism and increased catabolic

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hormones(glucagon and cortisol)


 Changes in glucose metabolism­Elevated circulating levels of catecholamine, glucagon,
cortisol and gluconeogenic hormones in response to severe thermal injury propagate
(results into) inefficient glucose production in the liver.
 Sex hormones and growth levels decrease around 3 weeks post burn. This results in
growth retardation
 Decrease in protein synthesis
 Increase in gluconeogesis­ increase in glucose production
 Increase in cytokines
 Increase in basal metabolic rate­increase in energy expenditure

The flow stage lasts for days, weeks, or months until the injury is healed

N/B.The hypermetabolic response is believed to be as a result of increased oxygen consumption,


increased production of catecholamine, increased production of catabolic hormones (cortisol,
epinephrine and glucagon, leading to inhibition of protein synthesis and lipogenesis) and
inflammatory cells (cytokines). Glucagon promotes gluconeogenesis, amino acid uptake,
ureagenesis and protein catabolism while Cor tisol, which is released from the adrenal cortex
enhances skeletal muscle catabolism and promotes hepatic use of amino acids for
gluconeogenesis, glycogenolysis, and acute­phase protein synthesis.

Nutr ition challenge of bur n patients/ Special concer ns for bur n patients/Effects of bur n

Adequate and prompt nutrition is extremely important for preventing numerous complications
that comes with burn
 Increased nitrogen losses that exceed any other type of stress or trauma. There is
increased nitrogen loss in the urine because of increased movement of amino acids from
skeleton muscle to the liver where amino acid (protein) serve as source of glucose.
Nitrogen is a by­product of protein synthesis

Nitrogen is also lost from wound exudate and blood loss during surgery, leading to an
extraordinarily negative nitrogen balance.

 Increased energy needs due to hyper metabolism that increase with size of the burnt area
peaking up to 2 to 2.5 times above the normal metabolic rate for burns involving as much
as 40% of the body surface.
 Severe protein catabolism
 Susceptible to infection due to destruction of the skin surface. Skin is the body’s first line

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of defense against infection


 Loss of skin also results in increased water and heat loss. The larger the burnt area the
greater the loss of water vapor and heat. Approximately 2.5­4l/day of water vapor may be
lost from a major burnt wound
 More protein loss as burnt surface allows leakage of a protein rich fluid containing
approximately two thirds as much proteins as plasma.
 Malnutrition. Many are anorexic and unable to consume a sufficient amount of
kilocalories to satisfy energy requirements. Also, burn patients do not feed well because
of pain, generalized discomfort and depression
 Increased need for water. Large amounts of waste products (such as nitrogen and
potassium) must be excreted by the kidney­ fluids are required to keep these in solutions
 Curling ulcer or acute ulceration of the stomach or duodenum is frequently observed in
burn patients­large amount of vitamin A can reduce incidence of stress ulcer
 Edema.­Capillary permeability increases and plasma protein fluids and electrolytes
escape into the burn area and intestinal space
 Anemia
 Heat loss
 Loss of electrolytes
 Burn patients may develop an ileus( blockage of the intestine especially the ileum) as a
result of shock that results into lack of peristalsis
Other challenges in patients (Systemic Effects following a Bur n)

 Toxic gases ­Causes upper airway edema and difficulty in breathing


 Edema
 Airway obstruction
 Gastric effects
o Acute gastroduodenal mucosal lesions
o Prolonged gastroduodenal mucosal lesions
o Duodenal ulcer induced by surgery
o Stomach dilatation.

Nutr itional car e of the bur n patient

Goals/Aims
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 To offer energy, fluids and nutrients in adequate quantities to maintain vital functions and
homeostasis, recover the activity immune system, reduce the risks of overfeeding, to
provide protein and energy necessary to minimize the protein catabolism and nitrogen
loss.

N/B. Burn patients require specialized nutritional support because over­nutrition predisposes the
patient to hyperglycemia, overload of the respiratory system, and hyperosmolarity. When dealing
with under­nutrition, the patient could suffer from malnutrition and subsequent reduction of
immunocompetence, prolonged dependency on mechanical ventilation and delay in the healing
processes, increased risk of infection, morbidity and mortality

Nutr ition ther apy

 Monitor nutritional status and provide specialized nutrition. Provide enteral nutrition (within
24 hours) if the patient cannot consume enough food orally.
Why enter al nutr ition is impor tant.
It stimulates the production of specific hormones beneficial for the proliferation of gut
mucosal cells
Maintains gut integrity and prevention of bacterial translocation

Parenteral nutrition is not recommended but only for patients with non­functioning GI tract
 Vitamin A (As much as 5000 units/1000 calories for increased immunity. Supplementation
may be done
 Vitamin C (As much as 1000­2000mg/day or 1­2g/day). For collagen synthesis. Vitamin C is
also an antioxidant Supplementation may be done
 Adequate copper­copper assists in the formation of red blood cells and work with vitamin C
to form the connective tissues.2­4 mg/day is recommended during the first few weeks of
injury repair
 Zinc­Zinc is required for over 300 enzymes in the body and plays a role in DNA synthesis­all
necessary for tissue regeneration and repair
Zinc deficiency has been associated with poor wound healing and, as Zinc deficiencies is one
of the most common micronutrient deficiencies.15­30 mg/day is recommended especially
during the initial stages of healing(Balancing of copper and zinc should be ensured as excess
of can create deficiency of the other)
 Mineral supplementation or adequate minerals e.g. calcium (it is affected during burns) and
vitamin. Calcium is needed for fracture repair/healing
 Adequate iron to compensate for the lost iron(to prevent anemia) and increase the volume of
oxygen for the organs and tissues
 Adequate energy to prevent weight loss of greater than 10% usual body weight.
 Provide adequate protein to promote wound healing, for positive nitrogen balance and
maintenance or repletion of circulating proteins. Protein degradation in burn patients
proceeds despite adequate protein supplementation.
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 Protein requirements are also increased in burn patients because of the increased catabolism
of skeletal muscle, more protein is also lost as the burnt surface allows leakage of a protein
rich fluid leading to average losses of 260 mg protein/kg/hr. Pr otein intake should var y
between 1.5–2.0 g/kg of ideal body weight on a daily basis. The extra protein is needed
for:
o Wound healing,
o Tissue building
o Blood regeneration.
o Optimize the immunize system

 Adequate fluids to prevent dehydration and for the removal of the nitrogenous wastes

Estimation of nutr itional r equir ements in bur n patients (Ener gy and pr otein)

 The most common formulas utilized in these patients are the Curreri, Pennisi, Schofield,
IretonJones, Harris­Benedict and the ASPEN recommendations.
 For children is the Mayes,Harris­Benedict. pennisi and World Health Organization
formula. The majority of mathematical formulas overestimate the nutritional needs.
 Between 1970 and 1980 the most frequently used formula for estimating the nutritional
needs of burn patients was developed by William Cur r er i.
 In 1976, Pennisi created a more comprehensive formula, designed for adults and
children, estimating both the energetic needs in calories and protein needs in grams.
 Other formulas developed for critically ill and burn patients include Toronto, Schofield,
Ireton Jones, Harris­Benedict, and the American Society for Parenteral and Enteral
Nutrition (ASPEN) recommendations.

Formulas for calculating approximate nutritional needs in burn cases. Electronic archive study,
2010

Author Gender Formula

Harris & Estimated Energy Requirements: BMR x Activity factor x Injury


Benedict factor
Male
66 + (13.7 x weight in kg) + (5 x height in cm) ­ (6.8 x age)
Female
665 + (9.6 x weight in kg) + (1.8 x height in cm) ­ (4.7 x age)

Activity factor:

Confined to bed: 1.2

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Minimal ambulation: 1.3

Injury factor:

< 20% TBSA: 1.5

20­40% TBSA: 1.6

> 40% TBSA: 1.7

Curreri For all patients Estimated Energy Requirements: (25 kcal x w) + (40 x %TBSA)

Curreri equation

for patients aged 16 to 59 years:

TEE: 25 kcal x kg actual body weight + (40 kcal x % TBSABa)

If percent TBSAB > 50%, use a maximum value of 50%


a

Curreri Example:

30 year male weighing 70 kg with burns involving 50% TBSA.

TEE: 25 kcal x 70 kg + (40 kcal x 50) = 1750 kcal + 2000 kcal=


3750 kcal as total energy expenditure

Pennisi Adults Estimated Energy Requirements:

Calories (20 x w) + (70 x %TBSA)

Protein (1 g x w) + (3g x %TBSA)

Children

Calories (60 kcal x w) + (35 Kcal x %TBSA)

Protein (3 g x w) + (1 g x %TBSA)

WHO For Children

Male < 3 years (60.9 x weight in kg) – 54

Male 3 to 10 (22.7 x weight in kg) + 495

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years

Female < 3 (61 x weight in kg) – 51


years
(22.5 x weight in kg) + 499
3 to 10 years

NUTRITION IN SURGERY

INTRODUCTION

Definition of ter ms

Sur ger y­This is a branch of medicine that involves the cutting, removal or closing of a body
tissue or organ with an aim of treating an injury, a disease or a disorder e.g. vasectomy, tooth
extraction and feeling, bariatric surgery, gastrectomy,

Elective sur ger y­It refers to surgery that is scheduled in advance because it does not involve
medical emergency. They can be delayed e.g. hernia, vasectomy etc. Most surgeries are elective

Emer gency sur ger y­It is one that must be performed immediately without delay

Surgery like any other injury to the body elicits a series of reactions including release of str ess
hor mones and inflammator y mediator s i.e. cytokines. This release of mediators to the
circulation has a major impact on body metabolism. They cause catabolism of glycogen, fat
and pr oteins with release of glucose, free fatty acids and amino acids into the circulation so that
substrate are diverted from their normal purposes e.g. physical activities to the task of healing
and immune response.
For optimal recovery and wound healing all patients undergoing surgery should be at optimal
nutritional status to help them tolerate the physiologic stress of the surgery and temporary
starvation that follows. But all too often, surgical patients may be malnourished secondary to the
medical condition causing the need for surgery. Additionally, they may experience anorexia,
nausea, or vomiting, which decrease their ability to eat.

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Fever may increase their metabolic rate. Or nutritional needs may not be met because of
malabsorption.

For surgery to be successful, patients who are malnourished or in danger of malnutrition must be
identified so corrective action may be arranged.

Measures to reduce stress of surgery can minimize catabolism and support anabolism
throughout surgical treatment and allow patients to recover substantially better and faster even
after major surgical operation.
The body metabolic responses like release of stress hormones and inflammatory mediators i.e.
cytokines and catabolism of glycogen, fat and proteins can result into malnutrition

Goal of nutr itional management


To enhance recovery of patients after surgery
Objectives
 To avoid long periods of preoperative fasting
 To improve or maintain nutritional status of preoperative patients as this will prevent
postoperative complications and malnutrition as well as improve the healing process
 To control metabolic processes
Pr eoper ative/pr e­sur ger y nutr ition car e
Surgery stresses the client regardless of whether it is elective (schedule in advance, not
emergency. One that can be postponed for 24 hours) or not. If the surgery is elective, the client’s
nutritional status should be evaluated before surgery; and if improvement is needed, it should be
undertaken immediately.

 High ener gy diet: Extra carbohydrates will be converted to glycogen and stored to help
provide energy after surgery, when needs are high and when clients may be unable to eat
normally. Encourage patients who do not meet their energy needs from normal foods to
take oral nutrition supplements during the preoperative periods
 High pr otein diet: Protein body stores should be assessed. The extra protein is needed
for:
o Wound healing,
o Tissue building
o Blood regeneration.
o Optimize the immune system
 Administer preoperative enteral nutrition preferably before admission to the hospital
 Vitamins and miner als: Any deficiency state such as anemia should corrected.
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Electrolytes and fluids should be normalized


o Vitamins A and C and zinc for wound healing,
o Vitamin D for the absorption of calcium,
o Vitamin K for proper clotting of the blood.
o Iron is necessary for blood building
o Calcium and phosphorus for bones
o The other minerals are needed for maintenance of acid­base, electrolyte,
and fluid balance in the body.
o The B vitamins are needed for the increased metabolism

In cases of overweight, improved nutritional status includes weight reduction before surgery
whenever possible. Excess fat is a surgical hazard because the extra tissue increases the chances
of infection, and fatty tissue tends to retain the anesthetic longer than other tissue.
 Immediate pr eoper ative per iod­ nutr ition car e
Many physicians order their clients to be NPO (nothing by mouth) after midnight the night
before surgery, i.e. in elective cases no food is allowed by mouth for at least 6 hours before
surgery. In emergency cases gastric lavage or suction is used to remove stomach contents before
anesthesia is started. This is done prevent to cases where food is regurgitated/vomiting then
aspirated into the lungs during surgery(Aspiration­a condition in which food, liquids, saliva or
vomit is breathed/inhaled through airways), upon awakening or to prevent vomiting or aspiration
that may be induced by anesthesia
 If there is to be gastrointestinal surgery, the colon should be free of residue to prevent
postoperative infection, fecal matter may interfere with the procedure itself and cause
contamination as colonic bacteria are reduced when less food residue is present.
Therefore a low­residue diet may be ordered for a few days before surgery (2­3 days).
This is intended to reduce intestinal residue.

The Low­Residue Diet

Low­fiber or residue­restricted diets may be used in cases of severe diarrhea, diverticulitis,


ulcerative colitis, and intestinal blockage and in preparation for and immediately after intestinal
surgery.

In some facilities, these diets consist of foods that provide no more than 3 grams of fiber a day
and that do not increase fecal residue (Tables 20­5 and 20­6). Some foods that do not actually
leave residue in the colon are considered “low­residue” foods because they increase stool volume
or provide a laxative effect. Milk and prune juice are examples. Milk increases stool volume, and
prune juice acts as a laxative.

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Foods to Allow and to Avoid on Low­Residue Dietsod

Foods to Allow Foods to Avoid

 Milk, buttermilk (limited to 2 cups daily) if  Fresh or dried fruits and vegetables
physician allows  Whole­grain breads and cereals
 Cottage cheese and some mild cheeses as  Legumes, coconut, and marmalade
flavorings in small amounts  Tough meats
 Butter and margarine  Milk, unless physician allows
 Eggs, except fried Rich pastries  Meats and fish with tough connective
 Tender chicken, fish, ground beef, and ground tissue
lamb (meats must be baked, boiled, or broiled)  Potato skin
 Soup broth
 Cooked, mild­flavored vegetables without
coarse fibers; strained fruit juices (except for
prune); applesauce; canned fruits including
white cherries, peaches, and pears; pureed
apricots; ripe bananas
 Refined breads and cereals, white crackers,
macaroni, spaghetti, and noodles
 Custard, sherbet, vanilla ice cream; plain
gelatin; angel food cake; sponge cake; plain
cookies
 Coffee, tea, cocoa, carbonated beverage
 Salt, sugar, small amount of spices as
permitted
 by physician

An example of low r esidue meal plan

Br eakfast Dinner Lunch/supper

Strained orange Chicken broth Tomato juice

Cream of rice with milk and Ground beef patty Macaroni and cheese
sugar
Boiled potato, no skin Green beans
White toast with margarine
and jelly Baked squash White bread and butter

Coffee with cream and sugar Gelatin dessert Lemon sherbet

Milk Tea with milk and sugar

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Examples of common sur ger ies


 Neck and head sur ger y­It is usually performed to remove a tumor due to neck and brain
cancer that inhibit a patient ability to chew and swallow normally.
 Esophageal sur ger y­ e.g. due to esophageal cancer. It can prevent swallowing
 Gastr ic /stomach sur ger y –e.g. partial gastrectomy/vagotomy(partial removal of the
stomach), total gastrectomy (removal of the entire stomach. A storage reservoir may be
created using a section of jejunum), gastroduodenostomy(removal of part of the stomach
and joining it directly to the duodenum), gastrojejunostomy(bypass the duodenum).They
are performed to remove a tumor, ulcer disease, hemorrhage, or to loss weight due to
morbid obesity) e.tc. Another surgical operation, bariatric surgery is often performed for
the treatment of obesity. Bariatric surgery(if it is passed with the purpose of losing
weight) limits the amount of food intake
Consequences of gastr ectomy
 Weight loss­gastrectomy leads to early satiety
 Absence of gastric juice pepsin and HCL acid­the entire digestion of protein must
occur in the small intestine
 Impaired fat utilization because of inadequate mixing of with food with digestive
enzymes
 intestinal sur ger y­It is where part of small or large intestine is removed e.g. colostomy
or ileostomy (These procedures involve creation of an artificial anus on the abdominal
wall by incision into the colon or ilium and bring it out to the surface, forming a stoma to
collect fecal matter).They are performed in cases of intestinal obstruction, inflammatory
bowel disease, diverticulosis etc. If more than 50% of the small intestine is removed ,
short­bowel syndrome may occur
Consequences

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 Weight loos
 Diarrhea
 Protein and fat metabolism

Post­sur ger y Nutr itional Car e

The post­surgery diet is intended to provide calories and nutrients in amounts sufficient to fulfill
the client’s increased metabolic needs and to promote healing and subsequent recovery.

The introduction of solid food depends on the condition of the gastrointestinal tract. Oral feeding
is often delayed for the first 24 to 48 hours after surgery to await the return of bowel sounds or
passage of flatus (flatus ­ gas in or from the stomach or intestines, produced by swallowing air
or by bacterial fermentation).
To some patients, oral intake including clear liquids can be initiated within hours after surgery if
bowel sound s back
In general, during the 24 hours immediately following major surgery, most clients will be given
intravenous solutions only. These solutions will contain water, 5% to 10% dextrose, electrolytes,
vitamins, and medications as needed. The maximum calories supplied by them is about 400 to
500 calories per 24­hour period. The estimated daily calorie requirement for adults after surgery
is 35 to 45 calories per kilogram of body weight. A 110­pound (50 kgs) individual would require
at least 2,000 calories a day. Obviously, until the client can take food, there will be a
considerable calorie deficit each day. Body fat will be used to provide energy and to spare body
protein, but the calorie intake must be increased to meet energy demands as soon as possible.

Because protein losses following surgery can be significant and because protein is especially
needed then to rebuild tissue, control edema, avoid shock, resist infection, and transport fats, a
high­protein diet of 80 to 100 grams a day may be recommended. In addition, extra minerals and
vitamins are needed. When peristalsis returns, ice chips may be given; and if they are tolerated, a
clear liquid diet can follow. (Peristalsis is evidenced by the presence of bowel sounds.)

Normally in postoperative cases, clients proceed from the clear­liquid diet to the regular diet.
Sometimes this change is done directly and sometimes by way of the full­liquid diet, depending
on the client and the type of surgery. The average client will be able to take food within 1 to 4
days after surgery. If the client cannot take food then, parenteral or enteral feeding may be
necessary.

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Sometimes following gastric surgery, dumping syndr ome occurs within 15 to 30 minutes after
eating. This is characterized by dizziness, weakness, cramps, vomiting, and diarrhea. It is caused
by food moving too quickly from the stomach into the small intestine. It occurs secondary to an
increase in insulin, in anticipation of the increase in food, which never comes.

Dumping syndr ome: nausea and diarrhea caused by food moving too quickly from the
stomach to the small intestine

To prevent dumping syndrome, the diet should be high in protein and fat, and carbohydrates
should be restricted. Foods should contain little fiber or concentrated sugars and only limited
amounts of starch. Complex carbohydrates are gradually reintroduced. Gradual reintroduction is
recommended because carbohydrates leave the stomach faster than do proteins and fats.

Fluids should be limited to 4 ounces (appr. 120 ml) at meals, or restricted completely, so as not
to fill up the stomach with fluids instead of nutrients. They can be taken 30 minutes after meals.
The total daily food intake may be divided and served as several small meals rather than the
usual three meals in an attempt to avoid overloading the stomach. Some clients do not tolerate
milk well after gastric surgery, so its inclusion in the diet will depend on the client’s tolerance.

The food habits of the postoperative client should be closely observed because they will affect
recovery. When the client’s appetite fails to improve, efforts should be made to offer nutritious
foods and supplements (either in liquid or solid form) that the client will ingest. The client
should be encouraged to eat and to eat slowly to avoid swallowing air, which can cause
abdominal distension and pain.

Sever e tr auma (sur ger y)


For patients with obvious under­nutrition at the time of surgery and for whom oral intake will be
inadequate (<60%) for more than 10 days;
 Initiate tube feeding for patients in need within 24 hours after surgery
 Start tube feeding with a low flow rate ( e.g. 10ml/hr to maximum of 20ml/hr) due to
limited intestinal tolerance
 It may take 5­7 days to reach the target intake and this is not considered harmful
 Reassess nutritional status regularly during the stay in the hospital and if necessary
continue nutritional support after discharge in patients who have received nutritional
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support preoperatively
 Progress over a period of several meals from clear liquids, and finally to solid foods

N/B. The postoperative nutrition care should be planned to address the nutrition challenges that
comes with surgery especially for patients who undergo alimentary canal surgery

Some of the nutrition challenges are:

 Weight loss due to inadequate intake of intake of food after surgery


 Increased protein loss due to catabolism
 Malabsorption of fats and fat soluble vitamins, simple sugars e.g. as a result of gastric
surgeries
 Malabsorption of vitamins e.g. fluids and electrolyte e.g. sodium, potassium and chloride
ions e.g. colon surgery
 Early satiety due to reduced storage capacity
 Rapid gastric emptying that may result into diarrhea, vomiting etc.
These nutrition challenges together with surgical metabolic responses if not checked can result
into malnutrition. Malnutrition is associated with low immune function, poor wound healing,
morbidity and mortality

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NUTRITION CARE AND SUPPORT IN THE INTENSIVE CARE


 Intensive care is a therapy unit concerned with the management of patients with acute life
threatening disorders. The severe or critical disease relates to a wide variety of clinical or
surgical conditions.
 Changes in most patients in the ICU include hyper metabolism, hyper glycemia with
insulin r esistance, accentuated lipolysis and incr eased pr otein catabolism.
 The impact of the combination of these metabolic changes and absence of nutritional
support may lead to rapid and severe depletion of lean body mass. The implications are;
 Multiple organ failure
 Increased risk of infection
 Hyper metabolism
 Decreased immunity
 Increased nutritional requirements
NB: The goal of nutrition management is to preserve lean body mass
Nutr ition car e and feeding

 Enteral nutrition (EN) via tube feeding is the preferred way of feeding the critically ill
patients and an important means of counteracting for the catabolic state induced by
severe diseases.
Indications for and implementation of enter al nutr ition (EN) in the ICU
 All patients who are not expected to be on full oral diet within 3 days should receive
enteral nutrition (EN)
 Haemodynamically stable critically ill patients who have a functioning GI tract should be
fed early (<24hours) using an appropriate amount of feed
 With an inadequate oral intake, undernutrition is likely to develop within 8­12 days
following surgery
 No general amount can be recommended as EN therapy has to be adjusted to the
progression/ course of the disease and gut tolerance
 During the acute and initial phase of critical illness: an exogenous energy supply in
excess of 20­25kcal/kg/day may be associated with a less favorable outcome and thus
should be avoided whereas during the recovery (anabolic flow phase) the aim should be
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to provide 25­35kcal/kg/day to support the anabolic reconstitution


 Patients with severe under nutrition should receive EN up to 25­35 total kcal/kg/day. If
these target values are not reached supplementary parenteral nutrition should be given
Route of administr ation
 In patients who tolerate EN and can be fed approximately to the target values no
additional parenteral nutrition should be given. In patients who cannot be fed sufficiently
enterally, the deficit should be supplemented parenterally
 Carefully consider parenteral nutrition in patients intolerant to EN at a level equal to but
not exceeding the nutritional needs of the patients thus overfeeding should be avoided
 There is no significant difference in the efficacy of jejuna versus gastric feeding in
critically ill patients
Types of for mula
 Whole protein formulas are appropriate in most patients because no clinical advantage of
peptide based formula has been shown
 Immune­modulating formulae (formulae enriched with Arginine, nucleotides and α ­3
fatty acids) are superior to standard enteral formulae (these acts as energy substrate for
immune cells, reduce inflammatory stimuli and cell mediated immunity as well as
scavenge free radicals)
In elective upper GI surgical patients:­
 In patients with mild and severe sepsis immune modulating formulae may be harmful and
therefore are not recommended
In patients with trauma
 In patients with ARDS (formula containing omega 3 fatty acids and antioxidants are
recommended)
 For burn patients trace elements (Cu, Se and Zn) should be supplemented in a higher than
standard dose
 ICU patients with very severe illness who do not tolerate more than 700ml enteral
formulae per day should not receive an immune modulating formulae enriched with
Arginine, nucleotide and omega 3 fatty acids

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 Glutamine should be added to standard enteral formula in burn and trauma patients
 Glutamine decreases infection complications, strengthens immune defense, improves
protein synthesis and nitrogen balance, improves metabolic homeostasis (glucose) and
improves gut functions
 There are no sufficient data to support enteral glutamine supplementation in surgical or
heterogeneous critically ill patients
FEEDING OF LOW BIRTH WEIGHT AND PRETERM INFANTS
 Low birth weights are defined as babies having less than 2500g at birth.
 Very low birth weights are those born with less than 1500g.
 About a third of low birth weight infants are small for gestational age and show intra
uterine growth retardation.
Pre­term babies are subdivided into three categories depending on the degree of maturity i.e.
 Less than 30 weeks( extremely premature)
 31­32 weeks
 35­36 weeks (borderline)
 The clinical management and nutritional requirement of the immature or preterm infants
is different from a mature infant born after 37 weeks.
 Preterm infants experience renal, hepatic, gastrointestinal and respiratory problems due to
immaturity of organ systems. They are more likely to need assistance with breathing and
are less likely to tolerate oral feeds.
Factor s that cause var iation in weight at bir th
 Mother’s health
 Mother’s nutritional status
 Mother’s diet during pregnancy
Factor s affecting women’s nutr itional status which might pr edispose the infant bor n
pr ematur ely or of low bir th weights ar e
 Nutritional intake
 Drug abuse
 Maternal under nutrition­is the major factor causing LBW (Low Birth weight) in
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developing countries
 Mothers pre­pregnancy weight i.e. preconception weight of 40kg and a height 150 cm
 Low pregnancy weight gain
 Anemia
 Malaria
 Acute and chronic infections e.g. tuberculosis
Challenges to optimal nutr ition for pr eter m infants

 Providing adequate nutrition to preterm infant is complicated by immature organ systems,


particularly the GI system and metabolic processes.

GI immatur ities in the pr eter m infant include:


 Face and oral musculature
 Inability to coordinate sucking and swallowing, breathing (synchronization)
 Poor pastoral control
 Low esophageal sphincter pressure
 Pharyngeal swallow
 Delayed gastric emptying and stool passage
 Slower upper and lower intestinal motility
 Immature digestion and absorption of carbohydrates, protein and lipids

Renal (kidney) functions


 Concentrating controlling ability
 Sodium excretion
 Ability to maintain acid base balance
 Glucose re­absorption
 Energy glycogen and fat
 Proteins hardly any muscles
 Minerals and micronutrients – low level of Ca, Zn, Iron and others most of which are
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accumulated in the last ten weeks

In addition, prior to birth the GI tract is sterile and therefore immunologically immature. Normal
gut colonization, acquired through contact with the mother and feeding, may be delayed or
absent following birth due to isolation of the infant and residence in the new inborn care unit
(NICU) setting. Preterm infants may therefore be at risk of acquiring abnormal bacterial flora
and developing nosocomial infections.

Key issues in pr eter m infants


 Preterm infants, especially those who have been growth restricted in uterus have fewer
nutrient reserves at birth than term infants
 Additionally, preterm infants are subject to physiological and metabolic stresses that can
affect their nutritional needs, such as respiratory distress or infection
Feeding Pr ematur e Infants

 The premature infant’s nutritional requirements are substantially different from those of
the term infant, and meeting their unique needs can be challenging.

 The aim of feeding the premature is to provide optimal nutrition early in life, in order to
improve survival as well as promote growth and development. This is the cornerstone of
the care of preterm infants.

 Avoiding early malnutrition can have both short­ and long­term benefits for the infant.
Early care in the new inborn care unit (NICU) is therefore focused on vital organ
development
Objectives of nutr ition management
 To promote feeding tolerance
 To improve digestibility
 To promote progress to full feeds
 To promote weight gain
 To enhance neurodevelopment, organ maturity and functioning
 To prevent infections and promote development of immune system
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Recommendations for nutritional requirements for pre­terms is based on data from intrauterine
growth and nutrient balance studies and assume that optimal rate of postnatal growth for preterm
infants should be similar to that of normal fetuses of the same post conception age. In practice,
however, target levels for nutrient input are not always achieved and this may result in important
nutritional deficits.

Nutr itional r equir ements for pr eter m


The recommended nutritional requirements for preterm are as shown in table 67 below:

Table 1: Recommended Nutr itional r equir ements for Pr e ter m Infants


Nutr itional Requir ements Recommended amounts
Fluid 150 – 200 Mmol
Energy 110 – 130 kcal/kg/day
Protein 3 ­4 g/kg/day
Fat 4.5 – 6.8 g/kg/day
Calcium 120 – 230 mg/kg/day (2 – 4.5 Mmol)
Phosphorus 60 – 140 mg/kg/day (Ca: P 1.4 – 2.0: 1)
Sodium 1.3 Mmol
Iron 35 – 45 μmol
Vitamin K 2 – 3 μg

Feeding options;
There are a number of feeding options available for pre­term babies. These are
 Mother’s own unmodified breast milk
 Mother’s own breast milk fortified
 Preterm formula
 Parenteral nutrition
Feeding Pr e­ter ms
 Enter al feeds: should be given as soon as possible to prevent gut atrophy. If the baby’s
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condition is unfavorable give minimal feeds to keep the gut functional i.e. 10­20ml
/kg/day
 Par enter al feeds: if the baby is unable to take enteral feeds, parenteral feeds should be
started as soon as possible to prevent severe malnutrition

Choice of feeding methods


The choice of feeding method is determined by several factors. Nonetheless;
 The methods outlined above can be used singularly or in combination depending on the
baby’s ability
 For small babies (L1500g) breast can be used in combination with kangaroo care
 Babies in kangaroo care gain weight faster and infection rate is reduced
Well infants of gestational age > 34 weeks are usually able to coordinate sucking, swallowing,
and breathing, and so establish breast or cup feeding. In less mature infants, oral feeding may not
be safe or possible because of neurological immaturity or respiratory compromise. In these
infants milk can be given as a continuous infusion or as an intermittent bolus through a fine
feeding catheter passed via the nose or the mouth to the stomach.
Note: A major concern with the introduction of enteral feeds (especially to preterm, IUGR infant
or sick infants) is the additional physiological strain on the immature gastrointestinal tract
which predisposes them to development of necrotizing Enterocolitis whose risk is inversely
related to gestational age and birth weight. The incidence of necrotizing Enterocolitis in very
low birth weight infants is 5­10%. The conditions long term morbidity may include substantial
neuro­developmental problems, undernutrition and associated infection during a vulnerable
period of growth and development.
Clinical featur es of necr otising enter ocolitis include
 Abdominal distension, tenderness or rigidity
 Lethargy, hypotonia, or apnoea
 Hepatic portal gas on abdominal x ray
 Intramural gas (pneumatosis intestinalis) on abdominal x ray
 Intestinal perforations
 Blood or mucus in stool
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Modes of feeding
 Enteral feeding/oral
 Breastfeeding
 Cup feeding
Enter al nutr ition
Most preterm infants who develop necrotizing enterocolitis receive enteral feeds. Start minimal
enteral nutrition within the first days of life of preterm infants, particularly those who are
clinically stable. Initiate using extremely small volumes to “prime” the digestive system and
increase the volume as the infant becomes more stable and tolerance is confirmed.
 Feeds nutritionally insignificant volumes of enteral milk (0.5­1.0 ml/hour)
 Aims to stimulate postnatal development of gastrointestinal system
 Use in parallel with total parenteral nutrition
 Increase enteral feeds' volume after pre specified interval, typically 7­14 days
 Calculate feeds based on weight
 Consider starting volume for either expressed breast milk or formula milk
 Babies who weigh less than 2.5kg (low birth weight) start with 60ml/kg/day
 Increase the total volume by 20ml/kg/day until the baby is taking a total of 200ml/kg/day
 Provide breast milk up to 240ml/kg/day but no other types of milk
 Feed 2­3 hourly including night feeds
 Continue until the baby weighs 1800g or more and is fully breastfeeding
 Check the baby’s 24 hr intake
 The size of individual feed may vary

NOTE: When feeding pre­term infants strictly use preterm formulas. Cow’s milk or any other
form of milk is contra indicated

Br east milk
 Breast milk provides same advantages to preterm infants as to the full term infant and it is
the recommended form of enteral nutrition for preterm infants
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 Early immune system development is particularly important for preterm infant to help
protect against infection, including NEC. Contributions of breast milk to immune
development are well confirmed
 Human br east milk may not consistently pr ovide all the nutr ient r equir ements of
pr eter m infants and may vary depending on the stage of lactation at which it is
collected. Micr onutr ient for tifier s should therefore be added to br east milk to achieve
desir ed tar gets. Fortification of human milk with calcium and phosphate may improve
bone mineral content
 Monitoring of the infant’s nutritional status is important to ensure that breast milk is
meeting the infant’s needs
 Breast milk has non­nutrient advantages for preterm infants including immuno­protective
properties and growth factors to the immature gut mucosa
 Some evidence show that preterm infants who receive human breast milk rather than
formula milk have a lower incidence of feed intolerance and gastrointestinal upset, as
well as lower incidence of necrotising enterocolitis

Suppor ting mother s to expr ess br east milk


Mothers may be very anxious after preterm delivery, especially if their infant needs intensive
care. Although feeding might not be seen as an immediate concern, mothers should be aware that
providing breast milk is one of the most important parts of their infant's care. Supporting mothers
to provide expressed breast milk may be the most important intervention available for preterm
infants. Feeding with expressed human milk reduces the risk of serious infection, which is a
major cause of neonatal morbidity and mortality in preterm infants in developing countries.
Several initiatives may help mothers to express breast milk successfully:
 Supporting the mother on how to correctly position and attach their infants to the breast
 Stimulation of oxytocin reflex
 Early discussion of the importance of breast feeding
 Provision of relevant written information, education and communication (IEC)materials
 Encouraging frequent breast milk expression to empty the breast
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 Simultaneous expression of both breasts


 Breast massage
 Skin to skin contact (Kangaroo method)
How to expr ess br east milk
 Place finger and thumb each side of the areola and press inwards towards the chest wall.
 Press behind the nipple and areola between your finger and thumb
 Press from the sides to empty all segments
For mula milks
Despite optimal maternal support, expressed breast milk may not always be available. As an
alternative, preterm infants may be fed with a variety of artificial formula milks. Broadly, these
may be "term" formulae (based on the composition of mature breast milk), or calorie, protein,
and mineral enriched "preterm" formulae (tailored to support intrauterine nutrient accretion
rates). Concerns about feeding tolerance with cow’s milk formula – characterized by vomiting,
larger gastric residuals, gas and constipation – have prompted studies on the implications of
protein source and type. In term formulas, improved digestibility has been observed with
hydrolyzed formulas as compared to formulas with intact protein, and whey protein­based
formula has been shown to promote a faster gastric emptying rate than casein. Therefore cow’s
milk should be discouraged. It is difficult to develop optimal recommendations for minimal
effective volumes and quantity of volume increases considering that preterm infants differ
widely with respect to developmental stage, particularly GI maturity.

Ver y pr eter m infants often have relatively delayed gastric emptying and intestinal peristalsis
and may be slow to tolerate the introduction of gastric tube feeds. In such circumstances give
intravenous nutrition (e.g. Amino venous, dextrose or Lipovenous 10% formulations) while
enteral nutrition is being established or when enteral nutrition is not possible (e.g. because of
respiratory instability, feed intolerance, or serious gastrointestinal disease).
Total par enter al nutr ition should consist of glucose and amino acid solution with electrolytes,
minerals, and vitamins, plus fat as the principal non­protein energy source. Bloodstream
infection is the most common important complication of parenteral nutrition use. Delivery of the
solution via a central venous catheter rather than a peripheral catheter is not associated with a

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higher risk of infection. Extravasation injury is a major concern when parenteral nutrition is
given via a peripheral cannula. Subcutaneous infiltration of a hypertonic and irritant solution can
cause local skin ulceration, secondary infection, and scarring.
Routes of administr ation of par enter al nutr ition
Intravenous solutions can be provided in different ways. The methods used depend on the
person’s immediate medical and nutrient needs, nutrition status and anticipated length of time on
IV nutrition support. They include:
 Peripheral Parenteral Nutrition (PPN)
 Central Parenteral Nutrition (TPN)

TOPIC: NUTRITION THERAPY IN CANCER


MEDICAL NUTRITION THERAPY FOR CANCER
Content
 Cancer disease overview
 Relationship between cancer and nutrition
 Effect of cancer on nutrient intake
 Nutrition care

Definition of ter ms
 Cancer :
Refers to abnormal division and reproduction of cells that can spread throughout the
body, crowding out normal cells and tissues OR
Refers to diseases characterized by the uncontrolled growth of a group of cells, which can
destroy adjacent tissues and spread to other areas of the body via lymph or blood
 Malignant – describes a cancerous cell or tumor which can injure healthy tissues and
spread cancer to other regions of the body.
 Malignant neoplasm ­ a mass of cancer cells that invades surrounding tissues or spreads
to distant areas of the body; if left untreated, it will likely worsen and become possibly
fatal
 Car cinogen – an agent (physical, chemical, or viral) that induces cancer in humans and
animals OR It refers to substances that can cause cancer
 Car cinogenesis – the process of cancer development
 Cancer cachexia ­a specific form of malnutrition characterized by loss of lean body
mass, muscle wasting, and impaired immune, physical, and mental function that
accompany advanced cancer, even with adequate nutrition. It may be related to elevated

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levels of tumor necrosis factor


 It is a multifactorial syndrome defined by an ongoing loss of skeletal muscle mass (with
or without loss of fat mass) that cannot be fully reversed by conventional nutritional
support and leads to progressive functional impairment.
 Tumor (neoplasm) – an abnormal tissue mass that has no physiological functions, a solid
cancer that causes a swelling or a lump; commonly defined as a malignant neoplasm
­Tumors can be benign or malignant (cancerous). Malignant tumor cells invade nearby
tissues and spread to other parts of the body. Benign tumor cells do not invade nearby
tissues or spread.
 Metastasize – to spread by cancer cells from one part of the body to another
 metastasis ­ growth of malignant tissue that spreads to surrounding tissues or organs
 Palliative car e – to provide support and comfort when cure or control is not possible; to
improve quality of life; to reduce tumor burden and help relieve cancer­related symptoms
 Contr ol – to extend the length of life when a cure is not possible; to obscure
microscopic metastases after tumors are surgically removed; to shrink tumors before
surgery or radiation therapy
 Cur e ­ to obtain a complete response to treatment of a specific cancer

How cancer develops

It is caused by mutations (changes) to the DNA within the cell. DNA is in the genes of the cell.
Cells are the smallest units of the body and they make up the body’s tissues. The DNA inside a
cell contains a set of instructions telling the cell what functions to perform, as well as how to
grow, repairs itself and divide. Errors in the instructions can cause the cell to stop its normal
function and may allow a cell to become cancerous.

Changes (mutations) in genes occur dur ing car cinogenesis.

Changes (mutations) in genes can cause normal controls in cells to break down. When this
happens, cells do not die when they should and new cells are produced when the body does not
need them. The buildup of extra cells may cause a mass (tumor) to form.

Tumors can be benign or malignant (cancerous). Malignant tumor cells invade nearby tissues and
spread to other parts of the body. Benign tumor cells do not invade nearby tissues or spread.

What causes gene mutations/factor s that incr ease the r isk of cancer ?
Gene mutations can occur for sever al r easons:
1. Gene mutations you'r e bor n with. You may be born with a genetic mutation that you

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inherited from your parents. This type of mutation accounts for a small percentage of
cancers.

2. Gene mutations that occur after birth. Most gene mutations occur after you're born and
aren't inherited. The mutations are caused by e.g. as smoking, radiation, viruses, cancer­
causing chemicals, diet, obesity, hormones, chronic inflammation and a lack of exercise.

 Cigarette Smoking and Tobacco Use

Tobacco use is strongly linked to an increased risk for many kinds of cancer. Smoking
cigarettes is the leading cause of the following types of cancer:

 Acute myelogenous leukemia (AML), Bladder cancer., Esophageal cancer, Renal


cancer, Pelvis cancer, Rectum cancer, Liver cancer, Mouth cancer, Kidney cancer,
Lung cancer, Colon cancer, Oral cavity/nasal cavity cancer., Pancreatic cancer,
Stomach cancer.

 Infections

Certain viruses and bacteria are able to cause cancer. Viruses and other infection ­causing


agents cause more cases of cancer in the developing world (about 1 in 4 cases of cancer)
than in developed nations (less than 1 in 10 cases of cancer). Examples of cancer­causing
viruses and bacteria include:

 Human papillomavirus (HPV) increases the risk for cancers of


the cervix, penis, vagina, anus
 Hepatitis B and hepatitis C viruses increase the risk for liver cancer.
 Helicobacter pylori increases the risk for gastric cancer.
 Aflatoxins(toxins in moldy peanuts or grain)­liver cancer

Two vaccines to prevent infection by cancer­causing agents have already been developed


and approved by theU.S. Food and Drug Administration (FDA). One is a vaccine to
prevent infection with hepatitis B virus. The other protects against infection with strains
of human papillomavirus (HPV) that cause cervical cancer.

 Radiation

Being exposed to radiation is a known cause of cancer. There are two main types of
radiation linked with an increased risk for cancer:

Ultraviolet radiation from sunlight: This is the main cause of nonmelanoma skin cancers.

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Ionizing radiation including:
o Medical radiation from tests to diagnose cancer such as x­rays, CT
scans, fluoroscopy, and nuclear medicine scans.
o Radon gas in our homes.

Ionizing radiation causes leukemia, thyroid cancer, and breast cancer in women. Ionizing


radiation also causes cancers of the lung, stomach, colon, esophagus, bladder, andovary.
Being exposed to radiation from diagnostic x­rays increases the risk of cancer in patients
and x­raytechnicians.

The growing use of CT scans over the last 20 years has increased exposure to ionizing
radiation. The risk of cancer also increases with the number of CT scans a patient has and
the radiation dose used each time.

 Immunosuppressive Medicines
Immunosuppressive medicines are linked to an increased risk of cancer. These medicines lower
the body’s ability to stop cancer from forming. For example, immunosuppressive medicines may
be used to keep a patient from rejecting an organ transplant.

 Alcohol

Studies have shown that drinking alcohol is linked to an increased risk of the following
types of cancers: Oral, Esophageal cancer., Breast cancer, Colorectal cancer (in men),
Drinking alcohol may also increase the risk of liver cancer and female colorectal cancer.

 Physical Activity

Studies show that people who are physically active have a lower risk of certain cancers
than those who are not

Studies show a strong link between physical activity and a lower risk of colorectal
cancer. Some studies show that physical activity protects against postmenopausal breast
cancer and endometrial cancer.

 Obesity

Studies show that obesity is linked to a higher risk of the following types of cancer:
Postmenopausal breast cancer, Colorectal cancer, Endometrial cancer, Esophageal
cancer, Kidney cancer, Pancreatic cancer. Some studies show that obesity is also a risk
factor for cancer of the gallbladder.
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 Environmental Risk Factors

Being exposed to chemicals and other substances in the environment has been linked to
some cancers:

Links between air pollution and cancer risk have been found. These include links
between lung cancer and secondhand tobacco smoke, outdoor air pollution, chromium
and asbestos.
Drinking water that contains a large amount of arsenic has been linked to skin, bladder,
and lung cancers.

 Diet ­
Diets contain both inhibitors and enhancers of carcinogenesis. Examples of dietary
carcinogen inhibitors include: antioxidants (e.g. vitamin C, vitamin E, selenium, and
carotenoids) and phytochemicals. Dietary enhancers of carcinogenesis may be the fat in
red meat or the polycyclic aromatic hydrocarbons that form with the grilling of meat at
high heat
Some studies have shown that a diet high in fat, proteins, calories, and red meat increases
the risk of colorectal cancer. Some studies show that fruits and non­starchy
vegetables may protect against cancers of the mouth, esophagus, and stomach. Fruits may
also protect against lung cancer.

Dietar y factor s that contr ibute to incr eased r isk of cancer


Over Consumption of Ener gy (Calor ies)
Eating too much food is one of the main risk factors for cancer. This can be shown two ways:
i. By the additional risks of malignancies caused by obesity,
ii. By the protective effect of eating less food.

Overweight and obesity account for 14 percent of all cancer deaths (esophagus, colon and
rectum, liver, gallbladder, pancreas, kidney, stomach (in men), prostate, breast, uterus, cervix,
and ovary) in men and 20 percent of those in women
Glucose Metabolism
Refined sugar is a high energy, low nutrient food – junk food. "Unrefined" sugar (honey,
evaporated cane juice, etc) is also very concentrated and is likely to contribute to the same
problems as refined sugar. Refined wheat flour products are lacking the wheat germ and bran, so
they have 78 percent less fiber, an average of 74 percent less of the B vitamins and vitamin E,
and 69 percent less of the minerals.
Some case control studies have found consistent increased risk of a high glycemic load (index)
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with gastric, upper aero digestive tract, endometrial, ovarian, colon or colorectal cancers
Low Fiber
Unrefined plant foods typically have an abundance of fiber. Dairy products, eggs, and meat all
have this in common – they contain no fiber. Refined grain products also have most of the
dietary fiber removed from them. So, a diet high in animal products and refined is low in fiber.
Refined grains have been found to be associated with increased risk of rectal cancer.
Red Meat
Red meat has been implicated in colon and rectal cancer. In some studies, meat and the
heterocyclic amines formed in cooking have been correlated to breast cancer.
Omega 3:6 Ratio Imbalance
In animal studies, omega 3 fats (alpha­linolenic acid, EPA, DHA) have been shown to be
protective from cancer, while omega 6 fats (linoleic acid, arachidonic acid) have been found to
be cancer promoting fats.
Flax seed
Flax seed is an excellent source of dietary fiber, omega 3 fat (as alpha­linolenic acid), and
lignans. The lignans in flax seed are metabolized in the digestive tract to enterodiol and
enterolactone, which have estrogenic activity. In fact, flax seed is a more potent source of
phytoestrogens than soy products, as flax seed intake caused a bigger change in the excretion of
2­hydroxyestrone compared to soy protein.
Studies have found flax seed to be protective against cancer
Fr uits and vegetables
The consumption of fruits and vegetables may provide some benefits in protecting against the
development of cancer. Fruits and vegetables contain both nutrients and phytochemicals with
antioxidant activity, and these substances may prevent or reduce the oxidative reactions that
cause DNA damage.
Phytochemicals may also help to inhibit carcinogen production in the body, enhance immune
functions that protect against cancer development or promote enzyme reactions that inactivate
carcinogens.
The B vitamin folate, which is provided by certain fruits and vegetables plays roles in DNA
synthesis and repair, thus inadequate folate intakes may allow DNA damage to accumulate.
Fruits and vegetables also contribute dietary fiber, which may help to protect against colon and
rectal cancers by diluting potential carcinogens in fecal matter and accelerating their removal
form the GI tract.
Summar y: Nutr ition­r elated factor s that influence cancer r isk

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Nutr ition­r elated factor s Cancer sites


Factor s that may incr ease cancer r isk
Obesity Esophagus, colon, rectum, pacrease,
gallbladder, kidney, breast (postmenopausal),
endometrium
Red meat, processed meats Colon, rectum
Salted and salt­preserved foods Stomach
Beta­carotene supplements Lung
High calcium diets (over 1500 mg daily) Prostate
Alcohol Mouth, pharynx, larynx, esophagus, colon,
rectum, liver, breast (postmenopausal)
Low level of physical activity Colon, breast (postmenopausal), endometrium
Factor s that may decr ease cancer r isk
Fruits and nonstarchy vegetables Lung, mouth, pharynx, larynx, esophagus,
stomach
Carotenoid­containing foods Lung, mouth, pharynx, larynx, esophagus
Tomato products Prostate
Allium vegetables (onion, garlic) Stomach, colon, rectum
Vitamin C – containing foods Esophagus
Folate – containing foods Esophagus
Fiber­ containing foods Colon, rectum
Milk an calcium supplements Colon, rectum
High level of physical activity Colon, breast (postmenopausal), endometrium

N/B. Food preparation methods are responsible for producing certain types of carcinogens.
Cooking meat, poultry, and fish at high temperatures (frying, broiling) causes the amino acids
and creatine in these foods to react together and form carcinogens. Carcinogens also accompany
the smoke that adheres to foods during grilling and are present in the charred surfaces of grilled
meat and fish.

N/B. Gene mutations occur frequently during normal cell growth. However, cells contain a
mechanism that recognizes when a mistake occurs and repairs the mistake. Occasionally, a
mistake is missed. This could cause a cell to become cancerous. Carcinogenesis often proceeds
slowly and continues for several decades.
Classification of cancer s
Cancers are classified by the tissues or cells from which they develop
 Adenocarcinomas – arise from glandular tissues
 Carcinomas – arise from epithelial tissues
 Leukemias – arise from white blood cell precursors
 Lymphomas – arise from lymphoid tissues
 Melanomas – arise from pigmented skin cells
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 Myelomas – arise from plasma cells in the bone marrow


 Sarcomas – arise from connective tissues, such as muscle or bone

All this has resulted into e.g. Cancer of the ureter, leukemia (Cancer of the blood and bone
marrow), Anal cancer, Basal cell carcinoma(Cancer of the skin), Gallbladder cancer, Breast
cancer, Carcinoid tumors, Cervical cancer, Colon cancer, Esophageal cancer, Eye melanoma,
Stomach cancer, Vaginal cancer, Tonsil cancer, Tongue cancer, Thyroid cancer, Throat cancer,
Testicular cancer, Prostrate cancer, Small bowel cancer, Skin cancer, Kidney cancer, Rectal
cancer, Osteosarcoma, Ovarian cancer, Pancreatic cancer, Oral/ Mouth cancer, Male breast
cancer, Lip cancer, Liver cancer. Lung cancer, Head and neck cancer e.t.c

Consequences of cancer
Nonspecific effects of cancer include:
 Anorexia
 Lethargy
 weight loss/wasting
 night sweats
 fever

NB: During the early stages, many cancers produce no symptoms, and the person may be
unaware of the threat to health.
 Wasting associated with cancer
 Anorexia, muscle wasting, weight loss, anemia and fatigue typify cancer cachexia.

Cancer cachexia – Is a multifactorial syndrome defined by an ongoing loss of skeletal muscle


mass (with or without loss of fat mass) that cannot be fully reversed by conventional nutritional
support and leads to progressive functional impairment
 In addition to weight loss, cancer patients often experience loss of lean body mass, or
muscle mass. Loss of muscle mass can result in decreased immunity, increased
infections, increased skin breakdown, decreased healing, and increased mortality.

How is wasting is br ought about?


 Metabolic changes
Cancer patients exhibit an increased rate of protein turnover but reduced muscle protein
synthesis. Muscle contributes amino acids for glucose production, further depleting the
body’s supply of protein. Triglyceride breakdown increases, elevating serum lipids. Many
patients also develop insulin resistance.
 Anor exia and r educed food intake
Anorexia is a major contributor to the wasting associated with cancer. Some factors that
contribute to anorexia or otherwise reduce food intake include:
 Chronic nausea and early satiety
 Fatigue
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 Pain
 Mental stress
 Gastrointestinal obstructions e.g. a tumor obstructing a portion of the GI tract
 Effects of cancer therapies – chemotherapy and radiation treatments for cancer
frequently have side effects that make food consumption difficult, such as nausea,
vomiting, altered taste perceptions, mouth sores, inflammation of mucosal tissue,
abdominal pain or discomfort, and diarrhea

Tr eatments for cancer


Treatment for cancer include: sur ger y, chemother apy, r adiation ther apy, or any combination
of the thr ee; with the aim to:
­ Remove cancer cells
­ Prevent further tumor growth
­ Alleviate symptoms

(i) Sur ger y – is performed to remove tumors, determine the extent of cancer, and protect
nearby tissues
The acute metabolic stress caused by surgery raises protein and energy needs and can
exacerbate wasting. Surgery also contributes to pain, fatigue, and anorexia.
(ii) Chemother apy – relies on use of drugs to treat cancer, and is used to inhibit tumor
growth, shrink/localized tumors before surgery, and prevent or eradicate metastasis. Some
cancer drugs interfere with the process of cell division; others sterilize cells that are in a
resting phase and not actively dividing.
(iii) Radiation ther apy – treats cancer by bombarding cancer cells with X­rays, gamma rays,
or various atomic particles. These treatments damage cellular DNA and cause cell death.
It can cause damage of healthy tissues and sometimes has long term detrimental effects on
nutrition status. Radiation to the head and neck area can damage the salivary glands and taste
buds, causing inflammation, dry mouth, and reduced sense of taste.
(iv) Hematopoietic stem cell tr ansplantation – replaces the blood­forming stem cells that
have been destroyed by high­dose chemotherapy or radiation therapy. These procedures may
be used to treat leukemia, lymphomas and multiple myeloma.
(v) Biologic Ther apies – Use of biological molecules that stimulate immune responses
against cancer cells (also called immunotherapy). These substances include antibodies,
cytokines, and other proteins that strengthen the body’s immune defenses, enable the
destruction of cancer cells, or interfere with cancer development in some way. Many of these
treatments can cause anorexia, GI symptoms, and general discomfort, reducing a person’s
ability or desire to consume adequate amounts of food.

(vi) Nutr ition Ther apy –Use of diet to improve patients’ nutritional status and help patients
to maintain body weight, maintain lean body mass, better tolerate treatment, and improve
quality of life. Cancer patients face many challenges, including poor nutritional status,
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weight loss, and malnutrition For some patients, the nutritional deficits can proceed to cancer
cachexia, a specific form of malnutrition characterized by loss of lean body mass, muscle
wasting, and impaired immune, physical, and mental function

The objective of nutr ition ther apy for cancer patients ar e:


 To minimize loss of weight and muscle tissue
 Correct deficiencies
 Provide a diet that patients can tolerate and enjoy despite the complications of illness

Pr oper nutr ition helps patients maintain weight, toler ate tr eatment, maximize outcomes,
and impr ove quality of life

 Pr otein and ener gy


 For maintenance of body weight and lean tissue, suggest 1.0 to 1.5 g protein/kg body
weight; and 25­35 kcal/kg body weight daily.

 For weight regain and repletion of muscle tissue, suggest 1.5 to 2.0 g protein/kg body
weight; and 35 to 45 kcal/kg body weight daily.

 Increase calories e.g. by frying foods and using gravies, mayonnaise, and salad dressings.
Supplements high in calories and protein can also be used.

 Choose high­protein and high­calorie foods to increase energy and help wounds heal.
Good choices include: eggs, cheese, whole milk, ice cream, nuts, peanut butter, meat,
poultry, and fish.

Although weight loss is a problem for many cancer patients, breast cancer patients often gain
weight. The weight gain occurs during the first two years after breast cancer diagnosis and is
associated with an increase in total body fat. Thus, there is need to help these patients avoid
unnecessary weight gain.
 Enter al and par enter al nutr ition suppor t

Nutrition support is used in limited situations during cancer treatment. Generally, tube feeding
and parenteral nutrition are provided to patients who have long­term or permanent
gastrointestinal impairment or are experiencing complications that interfere with food intake.
 Enteral nutrition (feeding liquid through a tube into the stomach or intestines), parenteral
nutrition (feeding through a catheter into the bloodstream).

 Nutr ition ther apy for side effects of cancer tr eatments and the caner itself

Loss of appetite : May be due to the cancer itself, tr eatment and psychological factor s
 Eat small, frequent, high­calorie meals and snacks such as juices, soups, milk, shakes, and fruit
smoothies at regular times each day(every 2hours)
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 Add extra protein and calories to food.


 Eat the largest meal at the time of day when you feel the best
 Include nutrient dense foods in meals, and consume them before other foods
 Indulge in favorite foods throughout the day. Serve foods attractively
 Avoid drinking large amounts of liquids before or with meals
 Eat in relaxed and pleasant environment. Eat with family members and friends when
possible
 Listen to your favourite music or enjoy a TV or radio program while eating
 Ask your doctor about appetite enhancing medications

Types of foods ar e usually r ecommended

 Cheese and crackers (a baked food typically made from flour. Flavorings or seasonings,
such as herbs, seeds, and/or cheese, may be added to the dough or sprinkled on top before
baking), Muffins, Puddings, Nutritional supplements, Milkshakes, Yogurt, Ice cream,
Powdered milk added to foods such as pudding, milkshakes, or any recipe using milk,
Finger foods (handy for snacking) such as deviled eggs, cream cheese or peanut butter on
crackers or celery, or deviled ham on crackers, Chocolate.

When food don’t just taste right/ Alterations of taste and smell: May be due to the cancer
itself, radiation, dental problems, chemotherapy infections (thrush) and medications
Taste dysfunction can result in food avoidance and dislike that may result into weight loss
 Brush teeth or use mouthwash, or rinse the mouth before eating
 Eat small, frequent meals and healthy snacks.
 Be flexible. Eat meals when hungry rather than at set mealtimes.
 Try favorite foods.
 Plan to eat with family and friends.
 Have others prepare the meal.
 Try new foods when feeling best.
 Use sugar­free lemon drops, gum, or mints when experiencing a metallic or bitter taste in
the mouth.
 Add spices and sauces to foods.
 Consume foods chilled or at room temperature.
 Use plastic utensils rather than metal eating utensils if foods taste metallic
 Choose eggs, fish, poultry and milk products instead of meats
 Add spices or flavorings to foods. Citrus may be tolerated well if no mouth sores or
mucositis/stomatitis is present.
 Experiment with sauces, seasonings, herbs, spices, and sweeteners to improve food taste
and flavor
 Save your favorite foods for times when you are not feeling nauseated
Nauseated a lot of the time and sometimes need to vomit

Nausea can affect the amount and types of food eaten during treatment. Eating before

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treatment is important, as well as finding foods that do not trigger nausea.

Frequent triggers for nausea include spicy foods, greasy foods, or foods that have strong odors.
 If nausea comes from chemotherapy treatment, then avoid eating for at least hours before
treatment
 Consume your largest meal at a time when you are least likely to feel nauseous
 Try consuming meals, and eat slowly. Experiment with foods to see if some foods cause
nausea more than others
 Frequent eating, and slowly sipping on fluids throughout the day may help.
 Eat dry foods such as crackers, breadsticks, or toast, throughout the day.
 Sit up or recline with a raised head for 1 hour after eating.
 Eat bland, soft, easy­to­digest foods rather than heavy meals.
 Avoid eating in a room that has cooking odors or is overly warm; keep the living space
comfortable but well ventilated.
 Avoid foods and meals that have strong odors or are fatty, greasy or gas forming
Pr oblems with chewing and swallowing food
 Experiment with food consistencies to find the ones you can manage best. Thin liquids, dry
foods, and sticky foods (such as peanut butter) are often difficult to swallow
 Add sauces and gravies to dry foods
 Drink fluids during meals to ease chewing and swallowing
 Try using a straw to drink liquids. Experiment with beverage thickness if you cannot
tolerate thin beverages
 Tilt head forward and backward to see if you can swallow more easily when your head is
positioned differently
Dr y mouth/xer ostomia: May be due r adiation dir ected at the head and neck, and
medications
Dry mouth may affect speech, taste sensation, ability to swallow, and use of oral
prostheses (is an artificial device that replaces a missing body part, which may be lost
through trauma, disease, or congenital conditions). There is also an increased risk of
cavities and periodontal disease because less saliva is produced to cleanse the teeth and
gums
 Try eating chilled or frozen foods, they are often smoothening
 Try soft foods such as ice cream, milk shakes, bananas, mashed potatoes, macaroni etc.
mix dry foods with sauces or gravies
 Cut foods into smaller pieces, so they are less likely to irritate the mouth
 Avoid foods irritate mouth sores, such as citrus fruits and juices, tomatoes & products,
spicy foods, foods that are salty, foods with seeds that can scrape the sores and coarse
foods such as raw vegetables, crackers, corn chips and toast
 Use straw for drinking liquids in order to bypass the sores
Dr y mouth
 Rinse mouth with warm salt water or mouthwash frequently. Avoid using mouthwash/rises
that contains alcohol
 Drink small amounts of liquid frequently between meals­plenty of liquids (25­30 mL/kg
per day) Perform oral hygiene at least 4 times per day (after each meal and before
bedtime).

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 Brush and rinse dentures after each meal.


 Keep water handy at all times to moisten the mouth.
 Consume very sweet or tart foods and beverages, which may stimulate saliva.
 Contact your doctor/pharmacist about medications or saliva substitute that can help a dry
mouth condition
 Use sour candy or chewing gum to stimulate the flow of saliva
 Slip fluids frequently while eating. Add broth, sauces, gravies, butter/margarine to foods
 Make sure to brush teeth and floss regularly to prevent tooth decay and oral infections
Constipation
Constipation is defined as fewer than three bowel movements per week. It is a very common
problem among individuals with cancer and may result from lack of adequate fluids or
dehydration, lack of fiber in the diet, physical inactivity or immobility, anticancer therapies
such as chemotherapy, and medications used in the treatment of side effects of anticancer
therapy such as antiemetics and opioids (medications that relieve pain).

 Drink plenty of fluids. Try warm fluids, especially in the morning


 Eat more fiber: whole­grain breads and cereals, nuts, fresh fruits and vegetables, prunes,
and prune juices. Avoid refined carbohydrate foods such as white bread, oatmeal, corn,
pears, popcorn, broccoli, carrots, cabbage, cauliflower, beans, oranges, popcorn, onions,
white rice and pasta. The recommended fiber intake is 25 to 35 grams per day. Fiber
should be gradually added to the diet, and adequate fluids must be consumed at the same
time.
 Engage in physical activity regularly

[Note: *These food items may cause gas; products containing alpha­galactosidase enzyme may be
helpful.]

Diar r hea: May be due r adiation, chemother apy, gastr ointestinal sur ger y, or emotional
distr ess
 To avoid dehydration and hypokalemia, drink plenty of fluids throughout the day. Salty
broths and soups, bananas, diluted fruit juices, and sports drinks are good choices.
 Avoid hot or cold liquids, caffeine and alcohol containing beverages. For severe diarrhea
try oral rehydration formulas that are commercially prepared
 Avoid foods and beverages that increase gas, such as legumes e.g. beans, onions,
vegetables of the cabbage family, foods that contain sorbitol or mannitol(gum made with
alcohol), chewing gum and carbonated beverages
 Drink plenty of fluids through the day; room­temperature fluids may be better tolerated, at
least 1 cup of liquid after each loose bowel movement.
 Limit milk to 2 cups or eliminate milk and milk products until the source of the problem is
determined.
 Try using lactase enzyme replacements when you use milk products in case you are
experiencing lactose intolerance. E.g. yogurt may be easier to tolerate than milk
 Avoid fatty foods if you are fat intolerant
 Eat small, frequent meals instead of large ones. Try consuming cool or lukewarm foods
instead of very cold or hot foods
 Ask your doctor about using bulk­forming agent or antidiarrheal medication

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Hydr ation and dehydr ation


 Drink 8 to 12 cups of liquids a day; take a water bottle whenever leaving home. It is
important to drink even if not thirsty, as the thirst sensation is not a good indicator of fluid
needs.
 Limit consumption of caffeine­containing products, including colas and other caffeinated
sodas, coffee, and tea (both hot and cold).
 Drink most liquids after and/or between meals to increase overall consumption of both
liquids and solids
 Use antiemetics (a drug that is effective against vomiting and nausea ) for relief from
nausea and vomiting

Mucositis/stomatitis
 Stomatitis, or a sore mouth, can occur when cells inside the mouth, which grow and divide
rapidly, are damaged by treatment such as bone marrow transplantation, chemotherapy,
and radiation therapy. These treatments may also affect rapidly dividing cells in the bone
marrow, which may make patients more susceptible to infection and bleeding in their
mouth
 Eat soft foods that are easy to chew and swallow such as soft fruits; bananas, pear,
watermelon; cottage cheese; mashed potatoes; macaroni and cheese; custards; puddings;
gelatin; milkshakes; scrambled eggs; oatmeal or other cooked cereals; pureed or mashed
vegetables such as peas and carrots; and pureed meats.
 Avoid foods that irritate the mouth, including citrus fruits and juices such as orange,
grapefruit, or tangerine; spicy or salty foods;
 Cook foods until soft and tender.
 Cut foods into small pieces.
 Use a straw to drink liquids. Eat foods cold or at room temperature; hot and warm foods
can irritate a tender mouth.
 Practice good mouth care, which is very important because of the absence of the
antimicrobial effects of saliva.
 Increase the fluid content of foods by adding gravy, broth, or sauces.
 Supplement meals with high­calorie, high­protein drinks.
 Numb the mouth with ice chips or flavored ice pops.

Neutr openia
 People with cancer may have a low white blood cell count for a variety of reasons, some
of which include radiation therapy, chemotherapy, or the cancer itself. Patients who have a
low white blood cell count are at an increased risk for developing an infection.
 Suggestions for helping people pr event infections r elated to neutr openia include the
following:
 Check expiration dates on food and do not buy or use if the food is out of date.

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 Do not buy or use food in cans that are swollen, dented, or damaged.
 Thaw foods in the refrigerator or microwave—never thaw foods at room temperature.
 Cook foods immediately after thawing.
 Refrigerate all leftovers within 2 hours of cooking and eat them within 24 hours.
 Keep hot foods hot and cold foods cold.
 Avoid old, moldy, or damaged fruits and vegetables.
 Cook all meat, poultry, and fish thoroughly; avoid raw eggs or raw fish.
 Buy individually packaged foods, which are better than larger portions that result in
leftovers.
 Limit exposure to large groups of people and people who have infections.
 Wash hands frequently to prevent the spread of bacteria.
 This list may be modified after chemotherapy or when blood count returns to norm

Effects of Cancer Tr eatment on Nutr ition


Sur ger y and Nutr ition (Sur ger y incr eases the body's need for nutr ients and ener gy)
Surgery increases the body's need for nutrients and energy for wound healing,
o
fight infection, and recover from surgery. If the patient is malnourished before
surgery, it may cause problems during recovery, such as poor healing or infection.
For these patients, nutrition care may begin before surgery.
o Surgery to the head, neck, esophagus, stomach, or intestines may affect nutrition
as they cause problems with Chewing, Swallowing, Tasting or smelling food,
Making saliva, Seeing. Stay away from carbonated drinks (such as sodas) and
foods that cause gas, such as: Beans, peas, broccoli, cabbage, Brussels sprouts,
green peppers, radishes and cucumbers. .
Nutrition therapy may include the following:
 Nutritional supplement drinks.
 Enteral nutrition (feeding liquid through a tube into the stomach or intestines).
 Parenteral nutrition (feeding through a catheter into the bloodstream).
 Medicines to increase appetite.

Chemother apy and Nutr ition


o Chemotherapy may cause side effects that cause problems with eating
and digestion. When more than one anticancer drug is given, more side effects
may occur or they may be more severe.
o The following side effects are common: Loss of appetite; inflammation, and sores
in the mouth; changes in the way food tastes; feeling full after only a small
amount of food; nausea; vomiting; diarrhea; constipation.

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Nutrition therapy may include the following:


 Nutrition supplement drinks between meals.
 Enteral nutrition (tube feedings).
 Changes in the diet, such as eating small meals throughout the day.

Radiation Ther apy and Nutr ition

Radiation ther apy can affect cancer cells and healthy cells in the tr eatment ar ea.
Radiation therapy can kill cancer cells and healthy cells in the treatment area. The
amount of damage depends on the part of the body that is treated; and the
total dose of radiation and how it is given.
Radiation ther apy may affect nutr ition.
Radiation therapy to any part of the digestive system often has side effects that cause nutrition
problems. Most of the side effects begin a few weeks after radiation therapy begins and go away
a few weeks after it is finished. Some side effects can continue for months or years after
treatment ends. The following are some of the more common side effects:
 For radiation therapy to the head and neck

Loss of appetite.
o
o Changes in the way food tastes.
o Pain when swallowing.
o Dry mouth or thick saliva.
o Sore mouth and gums.
o Narrowing of the upper esophagus, which can cause choking, breathing, and
swallowing problems.
 For radiation therapy to the chest

Infection of the esophagus.


o
o Trouble swallowing.
o Esophageal reflux (a backward flow of the stomach contents into the esophagus).
 For radiation therapy to the abdomen or pelvis
o Diarrhea.
o Nausea.
o Vomiting.
o Inflamed intestines or rectum
o A decrease in the amount of nutrients absorbed by the intestines.
Radiation therapy may also cause tiredness, which can lead to a decrease in appetite.
Nutr ition ther apy can help r elieve the nutr ition pr oblems caused by r adiation ther apy.
Nutrition therapy during radiation treatment can help the patient get enough protein and calories
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to get through treatment, prevent weight loss, help wound and skin healing, and maintain general
health. Nutrition therapy may include the following:
 Nutritional supplement drinks between meals.
 Enteral nutrition (tube feedings).
 Changes in the diet, such as eating small meals throughout the day.
Patients who receive high­dose radiation therapy to prepare for a bone marrow transplant may
have many nutrition problems and should see a dietitian for nutrition support.
Biologic Ther apy and Nutr ition
Biologic ther apy may affect nutr ition.
The side effects of biologic therapy are different for each patient and each type of biologic agent
The following nutrition problems are common:
 Fever.
 Nausea.
 Vomiting.
 Diarrhea.
 Loss of appetite.
 Tiredness.
 Weight loss

Stem Cell Tr ansplant and Nutr ition


Stem cell transplant patients have special nutrition needs.

Chemotherapy, radiation therapy, and medicines used for a stem cell transplant may cause side
effects that keep a patient from eating and digesting food as usual. Common side effects include
the following:
 Changes in the way food tastes.
 Dry mouth or thick saliva.
 Mouth and throat sores.
 Nausea.
 Vomiting.
 Diarrhea.
 Constipation.
 Weight loss and loss of appetite.
 Weight gain.

Nutr ition ther apy is ver y impor tant for patients who have a stem cell tr ansplant.
Transplant patients have a very high risk of infection. High doses of chemotherapy or radiation
therapy decrease the number of white blood cells, which fight infection. It is especially important
that transplant patients avoid getting infections.
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Patients who have a transplant need plenty of protein and calories to get through and recover
from the treatment, prevent weight loss, fight infection, and maintain general health. It is also
important to avoid infection from bacteria in food. Nutrition therapy during transplant treatment
may include the following:
 A diet of cooked and processed foods only, because raw vegetables and fresh fruit may
carry harmful bacteria.
 Guidelines on safe food handling.
 A specific diet based on the type of transplant and the part of the body affected by cancer.
 Parenteral nutrition (feeding through the bloodstream) during the first few weeks after the
transplant, to give the patient the calories, protein, vitamins, minerals, and fluids they
need to recover.

Nutr ition in Advanced Cancer

Advanced cancer is often associated with cachexia. Individuals diagnosed with cancer may
develop new, or worsening, nutrition­related side effects as cancer becomes more advanced. The
most prevalent symptoms in this population are the following:

 Weight loss.
 Early satiety.
 Bloating.
 Anorexia.
 Constipation.
 Xerostomia.
 Taste changes.
 Nausea.
 Vomiting.
 Dysphagia.

As defined by the WHO, palliative car e is an approach that improves the quality of life of
patients and their families facing the problems associated with life­threatening illness, through
treatment of pain and other problems, physical, psychosocial, and spiritual.

The goal of palliative care is to give relief of symptoms that are bothersome to the patient.
Although some of the symptoms listed above can be effectively treated, anorexia, though
common, is a symptom that is often not noted as problematic for most terminally ill patients but
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is distressing to most family members; this distress may vary according to cultural factors.
Terminally ill patients lack hunger, and of those who do experience hunger, the symptom is
relieved with small amounts of oral intake.

Decreased intake, especially of solid foods, is common as death becomes imminent. Individuals
usually prefer and tolerate soft­moist foods and refreshing liquids (full and clear liquids). Those
who have increased difficulty swallowing have less incidence of aspiration with thick liquids
than with thin liquids.

Dietary restriction is not usually necessary, as intake of prohibited foods (e.g., sweets in the
diabetic patient) is insufficient to be of concern. As always, food should continue to be treated
and viewed as a source of enjoyment and pleasure. Eating should not just be about calories,
protein, and other macronutrient and micronutrient needs.

TOPIC: MUSCULOSKELETOL DISORDERS

MUSCULOSKELETAL DISORDER

 Musculoskeletal disorders are injuries and disorders that affect the human body’s
movement or musculoskeletal system (i.e. muscles, tendons, ligaments, nerves, discs,
blood vessels, etc.).
 Musculoskeletal disorders include arthritis, gout, lupus, fibromyalgia, osteoporosis,
osteomalacia e.tc
 There are over 100 types of arthritis. The most common forms are osteoarthritis
(degenerative joint disease) and rheumatoid arthritis.

 Musculoskeletal disorders are one of the most common work­related ailments.


 Musculoskeletal disorders usually affect the back, neck, shoulders and upper limbs, but
lower limbs can also be affected. In more chronic cases, they can even lead to disability
and the need to give up work.

Causes of musculoskeletal disor der s

There is usually no single cause of MSDs; various factors often work in combination. Physical
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causes and risk factors include:

 Handling loads, especially when bending and twisting


 Repetitive or forceful movements
 Awkward and static postures
 Vibration, poor lighting or cold working environments
 Fast­paced work
 Prolonged sitting or standing in the same position

Types of musculoskeletal disor der s

Arthritis.

Arthritis comes from the Greek word arthron meaning “joint”

Arthritis therefore refers to an inflammation of one or more joints. Symptoms include Pain,
stiffness, swelling, redness, and decreased range of motion

The most common forms are osteoarthritis (degenerative joint disease) and rheumatoid arthritis

Rheumatoid ar thr itis

 Rheumatoid arthritis is an autoimmune chronic inflammatory disorder that mostly affects


the joints of the hips, hands, wrists, elbows, knees, ankles, arms, and feet, causing them
to become extremely painful, stiff, and even deformed but in some people, the condition
also can damage a wide variety of body systems, including the skin, eyes, lungs, heart
and blood vessels. Severe damage of the joint can result into disability.

Cause

It is an autoimmune disorder that occurs when your immune system mistakenly attacks your own
body's tissues. This creates inflammation that causes the tissue that lines the inside of joints (the
synovium) to thicken (inflamed) and secretes more fluid, resulting in swelling of the joints, and
pain in and around the joints.

The synovium makes a fluid that lubricates joints and helps them move smoothly.

If inflammation goes unchecked, it can damage cartilage, the elastic tissue that covers the ends of
bones in a joint, as well as the bones themselves. Over time, there is loss of cartilage, and the
joint spacing between bones can become smaller. Joints can become loose, unstable, painful and
lose their mobility. Joint deformity also can occur.

The joint effect is usually symmetrical. That means if one knee or hand if affected, usually the
other one is, too. Because RA also can affect body systems, such as the cardiovascular or
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respiratory systems, it is called a systemic disease. Systemic means “entire body.” 

Unlike the wear­and­tear damage of osteoarthritis, rheumatoid arthritis affects the lining of your
joints, causing a painful swelling that can eventually result in bone erosion and joint deformity.

The inflammation associated with rheumatoid arthritis is what can damage other parts of the
body as well.

Rheumatoid arthritis symptoms and signs include


 joint pain, such as in the joints of the feet, hands, and knees,
 swollen joints,
 afever,
 limping,
 polyarthritis,
 Non joint effects such as anemia due to chronic disease, decrease in saliva secretions and
dysphagia that can result into malnutrition

Medications

The types of medications recommended depend on the severity of the symptoms and how long
you've had rheumatoid arthritis.

 NSAIDs (Nonsteroidal anti­inflammatory drugs).They relieve pain and reduce


inflammation. Over­the­counter NSAIDs include ibuprofen and naproxen sodium
(Aleve). Stronger NSAIDs are available by prescription. Side effects may include ringing
in your ears, stomach irritation, heart problems, and liver and kidney damage.
 Ster oids. Corticosteroid medications, such as prednisone, reduce inflammation and pain
and slow joint damage. Side effects may include thinning of bones, weight gain and
diabetes.
 Disease­modifying antir heumatic dr ugs (DMARDs). These drugs can slow the
progression of rheumatoid arthritis and save the joints and other tissues from permanent
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damage. Common DMARDs include methotrexate (Trexall, Otrexup, Rasuvo),


leflunomide (Arava), hydroxychloroquine (Plaquenil) and sulfasalazine (Azulfidine).
 Dr ugs that tar get cytokines­cytokines are substances produced in tissues, that can cause
inflammatory changes in tissue cells( e.g. tumor necrosis factor and interleukin­1)

Side effects vary but may include liver damage, bone marrow suppression and severe
lung infections.

Ther apy

Your doctor may send you to a physical or occupational therapist who can teach you exercises to
help keep your joints flexible. The therapist may also suggest new ways to do daily tasks, which
will be easier on your joints. For example, if your fingers are sore, you may want to pick up an
object using your forearms.

Sur ger y

If medications fail to prevent or slow joint damage, surgery may be done to repair damaged
joints. Surgery may help restore your ability to use your joint. It can also reduce pain and correct
deformities.

Rheumatoid arthritis surgery may involve one or more of the following procedures:

 Synovectomy. Surgery to remove the inflamed synovium (lining of the joint).


Synovectomy can be performed on knees, elbows, wrists, fingers and hips.
 Tendon r epair . Inflammation and joint damage may cause tendons around your joint to
loosen or rupture. Your surgeon may be able to repair the tendons around your joint.
 J oint fusion. Surgically fusing a joint may be recommended to stabilize or realign a joint
and for pain relief when a joint replacement isn't an option.
 Total joint r eplacement. During joint replacement surgery, your surgeon removes the
damaged parts of your joint and inserts a prosthesis made of metal and plastic.

Surgery carries a risk of bleeding, infection and pain.

Nutr ition ther apy

Ener gy: Energy needs vary depending on individual needs. A high energy diet is needed
because of increased fever, sepsis, stressed of the disease skeleton injury or surgery

A high energy diet is also required if the patient is on physical therapy

Pr otein: Protein needs vary with protein status, surgical therapy, proteinuria, and nitrogen
balance. A well­nourished adult patient needs about 0.5 to 1 g of protein/kg/day during quit
disease periods. An increase to 1.5 to 2 g/kg/day is needed during active inflammatory disease
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periods.

Vitamin miner als. Adequate minerals and vitamins are required. Calcium and vitamin D may be
supplemented if the patient is undergoing steroid therapy or the disease is severe

Alter native medicine

Some common complementary and alternative treatments that have shown promise for
rheumatoid arthritis include:

 Fish oil. Some preliminary studies have found that fish oil supplements may reduce
rheumatoid arthritis pain and stiffness. Side effects can include nausea, belching and a
fishy taste in the mouth. Fish oil can interfere with medications.
 Plant oils. The seeds of evening primrose, borage and black currant contain a type of
fatty acid that may help with rheumatoid arthritis pain and morning stiffness. Side effects
may include nausea, diarrhea and gas.
 Tai chi. This movement therapy involves gentle exercises and stretches combined with
deep breathing. Many people also use tai chi to relieve stress in their lives. But don't do
any moves that cause pain.

Osteoar thr itis

 This is the milder and most common form of arthritis affecting millions of people
worldwide. It accounts for 60% to 70% of the joint diseases. It is sometimes called
degenerative joint disease or “wear and tear” because there is no inflammation involved.
 Osteoarthritis is a chronic condition that mostly affects older adults (over 40 years).
 It occurs when the protective cartilage of the bones wears down over time or when
cushion between joints breaks down leading to pain, stiffness and swelling.
 Although osteoarthritis can damage any joint in your body, the disorder most commonly
affects joints in your hands, wrist, knees, neck, hips and spine (back).
 Unlike many other forms of arthritis, such as rheumatoid arthritis and systemic lupus,
osteoarthritis does not affect other organs of the body.

Symptoms
 The main symptoms of osteoarthritis are joint pain and stiffness, particularly first thing
in the morning or after resting
 Some people also experience swelling, tender ness and a gr ating or cr ackling sound
when moving the affected joints. Affected joints may get swollen after extended activity.
 Other symptoms of osteoarthritis include bone spurs(feeling of hard lumps around the
affected joints)

The severity of osteoarthritis symptoms can vary greatly from person to person, and between
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different affected joints.

For some people, the symptoms can be mild and may come and go. Other people can experience
more continuous and severe problems which make it difficult to carry out everyday activities.

Almost any joint can be affected by osteoarthritis, but the condition most often causes problems
in the knees, hips and small joints of the hands.

In severe osteoarthritis, complete loss of cartilage causes friction between bones, causing pain at
rest or pain with limited motion.

Causes

Osteoarthritis has no specific cause. Several factors lead to the development of osteoarthritis
including:

 J oint injur y – overusing your joint when it hasn't had enough time to heal after an injury
or operation
 Other conditions (secondar y ar thr itis) – osteoarthritis can occur in joints severely
damaged by a previous or existing condition, such as rheumatoid arthritis or gout
 Age – your risk of developing the condition increases as you get older. It mostly occurs
in people aged 50 years or older
 Family histor y – osteoarthritis may run in families, although studies haven't identified a
single gene responsible
 Obesity/over weight – being obese puts excess strain on your joints, particularly those
that bear most of your weight, such as your knees and hips

In osteoarthritis, the protective cartilage on the ends of your bones breaks down, causing pain,
swelling and problems moving the joint. Bony growths can develop, and the area can become
inflamed (red and swollen).

Diagnosis

The diagnosis of osteoarthritis includes a medical history and a physical examination. These may
be followed by laboratory tests, X­rays, and a magnetic resonance imaging (MRI) scan.
Osteoarthritis may suspect if:

 you're aged 50 or older


 you have joint pain that gets worse the more you use your joints
 you have stiffness in your joints in the morning that lasts less than 30 minutes, or no
stiffness at all

If your symptoms are slightly different from those listed above, this may indicate another joint
condition. For example, prolonged joint stiffness in the morning can be a sign of rheumatoid
arthritis.

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Tr eatment

Osteoarthritis is a long­term condition and can't be cured, but it doesn't necessarily get any worse
over time and it can sometimes gradually improve. A number of treatments are also available to
reduce the symptoms.

Regular exer cise/ physical activity e.g. swimming, walking ar ound the neighbor hood

 One of the most beneficial ways to manage osteoarthritis is to get moving. While it may
be hard to think of exercise when the joints hurt, moving is considered an important part
of the treatment plan.
 Strengthening exercises build muscles around the affected joints, easing the burden on
those joints and reducing pain. Improve joint flexibility and reduce stiffness. Exercise
also help to reduce excess weight.

Losing weight if you'r e over weight.


 Excess weight adds additional stress to weight­bearing joints, such as the hips, knees,
feet and back.
 Losing weight can help people with osteoarthritis reduce pain and limit further joint
damage.
 The basic rule for losing weight is to eat fewer calories and increase physical activity

Wear ing suitable footwear

Medicines (Painkilling medications)

They are available as pills, syrups, creams or lotions, or they are injected into a joint. They
include:  

 Analgesics. These are pain relievers e.g. acetaminophen, opioids (narcotics).They are


available over­the­counter or by prescription.
 Nonster oidal anti­inflammator y dr ugs (NSAIDs). These are the most commonly used
drugs to ease inflammation and related pain. NSAIDs include aspirin, ibuprofen and
naproxen. They are available over­the­counter or by prescription. NSAIDs can cause
stomach upset, cardiovascular problems, bleeding problems, and liver and kidney damage
 Cor ticoster oids. Corticosteroids are powerful anti­inflammatory medicines. They are
taken by mouth or injected directly into a joint
 Hyalur onic acid. Hyaluronic acid occurs naturally in joint fluid, acting as a shock
absorber and lubricant. However, the acid appears to break down in people with
osteoarthritis. The injections are done in the hospital.

Occupational Ther apy

 An occupational therapist can help you discover ways to do everyday tasks or do your job
without putting extra stress on your already painful joint. For instance, a toothbrush with
a large grip could make brushing your teeth easier if you have finger osteoarthritis. A

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bench in your shower could help relieve the pain of standing if you have knee
osteoarthritis.

Tai chi and yoga.

 These movement therapies involve gentle exercises and stretches combined with deep
breathing.
 Many people use these therapies to reduce stress in their lives, and research suggests that
tai chi and yoga may reduce osteoarthritis pain and improve movement.
 When led by a knowledgeable instructor, these therapies are safe. Avoid moves that
cause pain in your joints.
 Massage and relaxation techniques can also help in reducing the pain

Sur ger y (joint r eplacement sur ger y)

 In a small number of cases, where the above treatments haven't helped or the damage to
the joints is particularly severe, surgery may be carried out to repair, strengthen or replace
a damaged joint, especially hips or knees.
 In joint replacement surgery (arthroplasty), your surgeon removes your damaged joint
surfaces and replaces them with plastic and metal parts. Surgical risks include infections
and blood clots. Artificial joints can wear out or come loose and may need to eventually
be replaced.

Sur gical and other pr ocedur es

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Knee osteotomy

Ar tificial hip


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Pr eventing osteoar thr itis

It's not possible to prevent osteoarthritis altogether. However, you may be able to minimize your
risk of developing the condition by avoiding injury and staying as healthy as possible.

 Exer cise
­Avoid exercise that puts strain on your joints and forces them to bear an excessive load,
such as running and weight training. Instead, try exercises such as swimming and cycling,
where your joints are better supported and the strain on your joints is more controlled.
­Try to do at least 150 minutes (2 hours and 30 minutes) of moderate­intensity aerobic
activity (such as cycling or fast walking) every week to build up your muscle strength
and keep yourself generally healthy.
 Postur e
­It can also help to maintain good posture at all times and avoid staying in the same
position for too long.
­If you work at a desk, make sure your chair is at the correct height, and take regular

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breaks to move around.


 Losing weight
­Being overweight or obese can increase the strain on your joints and increase your risk
of developing osteoarthritis. If you're overweight, losing weight may help lower your
chances of developing the condition.

Alter native medicine

Various complementary and alternative medicine may help with osteoarthritis symptoms.
Treatments that have shown promise for osteoarthritis include:

 Acupunctur e. Some studies indicate that acupuncture can relieve pain and improve
function in people who have knee osteoarthritis. During acupuncture, hair­thin needles
are inserted into your skin at precise spots on your body.
 Glucosamine and chondr oitin. Studies have been mixed on these nutritional
supplements. A few have found benefits for people with osteoarthritis, while most
indicate that these supplements work no better than a placebo.

Don't use glucosamine if you're allergic to shellfish. Glucosamine and chondroitin may
interact with blood thinners such as warfarin and cause bleeding problems.

 Avocado­soybean unsaponifiables. This nutritional supplement — a mixture of avocado


and soybean oils — is widely used in Europe to treat knee and hip osteoarthritis. It acts as
an anti­inflammatory, and some studies have shown it may slow down or even prevent

Osteopor osis

Osteoporosis is a bone disease as result of the body not forming new bone or of the body
reabsorbing too much bone, or both. It is characterized by low bone mass and deterioration of
bone tissue. This leads to increased bone fragility and risk of fracture (broken bones) as bones
become weak, particularly of the hip, spine, wrist and shoulder. So brittle that a fall or even mild
stresses like bending over or coughing can cause a fracture
 Osteoporosis literally leads to abnormally porous bone that is compressible, like a
sponge. This disorder of the skeleton weakens the bone and results in frequent fractures
(breaks)
 Osteoporosis is often known as “the silent thief” or “silent disease” because bone loss
occurs without symptoms.

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 Osteoporosis is sometimes confused with osteoarthritis, because the names are similar.
Osteoporosis is a bone disease; osteoarthritis is a disease of the joints and surrounding
tissue.
 Bone mass (bone density) decreases after 35 years of age, and bone loss occurs more
rapidly in women after menopause. In old age, osteoporosis is as a result of the body
reabsorbing too much bone
N/B. Calcium and phosphate are two minerals responsible for normal bone formation

Key r isk factor s for osteopor osis

 Genetics,
 Lack of exercise,
 Lack of calcium and vitamin D,
 Personal history of fracture as an adult,
 Cigarette smoking and excessive alcohol consumption
 Family history of rheumatoid arthritis,
 Low body weight and family history of osteoporosis.
 Age: The older you get, the greater the risk of osteoporosis
 Sex. Women are much more likely to develop osteoporosis than men. Older women who
are past menopause are at greater risk than young women/This is because of lowered sex
hormone, estrogen
 Body frame size. Men and women who have small body frames tend to have a higher risk
because they may have a higher less bone mass to draw from as they age
 Those who are on drugs for cancer, seizers, gastric reflux
 Thyroid hormone: Too much thyroid hormone can cause bone loss(hyperthyroidism)

Symptoms

There are typically no symptoms in the early stages of bone loss . But once bones have been
weakened by osteoporosis, you may have the following symptoms that include the following

 Back pain, caused by fracture or collapsed vertebra


 Loss of height over time
 A stopped posture
 A bone fracture that occurs much more easily than expected

Diagnosis

 Osteoporosis can be suggested by X­rays and confirmed by tests to measure bone density.

Tr eatments
 Medications
 Stopping use of alcohol and cigarettes
 Adequate exercise

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 Sufficient calcium, and vitamin D. This depends on age, sex and condition( pregnancy
and lactation) e.g. for adults aged 19 to 50 years, at least 1000 mg/day of calcium and 5
ug/day of vitamin D

Osteomalacia

 Osteomalacia refers to the softening of the bones, often caused by vitamin D deficiency.
Soft bones are more likely to bow and fracture than are harder, healthy ones
 Osteomalacia is not the same as osteoporosis, another bone disorder that also can lead to
borne fractures. Osteomalacia results from a defect in the bone­building process due to
vitamin D deficiency, while osteoporosis develops due to a weakening of previously
constructed bone. .
 Osteomalacia is most likely to occur in people with kidney, stomach, gallbladder or
intestinal disease and in those with cirrhosis of the liver.
 Osteomalacia is also known as the rickets for adults

Symptoms
 There are typically no symptoms in the early stages of osteomalacia. As osteomalacia
worsens, you may experience bone/aching pain that commonly affects the lower back,
pelvis, hips, legs and ribs. The pain may get worse at night , or when you are putting
weight on affected bones

Cause

Vitamin D deficiency

Diet Ther apy for Musculoskeletal

Ener gy: Energy needs vary widely and must be determined on individual basis and will depend
on increased metabolic activity factors such as stress of disease activity, sepsis, fever, skeletal
injury or surgery. If the client is receiving physical therapy, an additional physical activity factor
is used

Pr otein: Protein needs vary with protein status, surgical therapy, proteinuria and nitrogen
balance well­nourished adult patient needs about 0.5 to 1 g of protein/kg/day during quit disease
periods. An increase to 1.5 to 2g/kg/day

Vitamins and miner als: Standard recommendations for vitamins and minerals are used.
Specific supplementation may be used if needed, such as calcium and vitamin D if borne disease
is involved

Fat: A diet high in fat, especially saturated fat, may speed up the progression of knee
osteoarthritis

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