CHAPTER 3:

Infectious
and
Inflammator
y Disorders
EBOLA
 • known as Ebola Hemorrhage.

• Ebola Hemorrhagic Fever

• cause by a FILOVIRUSES

EBOLA • Rare and deadly disease caused by infection with

VIRUS
one of the Ebola virus strains.
• symptoms usually occurs rapidly and with both

DISEASE viruses, the course of illness often progresses rapidly

to profound hemorrhage, organ destruction, and

shock
• Mortality rate os 90%

• Recovery period is prolonged, with weakness,

malaisem and cachexia

• EBOLA VIRUS needs a host to survive abd creates a
MODE OF • Human to human transmission occurs
TRANSMISSION:
after exposure to blood or other body
fluids.
• Things that have the body fluids of an

infected person like clothes or sheets.

• Ebola enters the body through cuts in the

skin or when touching one’s eyes, nose

or mouth.
• Host – fruit bats of the Pteropodidae family

• Introduce into human through close contact with:

• a. blood
• b. secretions
• c. organ or other fluids of infected animals ( bat, chimpanzees, gorillas,

monkeys, forest antelope) found ill or dead in the rainforest.

• Close contact with patients.

• 5. Burial ceremonies that involve direct contact with the body of the

deceased.
• 6. People remain infectious as long as their blood contains the virus.

• Note: Pregnant women who get acute Ebola and recover from the disease

may still carry the virus in breast milk, or in pregnancy related fluids and
 • fever, high temperature
INITIAL (38.8C)
SYMPTOMS: • fatigue

• muscle pain

• headache

• sorethroat
• vomiting

• diarrhea

• internal and external bleeding

• rashes (hemorrhagic rash)

Incubation • Interval from infection with the

Period: virus to onset of symptoms is 2-21

days
• Humans are not infectious until

they develop symptoms

• A person with Ebola can only

spread the disease once they

have symptoms and as long as

their body contains the virus,

 • After recovering from Ebola, some people may have symptoms for
twoyears or longer.

Symptoms are:
a. feeling tired
b. headache
c. muscle and joint pain
d. eye pain and vision problems
e. weight gain
f. belly pain and loss of appetite
g. hair loss and skin problems
h. trouble sleeping
i. memory loss
j. hearing loss
k. depression and anxiety.
 • antibody-capture enzyme-linked immunosorbent

assay (ELISA)

Diagnosis • antigen-capture detection tests

• serum neutralization test
• reverse transcriptase polymerase chain reaction (RT-

PCR) assay
• electron microscopy
• virus isolation by cell culture.

• oral or IV fluids/ hydration

Treatment • Blood transfusion
• nutritional support
• oxygenation
Prevention and control
a. washing hands
b. avoiding touching the body fluids of people who have, or may have,
Ebola
c. not touching the bodies of people who have died from Ebola
d. Ebola vaccine (Ervebo vaccine) if they are at risk for the Zaire type of
Ebola.

Risk Reductions:
a. reducing the risk of wildlife-to-human transmission
b. reducing the risk of human-to-human transmission
c. outbreak containment measures, including safe and dignified burial of
the dead
d. reducing the risk of possible sexual transmission
e. reducing the risk of transmission from pregnancy related fluids and
tissue.
Standard precautions for Health Workers:
• Hand hygiene
• Respiratory hygiene
• use of personal protective equipment (to block splashes
or other contact with infected materials),
• safe injection practices
• safe burial practices.

Note:
Health-care workers caring for patients with suspected or
confirmed Ebola virus should apply extra infection control
measures to prevent contact with the patient’s blood and
body fluids and contaminated surfaces or materials such as
clothing and bedding.
WHO management:
1. Rehydration and the treatment of
symptoms improves survival.
2. WHO has made strong recommendations
for the use of two monoclonal antibody
treatments in treating Ebola:
• mAb114 (Ansuvimab; Ebanga)
• REGN-EB3 (Inmazeb).
MERS COV
Middle East Respiratory
Syndrome Coronavirus
MERS CoV
a newly discovered Betacoronavirus lineage C
that was first reported in Saudi Arabia in 2012
A zoonotic virus transmitted from animal to
humans
 Sign and Symptoms:
Mode of Transmission: • Fever
• Direct or Indirect contact with • Cough
camels, bats, goats, cow • Shortness of breath
• droplet through sneezing, • Pneumonia (common but not always
coughing present)
• Indirect transmission through • GI (diarrhea)
touching surfaces abd devices • Nausea and vomiting
• Kidney failure
contaminated with the virus

Incubation Period: Laboratory/Diagnostic Examination:

• Polymerase Chain Reaction Testing
• 14 days (PCR-RT)-with presence of antibodies
in blood 10 days after onset
symptoms
 Treatment:
• Supportive
Prevention and Control:
• Avoid contact with animals or sick animals
• Hand washing before and after touching animals
• Avoid consumption of raw or undercooked animal
products (high risk)
Complication:
• Severe Acute respiratory illness
• Pneumonia and kidney Failure

Note: seek immediate attention if an acute respiratory

illness with fever appears 14 days returning from travel.
 H1N1
SWINE FLU
 H1N1
a repiratory disease if the pigs caused by Type A influenza Virus

Also known as swine flu

Risk Factors:
1.Age – below 2 years old and 65 years old
2.Living or working condition
3.Weakened immune system
4.Chronic illness
5.Race – American Indians/Alaska Native
6.Aspirin use – below 19 years old
7.Pregnancy
8.Obesity
Symptoms:

• a. Fever, but not always.

• b. Aching muscles.
• c. Chills and sweats.
• d. Cough.
• e. Sore throat.
• f. Runny or stuffy nose.
• g. Watery, red eyes and eye pain
• h. Headache
• i. Tiredness/weakness
• j. Diarrhea
• k. Feeling sick to the stomach, vomiting – common in children (Influenza A virus)
 • droplet (sneezing, coughing,
Transmission touching)
• Flu symptoms develop about
1 to 4 days after you're
exposed to the virus.
• You can infect 1 day before
symptoms develop and up to
7 days or more after
becoming sick

NOTE:You can't catch swine flu

from eating pork.
For emergency in adult the sign and
symptoms are:
a. Troubled in breathing or shortness
of breath.
b. Chest pain.
c. Signs of dehydration such as not
urinating.
d. Ongoing dizziness.
e. Seizures.
f. Worsening of existing medical
conditions.
g. Severe weakness or muscle pain.
Emergency symptoms in
children can include:
a. Trouble breathing.
b. Pale, gray or blue-colored
skin, lips or nail beds
depending on skin color.
c. Chest pain.
d. Dehydration.
e. Severe muscle pain.
f. Seizures.
g. Worsening of existing
medical conditions.
 02 03
Complications: Complications:

01 a. Worsening of chronic
conditions - such as heart
a. Worsening of chronic
conditions - such as heart
disease and asthma. disease and asthma.
b. Pneumonia. b. Pneumonia.
Prevention:
c. Neurological symptoms, c. Neurological symptoms,
Seasonal flu
ranging from confusion to ranging from confusion to
vaccination
seizures. seizures.
d. Bronchitis and respiratory d. Bronchitis and respiratory
failure failure
e. Muscle tenderness. e. Muscle tenderness.
f. Bacterial infections. f. Bacterial infections.
Measures to prevent and limit the
spreading of flu:
1.Wash your hands often for at least
20 seconds by using soap and water
or use an alcohol-based hand sanitizer
that has at least 60% alcohol.
2. Cover your coughs and sneezes.
3. Avoid touching your face, eyes, nose
and mouth.
4. Clean and disinfect surfaces
regularly.
5. Avoid people who are sick or have
symptoms of flu.
 is a widespread inflammation of liver cells

resulting from viral or bacterial infections,

Hepatitis drugs, alcohol or chemical toxic to the liver and

some metabolic and vascular disorder

CLASSIFICATION:
• Viral

• Bacterial

• Toxic and drug induced

• Alcoholic hepatitis

• Autoimmune Hepatitis
 Non-Viral

is an inflammation of the liver that usually Most patient recover from non-viral
results from exposure to certain hepatitis although a few develop
chemicals or drugs. fulminating hepatitis or cirrhosis
 • is an acute inflammation of the liver marked by liver cell
destruction, necrosis, and autolysis.
• Systemic, viral infection in which necrosis and inflammation
of liver cells produce a characteristic cluster of clinical,
biochemical and cellular changes.
• Hepatic cells eventually regenerate with little or no residual
damage.
• Prognosis is poor if edema and hepatic encephalopathy
develop.
• Types:
1.Hepatitis A
2.Hepatitis B

Viral 3.Hepatitis C
4.Hepatitis D
5.Hepatitis E

Hepatitis
Phases of Infectious Hepatitis:
1. Viral replication phase/ Incubation phase
-asymptomatic
-laboratories – reveal markers of hepatitis
- patient remains asymptomatic during this phase but the infectivity is
highest during the last days if incubation periods
2. Preicteric phase –prodormal phase
- marked by prodromal constitutional symptoms and earliest laboratory
evidence of hepatocellular injury in pre-icteric phase is the elevation of serum
transaminases
-anorexia, nausea, vomiting, fatigue, pruritus
3. Icteric phase (1-2 weeks)
- commenced y the onset of clinical jaundice and the constitutional
symptoms diminish
- jaundice and dark urine
4. Convalescent Phase (2-12 weeks)
- sign and symptoms resolve and laboratory values return to normal
- last 1-4 weeks is usually followed by clinical and biochemical recovery in
2-12 weeks.
- Recovery phase is more prolonged in Hep B and Hep C
 Formerly called Infectious Hepatitis

Transmission:
• Fecal-oral route by ingestion of food or liquids
infected with the virus.

Characteristics:
• Prevalent countries with overcrowding and poor
sanitation.
• Found in the stool of infected patients before the
onset of symptoms.
• Acquire through poor hygiene, hand to mouth
contact or other close contact.
Hepatitis A • An infected food handler can spread the disease.
• People can contract the hepatitis by consuming

Virus water or shellfish from sewage-contaminated waters.

• Transmitted during sexual activity – oral-anal contact
or anal intercourse with multiple sex partners.
 Clinical Manifestations:
1. Anicteric (without
jaundice)-symptomless
2. Mild flu-like URTI (low
grade fever)
3. Anorexia – early
Incubation Period: symptom
2-6 weeks (mean 4 due to release of a
weeks) toxin by the damage
liver
4. Jaundice and dark
urine
5. Indigestion –
epigastric distress,
nausea, heartburn
flatulence
 HEPA A

Diagnostic Findings: Prevention: Medical Nursing

• Liver and spleen- • Scrupulous Management: Management:
moderately hand • Bed rest 1.Diet, rest and
enlarged washing. • Nutritious follow-up of
• HAV antigen – • Safe water diet – blood work
found in the supplies. frequent 2.Avoidance of
stool 7-10 days • Proper small alcohol
before the illness control of feedings, IV 3.Sanitation and
• HAV antibodies – sewage fluids with hygiene
found din serum disposal. glucose measures.
• HAV vaccine
 Risk factors:
Hepatitis B Virus 1. Exposure to blood,
• It is transmitted blood products or other
primarily through body fluids
blood. 2. Hemodialysis
• HBV found – blood, 3. IV injection/drug use
saliva, semen, and 4. Gay men and
vaginal secretions. bisexual activity
• Transmitted through 5. Mother to child
mucous membranes transmission
and breaks in the 6. Multiple sexual
skin. partners
• Transferred from 7. Receipt of blood or
carrier mothers to blood products
their infants via 8. History of sexually
umbilical vein and transmitted infection
during close contact. 9. Tattooing
Clinical Manifestations:
• Arthralgia's and rashes
• Loss of appetite
• dyspepsia
• Abdominal pain
• Generalized aching
• Malaise and weakness
• Jaundice may or may not be evident
• Light colored colored stools and dark urine
• Liver maybe tender and enlarged and spleen is enlarged

Preventing Transmission:
1.Screening of blood donors
2.Use of disposable syringes, needles and lancets.
3.Gloves are worn when handling all blood and body fluids

Active Immunization: HBV

Hepatitis B vaccine
 • provides passive immunity to HBV.
Passive Immunity: • indicated for people exposed to HBV who

Hepatitis B have never had Hepatitis B and have

never received hepatitis B vaccine.

Immune Globulin

• Goal-minimize infectivity and liver

Medical inflammation

Management: • Alpha-interferon
• Bed rest
• Activities are restricted until hepatic
enlargement and liver enzymes have
decreased.
• Adequate nutrition
• Proteins - not restricted
 H E PAT I T I S D
VIRUS
H E PAT I T I S E
Common in IV VIRUS
H E PAT I T I S C
injection, T RA N S M I TT E D
VIRUS
hemodialysis, BY T H E F E C A L -
Common in Blood O RA L R O U T E
blood
transfusion and THROUGH
transfusions. C O N TA M I N AT E
sexual contact
D WAT E R I N
and other POOR
Mode of
parenteral means. S A N I TAT I O N .
transmission –
sexual contact
Guillain-Barre
Syndrome
(GBS)
Idiopathic
Polyneuritis
 Guillain-Barre Syndrome (GBS) Idiopathic Polyneuritis
• a peripheral nervous system disease characterized by sudden onset of
muscle paralysis or paresis
• an acute, rapidly progressive, and potentially fatal form of polyneuritis that
causes mild weakness and mild distal sensory loss
• Autoimmune attack on the peripheral nerve myelin resulting in acute,
rapid segmental demyelination of peripheral nerves and some cranial
nerves producing ascending weakness with dyskinesia, hyporeflexia and
paresthesias.
• although the cause is unknown, the disease usually occurs 1-4 weeks after
a viral infection or immunization
• Antecedent – viral infection (Epstein-Barr Virus)

Subtypes:
1. Weakness in lower extremities which progresses upward and respiratory
failure (potential)- most common
2. Motor with no sensation
3. Descending GBS – affects the head and neck muscles
Clinical Manifestations:
• Muscle weakness and diminished reflexes of the lower
extremities.
• Hyporeflexia and weakness may progress to tetraplegia.
• Neuromuscular respiratory failure – demyelination of the
nerves that innervate the diaphragm and intercostal
muscles.
• Sensory symptoms – paresthesias of the hands and feet and
pain – due to demyelination of sensory fibers.
• Cranial nerve demyelination
• Optic nerve demyelination – blindness
• Bulbar muscle weakness – demyelination of the
glossopharyngeal and vagus nerves resulting in the inability
to swallow or clear secretions.
• Vagus nerve demyelination resulting in autonomic
dysfunction (tachycardia, bradycardia, hypertension and
orthostatic hypotension)
 Assessment and
Diagnostic Findings:
• Symmetric weakness
• Diminished reflexes
• Upward progression of
motor weakness
Note: GBS does not • Elevated protein levels –
affect cognitive detected in CSF
• CBC - leukocytosis
function or LOC • Nerve conduction test
will demonstrate neural
dysfunction
• Note: history of a viral
illness (few weeks
previously)- suggest
diagnosis
 Goal:
• Preventing the complications of
immobility.
• Use of anti-coagulant
• Compression boots – prevent
venous thromboembolism
(VTE)and DVT.
Medical Management: • Therapeutic plasma exchange
Respiratory therapy/mechanical
and IVIG – affect the peripheral
ventilation.
nerve myelin antibody level.
• Continuous ECG monitoring
• Alpha adrenergic blocking
agents – treat tachycardia and
hypertension
• IV fluid administration – to treat
hypotension
Complications: • Respiratory failure
• Cardiac failure
• Cardiac arrhythmias

Nursing Process: • Impaired breathing associated with rapidly

progressive weakness and impending respiratory
failure.
• Impaired mobility associated with paralysis.
• Impaired nutritional intake associated with
inability to swallow.
• Impaired verbal communication associated with
cranial nerve dysfunction.
• Anxiety associated with loss of control and
Planning Enhancing
and Goals: Physical
• Maintaining Respiratory Function
Mobility
• Incentive spirometry
• Chest physiotherapy • Passive and active range of
• Suctioning motion
• Anti-coagulant
• Anti-embolism stockings
• Adequate hydration
 3. Providing
Adequate
Nutrition
Paralytic ileus –
due to 4. Improving
insufficient Communication
5. Decreasing
parasympathetic Use with picture
Anxiety
activity. cards/eye blink
IVF and system
parenteral
nutrition
Gastrostomy
tube
Sexually Transmitted
Diseases

(STD’s)
 most common infection

may develop in anyone having sexual contact

STD/STI with multiple partners or with one partner who

has sexual contact with other

STI may be passed via semen or vaginal

secretions or by skin to skin contact
A. Candidiasis
• Fungal or yeast infection caused by Candida Albicans

Clinical Manifestations:
• pruritus, irritation
• Discharges – watery or thick, white, cottage cheese-like
appearance.

Medical Management:
• anti-fungal – miconazole, nystastin
• Inserted into the vagina with an applicator during bedtime.
• Oral medication – fluconazole
• Vaginal creams
B. Trichomoniasis
• Flagellated protozoan – called as
Trichomonas vaginalis
• Vaginal ph – greater than 4.5
• Trichomoniasis may be asymptomatic or
may be present with greenish discharge
and itching.
• Pain with intercourse is common and
men are seldom symptomatic.

Medical management:

1.Metronidazole
-Abstain from alcohol during treatment
-Abstain from sexual activity for 7-10 days
after treatment.
2. Topical Clotrimazole during pregnancy
C. Genital warts
• Causative Agent: Human Papilloma Virus
with 100 types
• Mode of transmission: Direct contact with
infected skin mucous membranes,
childbirth
• Incubation Period: 2-3 months, range 1-20
months
• Period of Communicability: as long as
lesions persist

Sign and Symptoms:

• Circumscribed lesions in cervix, vulva,
anus, penis, vagina, oropharynx (vary in
sizes)
 Laboratory/Diagnostic Examination:
Visualization of lesion
Excision and histological exam of lesion

Risk Factors:
1.young, sexually active
2.Multiple sex partners
3.Sex with a partner who has had multiple partners

Medical Management:
1.External genital warts – topical application of trichloroacetic acid
2.Electrocautery
3.Condom
4.Removal of warts by freezing with liquid nitrogen
Note: transmission can occur during skin-skin contact

Prevention:
-HPV vaccine for individuals 11-12 years old and safe sexual practices
d. Herpes Virus Type 2 Infection
(Herpes Genitalis)
Causative Agent: Herpes simplex
virus

Mode of Transmission:
-direct contact with infected skin
and mucous membranes,
childbirth

Incubation Period: 2-12 days

Period of Communicability:
-during and up to 7 weeks after
primary lesions appear
Clinical Manifestations:
• itching, pain, redness, edematous in the infected area
• -macules and papules then progress to vesicles and ulcers but may spread to
surrounding tissues or disseminated in body.
• Labia- primary site (female)
• Glans penis, foreskin, penile shaft (male)-site
• 2. Influenza like symptoms – 3-4 days after the lesions appear
• 3. Inguinal lymphadenopathy
• 4. Elevated temperature, malaise, headache, myalgia, dysuria

Medical management/Treatment:
• 1.No cure for genital herpes infection
• 2.Anti viral agents - acyclovir
• 3. Antispasmodic
• 4. Saline compress

Prevention:
• 1.Safe sexual practices
• 2.CS delivery if lesions are present during late pregnancy
Nursing Process:
1.Assessment:
- Health history
- Pelvic examination
2. Diagnosis:
- Acute pain associated with the genital lesions
- Risk for infection
- Anxiety associated with worry about the
diagnosis
3. Nursing Interventions:
- Relieving pain
- Preventing infection and its spread (proper
hand washing)
- Relieve anxiety
E. Chlamydia
Causative Agent: Chlamydia trachomatis

Mode of transmission:
Sexual contact or contact with exudates from mucous membranes, childbirth

Incubation Period: 7-14 days

Sign and symptoms:

• Chlamydia may be asymptomatic or may present wth urethritis or cervicitis characterized by
discharge, itching and burning on urination.
• In women, spotting between periods or after intercourse may occur
• Urethritis with purulent discharge from anterior urethra (males)
• Mucopurulent cervicitis often asymptomatic (females) – lead to endometritis, salphingitis and pelvic
peritonitis

Diagnostic Examination:
• Culture and ,Nucleic acid amplification test (NAAT) of urine or swab samples.

Treatment:
• Macrolide (Clarithromycin, Erythromycin) , Doxycycline, Azithromycin (single dose)
Complication Nursing
Management:
• infection may cause infertility in men and
women and epidymitis in males, PID and
ectopic pregnancy may occur in infected • 1.Use of condom and spermicide
women. • 2.Educational counseling
• If passed to a NB, conjunctivitis may occur. • Prevention and Control:
• 1. Safe sexual practices
• 2. Test pregnant women
F. Syphilis

Causative Agent:
-Treponema Pallidum
Mode of Transmission:
-Sexual Contact

Incubation Period:
10-90 days

Four different stages.

Note: People are very contagious in the first and second stages and can easily
pass the infection to their sex partners.

Types and sign and symptoms:

1. primary- chancre that appears within 3 weeks at area of contact.
2. secondary – condylomata, sore throat, mucous patches of the mouth and
macupapular rash.
3. Tertiary – gamma formation, cardiovascular and nervous system involvement.
Stages of A. Primary Syphilis
is characterized by painless genital ulcer of CHANCRE
Syphilis that spontaneously regresses

B. Secondary Syphilis
develop weeks to months later and is cahracterized by
a temporary skin rash, typically located on the palms
of the hands and soles of feet

C. Tertiary Syphilis
may develop decades after the initial infection and is
characterized by sensory loss, muscle weakness and
heart defects.
Diagnostic Treatment: Prevention and Complication:
Examination: 1.Penicillin (IM) Control: untreated syphilis
a. Darkfield 2.Tetracycline- if 1.Practice may cause heart
illumination test non-pregnant but monogamy failure and
b. venereal allergic to 2.Sex education neurologic
disease research penecillin deterioration
laboratory 3.Erythromycin/ if passed to fetus,
(VDRL) test Ceftraixone- if it can cause fetal
c. Fluorescent pregnant death or
treponemal neonatal
antibody test infection
G. Human Immunodeficiency Virus/Acquired Immuno
Deficiency Syndrome

Causative Agent: HIV 1 and 2

Mode of Transmission:
• Sexual contact
• Blood transfusion
• Contaminated syringes, needles, nipper, blades
• Direct contact of open wounds/mucous
membranes with contaminated blood, body
fluids, semen, and vaginal discharges
Incubation Period:
Varies from 3-6 months to many years (8-10 years)
Sign and Symptoms:
1. Clinical stage 1 – persistent generalized
lymphadenopathy
 Clinical stage 111
• Weight loss >10% of body
Clinical stage 11 weight
• weight loss of <10% of • Unexplained chronic
body weight diarrhea for 1 month
• Minor mucocutaganeous • Unexplained prolonged
manifestation fever for >1 month
• Herpes zoster within the • Oral candidiasis
last five years • Oral hairy leukoplakia
• Recurrent URTI • PTB within the past year
• severe bacterial infections
Clinical stage 1V
• Pneumocystic carini
pneumonia
• Toxoplasmosis of brain
• Herpes simplex virus infection
• Kaposis sarcoma
• Extra pulmonary tuberculosis
• Lymphoma
• Acquired immunodeficiency
syndrome – most advanced
stages of HIV infection.
• Occurrence of any more
than 20 opportunistic
infections or HIV-related
• cancers (WHO, 2018)
Diagnostic Examination:
• Enzyme Linked Immuno Sorbent
Assay (ELISA)- presumptive test
• Western blot – confirmatory test
Treatment:
• Antiretroviral drug – suppress the
virus
Prevention and Control:
Blood and blood products
a. Screen blood donors
b. Observe universal precaution
c. Refrain from using contaminated
needles and syringes
Sexual transmission
a. Abstain from promiscuous
sexual contact
b.Be faithful to your partner and
practice monogamous sexual contact.
c.Follow correct and consistent use of
condoms.
3.Mother-to-child transmission
Note: For HIV+ mothers,
consult with health workers to
have access
to care, treatment, and support
to services during pregnancy, labor
and
delivery, and post-partum
4.Pre-Exposure Prophylaxis for
people with a high risk of acquiring
HIV
by taking the drug Truvada.
Gonorrhea
• causative agent: Neisseria gonorrhea (bacteria)
• a bacterial infection transmitted by sexual fluids through oral,
vaginal or anal sex.
• primarily affects the genital organs
• it may be asymptomatic or may present with purulent discharge
from the urethra or vagina and burning on urination. Infants born
to mother with gonorrhea may develop conjunctivitis or
pharyngitis
• untreated gonorrhea may cause femake sterility or PID and
increased risk of ectopic pregnancy.
• Both men and women may develop disseminated infection with
arthritis, endocarditis, or conjunctivitis leading to blindness.
• If pass to NB: it causes blindness.
Inflammatory Disorders
(All Body Systems)

Gastro-intestinal System
 The DIGESTIVE
SYSTEM
The primary
functions
• Ingestion
• Digestion
• Elimination
• Absoprtion
QUADRANTS

1 2

RUQ LUQ

• LIVER • SPLEEN
• GALLBLADDER • STOMACH
• DUODENUM • LEFT COLIC FLEXURE
• HEAD OF THE PANCRE • TAIL OF PANCREAS
AS • LEFT KIDNEY
• RIGHT KIDNEY • LEFT SUPRARENAL GL
• RIGHT SUPRARENAL G AND
LAND
QUADRANT RLQ
•
•
ASCENDING COLON
APPENDIX

S •
•
•
CECUM
2/3 OF ILEUM
ILEOCECAL VALVE

LLQ
• DESCENDING COLON
• SIGMOID COLON
• 2/3 OF JEJUNUM
Lips to the orophaynx
Teeth, tongue, palate,
salivary glands and
tonsils
Initial digestion of
carbohydrates

MOUTH
Salivary 1. Parotid=
secretes

Glands
purely
serous,
Stensen’s
duct
2.Submandi
bular/
submaxillay
Your paragraph = secretes
text mixed
saliva, with
Wharton’s
duct
3.
Sublingual=
secretes
mixed
saliva, with
two ducts-
duct of
PHARYNX
Oropharynx is a
passageway of both food
and air
ESOPHAGUS
Muscular tube extending from
the pharynx to the stomach
With sphincter.
Function
propel food to the stomach
STOMACH CELLS IN THE STOMACH

• 1. Mucus cells- secret

e mucus for protectio
n of the mucosa
• 2. Chief cells/principal
cells/Zymogenic cells
• secrete Pepsinogen
needed for protein dig
estion
J-shaped dilatable • 3. Parietal cells/Oxynti
c cells- secrete Hydroc
Epigastric & RUQ hloric acid to activate
pepsinogen and Intrin
3 parts: sic factor needed to a
1. Fundus bsorb Vitamin B12
• 4. Argentaffin cells- se
2. Body crete Serotonin
3. Pylorus
 STOMACH

J-shaped, but varies in size and shape Lesser curvature: connected to the
with the volume of its contents porta hepatis of the liver by the lesser
Vary considerably from person to omentum
person, differing especially with the Greater curvature: from which the
build of the subject. greater omentum is suspended
Cardiac region: receives the esophagus
Fundus – dome-shaped upper part of
the stomach, normally filled with air
• Body of the stomach: main center portion

• Pylorus: has a thick muscular wall and narrow lumen that

leads to the duodenum

• Lined by mucosae that is thrown into folds called rugae

• Peritoneum covers the anterior and posterior surfaces of

the stomach and is continued between the lesser curve
and the liver as the lesser omentum, and beyond the
greater curve as the greater omentum.

• *omentum – a ligament that joins the stomach to another

structure.
DUODENUM
• The 2nd part of the duodenum has an opening halfway
down on its posteromedial aspect for the pancreatic and
common bile ducts, variously called the duodenal papilla
or ampulla of Vater.
• Guarded by the sphincter of Oddi.
• An accesory pancreatic duct (of Santorini) may also be
present proximally.
• Is in contact with the pancreatic head medially

• Extends from the pylorus to the duodenojejunal flexure.

• The first 2.5 cm of the duodenum, like the stomach, is attached t
o the greater and lesser omentum.
• The remainder of the duodenum is retroperitoneal, and, as a res
ult, less mobile than the small intestine.
• Curves in a C shape around the head of the pancreas
• DUODENU
M
• JEJUNUM
• ILEUM

• Begins where the intestine assumes a mesentery

at the duodenojejunal flexure and ends at the
ileocecal junction.
• Varies in the length from 3-10 meters (ave. 6
meters).
• Very mobile and lies in mobile coils in the central
abdomen.
• Jejunum – proximal 2/5 of the small intestine
• Ileum – distal 3/5 of the small intestine.
THE
APPENDIX
• Arises at the convergence of
the taenia coli on the
posteromedial wall of the
cecum.
• A thin structure containing
lymphoid tissue; length is
variable – between 12 and 24
cm.
• Its position is variable
• lIncidence of the commonest
positions: retrocecal – 64%,
inferomedial – 36%
THE LARGE
INTESTINE
(COLON)
Cecum
Ascending colon
Transverse colon
Descending colon
Sigmoid colon
Rectum
 Its length is very
variable, with an
average length of
1.5 meters.
THE LARGE
INTESTINE (COLON) Wider in diameter
than the SI, with a
maximum diameter
of the cecum at 9.0
cm and the
transverse colon at
5.5 cm.
ANUS

The anal canal is the last

portion of the tract,
surrounded by an internal and
external anal sphincter
PERITONEUM
Serous membrane lining
the abdominal cavity
Parietal peritoneum-
abdominal wall
Visceral peritoneum-
visceral organs
Pancreas
A pistol-shaped
organ both an
endocrine and
exocrine gland
Parts: head, body
and tail
Ducts: major is
Wirsung, minor is
Santorini
Described as having a head, neck,
body and tail.
It is retroperitoneal with the
exception of the tail, which lies in
the splenorenal ligament.

Pancreatic head
Lies in the curve of the duodenum,
with the pylorus and the duodenal
cap overlapping it slightly on its
anterior surface.
The common bile duct (CBD)
passes posterior to the head of
the pancreas in a groove or tunnel
towards its termination in the 2nd
part of the duodenum.
Pancreatic ducts
The pancreatic duct (of Wirsung) begins
in the tail by the union of the ductules
and passes transversely towards the
head.
At the neck the duct turns inferiorly,
somewhat posteriorly and to the right,
and joins the bile duct to form a
terminal, common dilated portion called
the ampulla (of Vater) before entering
the duodenum at the papilla
Accessory organ
• GALLBLADDER
• lPear-shaped organ on the right upper quadrant below
the liver
• lParts: fundus, body and neck
• lFunctions to store and concentrate bile
• A pear-shaped sac attached to the extrahepatic bile
ducts by the cystic duct.
• Described as having a fundus, body and neck, and it
hangs on its bed on the visceral surface of the liver
• Stores and concentrates bile
• The normal gallbladder has a capacity of 30 to 50 mL.
However, sonographic volume measurements are
difficult to perform, and reported values (17 to 27 mL)
for fasting volunteers vary widely
Movement

Mouth (Chewing or mastication) swallowing

• Process of digestion begins with act of • Regulated by CNS (medulla oblongata –
chewing swallowing center)
• Foods is broken down into small particles • Rhythmic activity of the smooth muscles of
then swallowed & mixed with digestive esophagus propels food to the stomach
enzymes
• Approx. 1.5L of saliva secreted daily
• Ptyalin or Salivary amylase • Salivary secretions- salivary amylase or
• Begins digestion of starches ptyalin begins the digestion of carbohydrates
 Stomach movement
Stomach Secretions
• Mixing waves
Mucus • Peristaltic movements
• Produced by the mucus cells for mucosal
protection Digestion for lipids
HCL from parietal cells • Gastric lipase
• Helps breaksdown nutrients (proteins)
• Helps eliminates bacteria & viruses Digestion for proteins
Pepsinogen from chief cells • Pepsin
• Activated by HCl into Pepsin
• Intrinsic factor from parietal or chief cells No enzyme for carbohydrates
Gastrin
• hormone from the antral G cells
• Enhance gastric mucosal growth
• Gastric motility
• Helps secretions of HCl through Histamine
activation
 • Duodenal secretions
come from the
accessory digestive
organs
• Pancreas, Liver, GB &
glands of the intestine
itself
• Pancreatic enzymes,
Bicarbonate, Biles
• Sphincter of Oddi –
Chyme in Duodenum controls flow of bile
• Role of cholecystokinin
-Secreted by the upper wall
of the SI
-Stimulated by HCL & other
chyme (proteins, fats, CHO)
from the stomach
-Stimulates GB to secretes
Biles
-Stimulates acinar cells of
pancreas to produce
enzymes & juices
-Relaxation of S.Oddi
Small intestine:
movement
Slow & weak peristaltic activity
• Allows for efficient reabsorption of water
• Wastes material distend the rectum usually
about 12H
Feces
• Undigested foodstuffs
• Inorganic material, water & bacteria
• 25% solid 75% fluid
• Brown color due breakdown of bile by
intestinal B
Defecation reflex
• moves the feces to the internal anal sphincter,
mediated by the parasympathetic nerves
• Distention causes the reflex
ELIMINATION • Begins with distention of the
rectum
• Contractions of the rectal
musculature & relaxes the
normally closed internal anal
sphincter
• Internal Anal Sphincter- Controlled
by ANS
• During DEFECATION
- Ext anal s. voluntarily relaxes to
allow colonic contents to be expelled
- Under spinal reflex by parasymp
nerve fibers
PANCREATIC LIVER
SECRETIONS SECRETION
Bicarbonate BILES- aids in emulsifying the fats
• to neutralize the acidic chyme from the stomach

Pancreatic amylase

• for carbohydrate digestion

Pancreatic lipase

• for fat digestion

Trypsin and chymotrypsin

• for protein digestion

 Upper GIT study: barium
COMMON swallow
Pre-test: NPO post-midnight
LABORATOR Post-test: Laxative is ordered,
Y increase pt fluid intake, instruct
that stools will turn white,
PROCEDUR monitor for obstruction
ES
 Lower GIT study: barium enema
Examines the lower GI tract

• Pre-test: Clear liquid diet and

laxatives, NPO post-midnight,
cleansing enema prior to the
test
• Post-test: Laxative is ordered,
increase patient fluid intake,
instruct that stools will turn
white, monitor for obstruction
Cholecystography
• Examination of the
gallbladder to detect stones,
its ability to concentrate,
store and release the bile

• Pre-test: ensure consent, ask

allergies to iodine, seafood
and dyes; contrast medium is
administered the night prior,
NPO after contrast
administration
• Post-test: Advise that dysuria
is common as the dye is
excreted in the urine, resume
normal activities
 Removal of peritoneal fluid for analysis

Paracentesis •Pre-test: ensure consent, instruct to VOID and

empty bladder, measure abdominal girth

•Intra-test: Upright on the edge of the bed, back

supported and feet resting on a foot stool
 Conditions of the PATHOPHYSIOLOGY
GASTRITIS
Stomach
Inflammation of the gastric mucosa
May be Acute or Chronic
Etiology: Acute- bacteria, irritating foods, NSAIDS,
alcohol, bile and radiation
Etiology: Chronic- Ulceration, bacteria, Autoimmune
disease, diet, alcohol, smoking
NURSING
INTERVENTIONS
1. Give BLAND diet
2. Monitor for signs
of complications like
bleeding,
obstruction and
pernicious anemia
3. Instruct to avoid
spicy foods,
irritating foods,
alcohol and caffeine
4. Administer
prescribed
medications- H2
blockers, antibiotics,
mucosal protectants
5. Inform the need
for Vitamin B12
injection if
deficiency is
APPENDICITIS
• Small, finger-like appendage Appendicitis
about 10cm long
• Attached to the cecum just below
the ileocecal valve
• With small lumen
• Prone to obstruction
• Most common emergency
abdominal surgery
• Common between ages of 10 &
30 years
• Once occluded (fecalith) or
kinked
• Intraluminal pressure increases
then initiates a progressive
severe periumbilical pain that
becomes localized to the RLQ for
4-6hours
• Inflamed appendix filled with pus
Pathophysiology
Hallmark S/Sx:
• Vague epigastric or periumbilical pain progresses
to RLQ
• Low grade fever
• N&V
• Loss of appetite
• Local tenderness at McBurney’s point
• Rebound tenderness
• If appendix curls around behind the cecum, pain &
tenderness felt in the lumbar region
• If the tip of appendix is in the pelvis, pain elicited
only during DRE
• If the resting in the rectal area, pain on defecation
• Dysuria, if tip near the UB or ureter
• Rovsings sign
• Psoas sign
• Obturator sign
SURGERY:
Appendectomy
1 2

Diagnostic exams Complications

• CBC- neutrophilia • Perforation- Occurs

• Urinalysis 24 hours after the o
nset of pain
• CRP- within the 12
• Peritonitis
hours
• Abscess formation
• Abdominal X-ray fil
ms
• UTZ studies
• CT scans
 1.Before surgery
a.IV infusion
b.Promote adequate renal function
c.Antibiotic
d.Analgesics

Goals: Note: Enema is contraindicated – lead to

perforation
• Relieve pain
• Preventing fluid 2. After surgery:
volume deficit 1.High fowler position – reduces tension
• Reduce anxiety on the incision and abdominal organ –
• Preventing or treating reducing pain.
Promotes thoracic expansion –
surgical site infection preventing atelectasis
• Preventing atelectasis 2. Incentive spirometer
• Maintaining skin 3. Opioid (morphine)
integrity 4. IVF
5. Oral fluid and food – when bowel
• Attaining optimal sound return
nutrition 6. Urine output
7. Ambulation the day of surgery –
reduce the risk of atelectasis and venous
thromboembolism
8. Heavy lifting is avoided
9. Normal activity resumed within 2-4
weeks.
NURSING MANAGEMENT
• Provide emotional support & needs to ventilate any fear of surgery
• Montor Fluid and Electrolytes
• Asses for signs of infections
• Semi fowlers to moderate fowlers position
• To help localize infection if the appendix ruptures

Prepares for Surgery

• NPO
• Start IVF
• Antibiotics as ordered

Post surgery
• High fowlers position: reduce tension on the incision site
• Pain meds as ordered
• Encourage early ambulation
• Assess return of BM, Bowel, sounds, Flatus
Peritonitis

Inflammation of the
peritoneum
Caused by perforation of
GIT or by chemical stress
like in Pancreatitis
 PERITONITIS

Causes: Types:
Bacterial infection or secondary to fungal Primary – spontaneous bacterial
or mycobacterial infection peritonitis
(E. Coli, Pseudomonas, Streptococcus, Secondary – due to perforation of
Klebsiella) abdominal organs causing spillage that
2. External sources ( abdominal surgery or infects the serous peritoneum ( perforated
trauma or inflammation that extends from appendix, peptic ulcer, diverticulitis).
an organ outside the peritoneal area)
 Diagnostic exams
Hallmark S/Sx • CBC- WBC Elevated
• Abdominal • Hgb/Hct- low
pain • ABG- reveals DHN
• Rebound and acidosis
• Blood cultures
tenderness • UTZ- abscess
• Nausea & formation
Vomiting • Abdominal X-rays-
• Fever shows free air and
• Rigid distended bowel
abdomen loops
• Elevated WBC
Clinical Manifestations:
• Pain is diffuse then constant, localized and intense.
• Abdomen is tender and distended, rigid.
• Rebound tenderness
• Anorexia, nausea, vomiting
• Peristalsis diminished resulting in paralytic ileus
• Increased in body temperature and pulse rate
• Hypotension, oliguria and anuria

Note: Sign and symptoms will mirror of sepsis and septic shock
Medical Management:
1.Fluid, colloid and electrolyte replacement
2.Isotonic solution administration – for hypovolemia
3.Analgesia
4.Anti-emetic
5.Intestinal intubation and suction – relieve abdominal distention
6. Oxygen therapy- for respiratory distress
7. Antibiotic therapy – broad spectrum antibiotic

NURSING MANAGEMENT:
• Maintain the semi-fowlers position
• To localize infection in the pelvic area
• Monitor VS
• Monitor IVF & Gastrointestinal decompression (NGT)
• Monitor I & O
• Auscultate for bowel sounds
• lNote passage of flatus
• Antibiotics as ordered
 • Refers to 2
chronic
inflammatory GI
disorders
-Regional enteritis
Inflammatory (Crohns disease)
Bowel Disease -Ulcerative colitis
(IBD) • Unknow cause
• Triggered by
-Pesticides exposure
-Food additives
-Tobacco & radiation
-NSAIDs
 Predisposing factors:
• 1.Family history
• 2.Caucasian
• 3.Living in
northern climate
• 4.Living in urban
Inflammatory areas
Bowel Disease Causes:
• 1.Genetic
(IBD) • 2.Altered immune
response
• 3.Altered
response to gut
microorganisms
IBD: Crohn’s Disease
• Regional enteritis
• Common in adolescents or young adults
• Commonly affects distal ileum & ascd colon but
occur anywhere along the GIT
• Common to smokers
• Begins with edema & thickening of mucosa
• Lesions are not continuous, separated by normal
tissue
• Cobblestone appearance
• Clusters of ulcers
• RLQ pain
• Diarrhea
• Crampy abdominal pains after meals
• Weight loss
• Malnutriion
• Secondary anemia
• Fever & Leukocytosis
• Seatorrhea (excessive fat in the feces)
Clinical Manifestations: Diagnostic findings
• Diarrhea • Proctosigmoidoscopy- If with inflamed
• Right lower quadrant abdominal pain rectosigmoid area
unrelieved by defecation • Fecalysis
• Crampy abdominal pain occur after
- Positve Occult blood
meals
- Steatorrhea
• Abdominal tenderness and spasm
• Barium study
• Weight loss, malnutrition, anemia
- Most conclusive
and dehydration
• Weeping, edematous intestine - Shows classic “STRING SIGN” on an
• Intra-abdominal and anal abscess x-ray film of terminal ileum
• Fever and leukocytosis - Ulcerations (cobblestone
• Stetorrhea (excess fat in the feces) appearance)
and anorexia - chronic symptoms • Endoscopy
• Arthritis • Colonoscopy
• Skin lesions (erythema nodusom) • Intestinal biopsies
• Uveitis • CBC (Hgb decrease, WBC elevated , ESR,
• Oral ulcers elevated )
 Complications:
Intestinal
obstruction/stricture
Enterocutaneous fistula –
formation
common type of small
Perianal disease
bowel fistula
Fluid and electrolyte
Note: patients with
imbalance
Crohn’s disease are risk
Malnutrition from
of colon cancer
malaborption
Fistula and abscess
formation
Ulcerative Colitis
• Chronic ulcerative and
inflammatory disease of the
mucosal and sub mucosal layers of
the colon and rectum
• Recurrent ulcerative &
inflammatory disease of the colon
& rectum
• May cause Colon CA
• Multiple ulcerations of the colonic
mucosa
• Bleeding due to ulcerations
• Contiguous lesions, occurring one
after the other
• Disease usually starts at rectum &
spreads proximally to involve the
entire colon
 ULCERATIVE COLITIS
Clinical Manifestation:
1.Remission and exacerbation
2.Diarrhea with passage of mucus, pus, or blood
3.Left lower quadrant pain
4.Intermittent tenesmus
5.Bleeding (mild or severe)
Characteristics: 6.Pallor, anemia and fatigue
7.Anorexia, weight loss
remission and exacerbation 8.Fever
9.Vomiting
Abdominal cramps and bloody 10.Dehydration
or purulent diarrhea 11.Cramping and passage of six or more liquid
stools each day
12. Hypoalbuminemia
13. Electrolyte imbalance
14. Skin lesion (erythema nodosum)
15. Uveitis
16. Arthritis
Assessment and Diagnostic
Findings:
• Abdominal X-ray
• Colonoscopy – definite
screening test
• Biopsies
• CT scan
• MRI
• Ultrasound
• Stool - + for blood
• Low hematocrit and
hemoglobin
• Elevated WBC
• Low albumin
• Electrolyte imbalance
• C-reactive protein -
elevated
• Elevated antineutrophil
cytoplasmic antibody
levels
Complications:
Toxic megacolon
Perforation
Bleeding
Risk:
Osteoporotic fracture
Colon cancer

Management of Inflammatory Bowel Disease:

1. Pharmacologic Therapy
Amino salicylates (Sulfazalazine)

Adverse effects:
Headaches
Nausea
Diarrhea
B. Antibiotics (Metronidazole, Ciprofloxaxcin)
C. Corticosteroids
D. Immuno modulators (Azathioprine)

Adverse Effects:
1.Depress bone marrow
-monitor for neutropenia
E. Anti-tumor necrosis factor medications (Infliximab)

11. Nutritional Therapy

a.Oral fluids and IV therapy
b.low residue, high calorie diet with supplemental vitamin therapy and iron replacement
c.Calcium and vitamin D – prevent osteopenia
d.Nutritional therapy
e.Cold foods and smoking – avoided
f.Probiotic supplements – indicated for ulcerative colitis
ULCERATIVE COLITIS
SURGERY
IBD: MANAGEMENT

MEDICAL MANAGEMENT:

• Adequate fluid
• Diet
• Low fiber, high protein,
high calorie
• IVF if admitted
• Avoid milk & milk
products
• Avoid cold foods &
smoking
• Antidiarrheal & HNBB
• Sulfasalazine
• Metronidazole
• Corticosteroids
• Prednisone if OPD
• Hydrocortisone if
MEDICAL MANAGEMENT:
Immunomodulators
• Azathioprine
• Methotrexate
Surgical interventions
• Strictureplasty
• Blocked or narrowed intestines are widened
• Small Bowel resection
• Total colectomy & ileostomy
Procedure of choice in severe crohn’s disease
Ileostomy
Creation of opening or stoma in the abdominal
wall
Allows drainage of fecal matter
Intestinal transplant
Proctocolectomy with ileostomy
Complete resection of colon, rectum & anus
IBD: NSG. MGT
• Maintaining normal elimination patterns
• Ready access to bathroom, commode or bedpan
• Antidiarrheal as ordered
• Encourage bed rest
• Relieving pain
• Nonpharmacologic
• Position changes
• Warm application
• Diversional activities
• Analgesic as ordered
• Accurate I&O
• Daily weights
• Replace fluid loss volume per volume
• Stress reductions
• Small frequent meals. Low fiber diet
Cholelithiasis
• Calculi or Gallstones
• 2 types
• Pigment stones

- Form when unconjugated pigments in the bile

precipitate to form stones
- 25% of cases
- Increased with Cirrhosis, Hemolysis, Infections of
the Biliary Tract
- Cannot be dissolved & must be removed

• Cholesterol stones

- 75% of cases
- Decreased bile acid synthesis & increased
cholesterol synthesis in the Liver resulting in bile
supersaturated with cholesterol, which precipitates out
of the bile to form STONES
- Cholesterol – Saturated bile predisposes to the
formation of gallstones & acts as an irritant that
produces inflammatory changes in the GB.
ASSESSMENT findings
1. Indigestion, belching and flatulence
2. Fatty food intolerance, steatorrhea
3. Epigastric pain that radiates to the scapula or localized at the RUQ
Bout of Biliary Colic
Contraction of the GB which cannot release bile because of obstruction by the stone at the cystic duct
Fundus of the GB comes in contact with the abdominal wall thus tenderness @RUQ
4. Mass at the RUQ due to Cholecystitis
5. Fever
5. Murphy’s sign
6. Jaundice
• Obstruction @ CBD
• Absorbed by the blood
7. dark orange and foamy urine
• Excretion of bile pigments by the kidneys
8. Feces
• No bile pigments
• Grayish (clay-colored)
9. Vits ADEK
• Due to obstruction of bile flow
 Ultrasonography
DIAGNOSTIC • can detect the stones
PROCEDURES • Replaced cholecystography
• Rapid & accurate
• No exposure to ionizing radiation
Abdominal X-ray
• Calcified stones
Cholecystography
• If no UTZ
• Given with oral iodide-containing contrast
agent
• GB will be filled by this radiopaque substance
• If with stones, shadows appears on x-ray film
 WBC count increased
DIAGNOSTIC Endoscopic Retrograde
PROCEDURES Cholangiopancreatography (ERCP)
• Direct visualization of structures
• reveals inflamed gallbladder with gallstone
• Flexible fiberoptic endoscope inserted through
the esophagus to the descending duodenum
• Fluoroscopy & Multiple x-rays are used during
ERCP to determine location of ductal stones
NURSING
INTERVENTIONS
• Maintain NPO in the active phase
• Maintain NGT decompression
• Administer prescribed medications to relieve pain
Morphine SO4 (cause spasm of S.of Oddi)
Meperidine (Drug of Choice)
• Instruct patient to AVOID HIGH- fat diet and GAS-forming foods
• Assist in surgical and non-surgical measures
• Surgical procedures
Cholecystectomy
Choledochotomy
-Reserved with patient with acute cholecystitis who is too ill to undergo surgery
-Making an incision in the CBD to remove stones
Laparoscopy
-Surgeon will make 4 small incisions in the abdomen
-Inserts a Laparoscope through the umbilical incision
CHOLEDOCHOTOMY- surgical
incision of the CBD
PHARMACOLOGIC
THERAPY
• Analgesic (narcotic)
• Ursodeoxycholic acid
• dissolve the gallstones
• 6-12 months of therapy
• Antacid
• Anti-emetics
Post-operative
nursing interventions

• Monitor for surgical complications

• Post-operative position after recovery from anesthesia- LOW FOWLER’s
• Encourage early ambulation
• Administer medication before coughing and deep breathing exercises
• Advise client to splint the abdomen to prevent discomfort during coughing
• Administer analgesics, antiemetics, antacids
• Care of the biliary drainage or T-tube drainage
• Fat restriction is only limited to 4-6 weeks. Normal diet is resumed
 • Inflammation of the
gallbladder
• Can be acute or chronic
• Acute cholecystitis
- usually is due to gallbladder
stones
• Chronic cholecystitis is usually
due to long standing gall
bladder inflammation
• Calculous cholecystitis
- 90% of acute cholecystitis
- A GB stone obstruct the bile
outflow
- Bile remaining the GB Cholecystitis
initiates a chemical reaction thus
edema occurs
- Bacterial factors (E.coli,
Klebsiella, Streptococcus)
• Acalculous cholecystitis
- Inflammation in the absence
of GB stones
- Due to major surgery, severe
trauma, burns
Pancreatitis
• Inflammation of the pancreas
• Pancreatitis duct temporary obstructed – hypersecretion of the exocrine
enzymes of the pancreas – enzymes enter the bile duct (activated) together
with the bile – reflux into the pancreatic duct – pancreatitis

• Autodigestion of the pancreas

- Usually trypsin
• Acute Pancreatitis
- Pancreatic becomes obstructed, reflux of enzymes into the pancreas causing
pancreatitis
- Or Gallstones in the ampulla of vater, obstruct the flow of the bile causing
reflux thus activation of the enzymes causing necrosis, erosion & hemorrhage
• Chronic Pancreatitis
- Long term use of alcohol
 Etiology and
predisposing factors
• Biliary tract disease
• Cholelithiasis (women)
• Bacterial disease
• PUD
• Mumps (viral infxn)
 Types
1. Interstitial edematous pancreatitis –
lack of pancreatic with diffuse
enlargement of the gland due to
inflammation and edema.
2. Necrotizing pancreatitis – tissue
necrosis in the pancreatic parenchyma
 ASSESSMENT findings

Abdominal pain- acute onset, occurring after a heavy meal or alcohol intake
Abdominal guarding
Bruising on the flanks and umbilicus
N/V, jaundice
Hypotension and hypovolemia
HYPERGLYCEMIA, HYPOCALCEMIA
Signs of shock
Clinical manifestations:
Severe abdominal pain and tenderness
(midepigastrium)– due to irritation and edema of
inflamed pancreas.
- occur 24-48 hours after a very heavy meal
or alcohol ingestion.
- can’t be relieved by antacid
- abdominal distention, palpable mass,
decreased peristalsis
- vomiting (bile stained)
- rigid or boardlike abdomen – peritonitis
- ecchymosis (flank or around the umbilicus)
– severe pancreatitis
- fever, jaundice
- mental confusion and agitation
- hypotension, tachycardia, cyanosis, cold
clammy skin
- respiratory distress and hypoxia
myocardial depression, hypocalcemia,
hyperglycemmia
-DIC
 DIAGNOSTIC TESTS
1. Serum amylase and serum lipase
2. Ultrasound
3. WBC elevated
4. Serum calcium decreased
5. CT scan
6. Hemoglobin and hematocrit
7. Transient hyperglycemia and
glycosuria
8. elevated serum Bilirubin
NURSING INTERVENTIONS

• Assist in pain management.

• Assist in correction of Fluid and Blood loss
• Place patient on NPO to inhibit pancreatic stimulation
• NGT insertion to decompress distention and remove gastric secretions
• Maintain on bed rest
• Position patient in SEMI-FOWLER’s to decrease pressure on the diaphragm
• Deep breathing and coughing exercises
• Provide parenteral nutrition
• Introduce oral feedings gradually- HIGH carbo, LOW FAT
• Maintain skin integrity
• Manage shock and other complications
 • Pain Management
• Opioid – Morphine
• NSAIDs – avoided (risk for
bleeding)
2. Intensive Care
• Correction of fluid and blood loss
and low albumin
• Insulin – in case of hyperglycemia
Medical Management: 3. Respiratory Care
• ABG monitoring
• Use of humidified oxygen
4. Biliary Drainage
5. Surgical Intervention
6. NPO – inhibit stimulation of the
pancreas
• Enteral feedings – recommended
7.NGT – relieve nausea, vomiting,
abdominal distention and paralytic
ileus
8.Proton-pump inhibitor