Gastrointestinal Disorders

By

Nguyo Patrick Mr.

Contents
1. Review of anatomy and physiology of GIT
including the biliary tract.
2. Etiology, pathophysiology, manifestations,
diagnosis, management & prognosis of
disorders (including tumors) of
1. The mouth 6. The liver
2. Esophagus 7. Biliary
3. Stomach 8. Rectum & Anus
4. Intestines
5. Peritoneum
Conditions to cover are:
 Gastritis
 Peptic Ulcer
 Pancreatitis
 Hernia

 Ulcerative colitis
 Intestinal obstruction
 Appendicitis
 Peritonitis
 Hemorrhoids
 Tumor's of Oesophagus,stomach,colon,rectum

and pancreas.
Conti-
 Biliarytract;Jaundice,Hepatitis,Cirrhosis of
the liver,Cholecystitis,Cholelithiasis,Portal
hypertension and Carcinoma of the Liver.
Review of anatomy and
physiology
 Gastrointestinal system consists of the GI
tract also known as the alimentary tract, and
the associated organs; the liver and the
pancreas.
 It is involved in intake, digestion, absorption
and excretion.
 The alimentary tract is a tube-like structure
modified at various levels, measuring btn 23-
26 feet and extends from the mouth through
the thorax, the abdomen and terminates
Cont.
at the anus.
 The esophagus is a distensible tube about

25 cm long communicating with oral-

pharynx superiorly and continuous with the
stomach inferiorly.
 It is in front of cervical and thoracic

vertebrae and behind the heart and

trachea.
 It enters the stomach through the

diaphragmatic hiatus.
Cont.
 The esophagus joins the stomach at the
oesophagogastric junction and the
communication between the two is
controlled by the cardiac sphincter.
 The stomach is a distensible sac with a

volume of about 1500 mls found on the

upper segment of the peritoneal cavity and
on the left.
 Anatomically, it has four parts:
 The cardia, fundus, body and the antrum.
 The stomach wall is lined by a mucus

membrane with goblets cells, chief and

parietal cells that produce secretions
necessary for digestion and protection in the
stomach.
 The stomach opens into the small intestines.

There is a pyloric sphincter between the two.

 Small intestines are divided into three:

duodenum, jejunum and ileum.

 They account for about two-thirds of the GI
length.
 The common bile duct joins the duodenum

at the ampulla of Vater and here it empties

the bile juices and pancreatic enzymes into
the duodenum.
 the junction between the ileum and large

intestine is called the caecum and is found

in the right lower portion of the abdomen.
 Vermiform appendix is located near this
junction.
 The large intestine is important in

absorption of water and drugs.

 The large intestine is divided into three

parts: the ascending colon, the transverse

colon and descending colon.
 The colon joins the rectum which serves as

a reservoir which terminates at the anus.

 The GI tract receives blood from arteries that
originate along the entire length of the
thoracic and abdominal aorta. Of particular
importance are the gastric artery and the
superior and inferior mesenteric arteries.
 Blood is drained from these organs by veins
that merge with others in the abdomen to
form a large vessel called the portal vein.
 Both the sympathetic and parasympathetic
portions of the autonomic nervous system
innervate the GI tract.
 In general, sympathetic nerves exert an
inhibitory effect on the GI tract, decreasing
gastric secretion and motility and causing
the sphincters and blood vessels to constrict.
Parasympathetic nerve stimulation causes
peristalsis and increases secretory activities.
The sphincters relax under the influence of
parasympathetic stimulation. The only
portions of the tract that are under voluntary
control are the upper esophagus and the
external anal sphincter.
Assessment of digestive
and G.I function
1. History and clinical
manifestations.
 The nurse begins by taking a complete
history, focusing on symptoms common to GI
dysfunction.
 Take complete history of the presenting

condition paying attention to:

1. Pain:-the character, duration, intensity,
pattern, location, distribution of referred
pain, aggravating factors and relieving
factors.
2. Indigestion:- upper abdominal discomfort
associated with eating.
Assessment cont’
3. Intestinal gas:- belching, flatulence, bloating and abdominal
distension.
4. Change in bowel habits:- diarrhea, constipation, bleeding,
stool changes.
-bulky, foamy stools with foul odor.
- clay/ light grey –absent urobilin.
- Mucoid stools.
- Small, dry, rock hard stool.
5.Nausea and vomiting.
6.Past GIT diseases.
7.Past and current medication use and any surgery.
8.Use of tobacco and alcohol use.
9.Changes in appetite/eating patterns.
10.Un explained weight gain or loss.
2. Physical assessment
 Inspect the mouth, teeth, buccal mucosa,
teeth and gums. Note any discoloration,
rashes/nodules, ulcers or bleeding.
 Pt lies supine with legs flexed at the knees.
 Inspect the abdomen noting any scars,

contour and symmetry.

 Auscultate noting the location, frequency

and character of bowel sounds.

Physical exam cont’d
 High-pitched and gurgling sounds are best
heard using the diaphragm of the
stethoscope
 Percuss the four quadrants of the abdomen

and note any tympany or dullness. Shifting

dullness is a sign of ascitis.
 Palpate to identify areas of tenderness and

swelling. Assess rebound tenderness.

 Inspect and examine the perineal and anal

area.
4. Diagnostic evaluation
a) blood tests:- complete blood count,
carcinoembryonic antigen, LFTs, serum
cholesterol levels and triglycerides.H.P.tests.
b) Stool tests:-inspect for consistency, color
and occult bleeding. Other tests asses for
parasites, pathogens, food residues, fat,
nitrogen, and fecal urobilinogen.
c) Breath tests:- urea breath tests, hydrogen
breath tests.
Diagnostic evaluation
cont’d
d) Abdominal ultrasonography.
e) Barium swallow or upper GI series.
f) CT scan, MRI.
g) Barium enema.
h) Endoscopic procedures.
- upper gastrointestinal fibroscopy/
esophagagogastroduodenoscopy.
-anoscopy, sigmoidoscopy
Esophageal conditions.
1 Achalasia
 also known as esophageal achalasia,
achalasia cardiae, cardio spasm, and
esophageal aperistalsis, is an esophageal
motility disorder involving the smooth muscle
layer of the esophagus and the lower
esophageal sphincter (LES). It is characterized
by incomplete LES relaxation, increased LES
tone, and aperistalsis of the esophagus
(inability of smooth muscle to move food
down the esophagus) in the absence of other
explanations like cancer or fibrosis
Signs and symptoms
 Dysphagia
 Regurgitation.
 Weight loss
 Coughing when lying in horizontal position.
 Chest pains that are easily mistaken for

heart burn.
S$s cont’d
 Due to the similarity of symptoms,
achalasia can be mistaken for more
common disorders such as
gastroesophageal reflux disease (GERD),
hiatus hernia, and even psychosomatic
disorders. Specific tests for achalasia are
barium swallow and esophageal
manometry. In addition, endoscopy of the
esophagus, stomach and duodenum
(esophagogastroduodenoscopy or EGD)
with or without endoscopic ultrasound, is
typically performed to rule out the
possibility of cancer. The internal tissue of
the esophagus generally appears normal in
endoscopy, although a "pop" may be
observed as the scope is passed through
the non-relaxing lower esophageal sphincter
with some difficulty, and food debris may be
found above the LES
Management
 Advice the patient to eat soft food, take it
slowly.
 Calcium channel blockers e.g nifedipine or

nitrates eg isosorbide dinitrate.

 Botulinum toxin.
 Surgery- Heller myotomy.

(esophagomyotomy)
 Pneumatic dilatation. stretch the

narrowed area of the esophagus

2 Gastroesophageal reflux
disease.(GERD)
 is chronic symptoms or mucosal damage
caused by stomach acid coming up from the
stomach into the esophagus. A typical
symptom is heartburn.
 The causes include abnormal relaxation of

the lower esophageal sphincter, which

normally holds the top of the stomach
closed; Pyloric stenosis, motility disorder,
impaired expulsion of gastric reflux from the
esophagus, or a hiatal hernia
Signs and symptoms
Adults
The most-common symptoms of GERD are:
 Heartburn(Burning sensation in the esophagus)

 Regurgitation

 Trouble swallowing (dysphagia)

Less-common symptoms include:

 Pain with swallowing (odynophagia) Excessive

salivation
 Nausea and chest pains

 Esophagitis
Common symptoms of Pediatric Reflux
 Irritability and pain, sometimes screaming

suddenly when asleep. Constant or sudden

crying or colic-like symptoms. Babies can be
inconsolable especially when laid down flat.
 Poor sleep habits typically with arching their

necks and back during or after feeding

 Excessive posseting or vomiting
 Frequent burping or frequent hiccups
 Excessive dribbling or running nose
 Swallowing problems, gagging and choking
 Frequent ear infections or sinus congestion
 Babies are often very gassy and extremely

difficult to “burp” after feeds

 Refusing feeds or frequent feeds for comfort
 Bad breath – smelling acidy Rancid/acid

smelling diapers with loose stool

Diagnosis

 A detailed historical knowledge is vital for

an accurate diagnosis
 Esophageal pH Monitoring,
 barium swallow X-rays,
 esophageal manometry,
 Esophagogastroduodenoscopy (EGD).
Pathophysiology
 GERD is caused by a failure of the cardia. In

healthy patients, the "Angle of His"—the

angle at which the esophagus enters the
stomach—creates a valve that prevents
duodenal bile, enzymes, and stomach acid
from traveling back into the esophagus
where they can cause burning and
inflammation of sensitive esophageal tissue.
Patho cont’d
 Factors that can contribute to GERD:
 Hiatal hernia, which increases the likelihood
of GERD due to mechanical and motility
factors.
 Obesity: increasing body mass index is
associated with more severe GERD. In a large
series of 2000 patients with symptomatic
reflux disease, it has been shown that 13 %
of changes in esophageal acid exposure is
attributable to changes in body mass index
factors
 Zollinger-Ellison syndrome, which can be
present with increased gastric acidity due to
gastrin production
 Hypercalcemia, which can increase gastrin

production, leading to increased acidity

 Scleroderma and systemic sclerosis, which

can feature esophageal dysmotility

 The use of medicines such as prednisolone
 Visceroptosis or Glénard syndrome
Management
 Eat low fat diet, avoid
caffein,tobacco,beer,milk,carbonated beverages.
 Avoid eating 2 hours before bed time.
 Maintain normal body weight.
 Elevate the upper body on pillows.
 Proton pump inhibitors (such as omeprazole,
esomeprazole, pantoprazole, lansoprazole, and
rabeprazole) are the most effective in reducing gastric
acid secretion.
 Gastric H2 receptor blockers (such as ranitidine,
famotidine and cimetidine) can reduce gastric secretion
of acid. These drugs are technically antihistamines. They
relieve complaints in about 50% of all GERD patients.
Management Cont.
 Antacids
 Prokinetics e.g. cisapride strengthen the

lower esophageal sphincter and hasten

gastric emptying.
 Sleeping on the left side reduces reflux at

night.
 Avoid smoking.
 An absolute treatment is vagotomy.
 Nissen fundoplication. In this procedure the
upper part of the stomach is wrapped around
the lower esophageal sphincter (LES) to
strengthen the sphincter and prevent acid
reflux and to repair a hiatal hernia
 Another treatment is transoral incisionless

fundoplication (TIF) with the use of a device

called Esophyx, which allows doctors to rebuild
the valve between the stomach and the
diaphragm by going through the esophagus
3. HIATAL HERNIA
 This is protrusion of the stomach into the
thoracic cavity through a widened opening
where the esophagus penetrates the
diaphragm.
 Hiatal hernias are of two types:
 Sliding hiatal hernia,
 Paraesophageal hernia
Cont..
Clinical features.
 Most patients are asymptomatic.
 Sliding hernia:

◦ Heartburn
◦ Regurgitation
◦ Dysphagia
 Paraesophageal
◦ Sense of fullness
◦ Pain when strangulation occur
◦ Risk of obstruction
management
 Frequent, small feeding
 Advice the patient not to recline for 1 hour
after feeding
 Elevate the head of the bed
 Medical and surgical management of a
paraesophageal hernia is similar to that for
gastroesophageal reflux; however,
paraesophageal hernias may require
emergency surgery to correct torsion (twisting)
of the stomach or other body organ that leads
to restriction of blood flow to that area.
Impaired Esophageal Motility
1. Types
a. Achalasia: characterized by impaired peristalsis
of smooth muscle of esophagus and impaired
relaxation of lower esophageal sphincter
b. Diffuse esophageal spasm: non-peristaltic
contraction of esophageal smooth muscle
2. Manifestations: Dysphagia and/or chest pain
3. Treatment
a. Balloon dilation of lower esophageal sphincter
b. May place stents to keep esophagus open
3. Cancer of the esophagus
 Is malignancy of the esophagus.
 There are various subtypes, primarily

squamous cell cancer (approx 90-95% of all

esophageal cancer worldwide) and
adenocarcinoma.(Cancer of mucus secreting
glands in the body).
 Squamous cell cancer arises from the cells

that line the upper part of the esophagus.

 Adenocarcinoma arises from glandular cells

that are present at the junction of the

esophagus and stomach.
Signs and symptoms
 Dysphagia-difficult swallowing
 Odynophagia-painful swallowing
 Weight loss.
 Lack of appetite.
 Pain of burning, heart burn-like nature
 Nausea
 Vomiting
 Regurgitation
 Persistent hiccups.
 Sub sternal pain.
Signs and symptoms cont.
 Coughing and increased risk of aspiration
pneumonia because of regurgitation.
 Upper air way obstruction in advanced tumor and
fistula may develop.
 Bleeding and Hematemesis.
 Superior vena cava syndrome.
 Sensation of mass in the throat.
 Regurgitation of food.
 Hemorrhage may take place.
 Progressive loss of weight and strength due to
starvation.
 Respiratory difficulty and foul breath.
Causes
Cause is unknown but there are factors that
increases the risk.
 Sex- more common to men.
 Age- most cases are 60 yrs plus.
 Smoking and heavy alcohol use
 GERD
 HPV infection.
 Presence of other head and neck cancers.
 Chronic irritation.
 Corrosive injury to esophagus by swallowing
strong alkalines (lye) or acids.
 Particular dietary substances, eg.
nitrosamine.
 Plummer-Vinson syndrome-is a condition that
can occurs in people with long-term (chronic)
iron deficiency anemia-D.I.S
 Tylosis and Howel-Evans syndrome
(hereditary thickening of the skin of the
palms and soles).
 Radiation therapy for mediastinum cancers.
Diagnosis
 Although an occlusive tumor may be
suspected on a barium swallow or barium
meal, the diagnosis is best made with
esophagogastroduodenoscopy (OGD,
endoscopy)
 Biopsies taken of suspicious lesions are then

examined histologically for signs of

malignancy.
 CT of the chest, abdomen and pelvis, can
evaluate whether the cancer has spread to
adjacent tissues or distant organs
(especially liver and lymph nodes)
 Esophageal endoscopic ultrasound (EUS)

can provide staging information regarding

the level of tumor invasion, and possible
spread to regional lymph nodes
Nursing Diagnosis
a. Imbalanced Nutrition: Less than body
requirements (may include enteral tube
feeding or parenteral nutrition in hospital
and home)
b. Anticipatory Grieving (dealing with
cancer diagnosis)
c. Risk for Ineffective Airway Clearance
(especially during postoperative period if
surgery was done)
Management
 The treatment is determined by the cellular
type of cancer (Adenocarcinoma or squamous
cell carcinoma vs. other types), the stage of
the disease, the general condition of the
patient and other diseases present. On the
whole, adequate nutrition needs to be assured,
and adequate dental care is vital.
 If the patient cannot swallow at all, a stent

may be inserted to keep the esophagus patent;

stents may also assist in occluding fistulas
Management Conti.
 Esophagectomy is the removal of a
segment of the esophagus; as this shortens
the length of the remaining esophagus,
some other segment of the digestive tract
(typically the stomach or part of the Colon
or jejunum]) is pulled up to the chest cavity
and interposed. If the tumor is unresectable
or the patient is not fit for surgery, palliative
esophageal stenting can allow the patient to
tolerate soft diet.
Management Cont.
 Types of esophagectomy:
 Thoracoabdominal approach- which opens the
abdominal and thoracic cavities together.
 Two stage Ivor Lewis (also called Lewis-Tanner)
approach- with an initial laparotomy and
construction of a gastric tube, followed by a
right thoracotomy to excise the tumor and
create an esophagogastric anastomosis.
 Three stage McKeown approach- where a third
incision in the neck is made to complete the
cervical anastomosis.
 Endoscopic Therapy for Localized Disease
 The two forms of endoscopic therapy that

have been used for Stage 0 and I disease

are endoscopic mucosal resection (EMR)
and mucosal ablation using photodynamic
therapy , Nd-YAG laser, or argon plasma
coagulation.
 Laser therapy
 Irradiation
 Chemotherapy depends on the tumor type,
every three weeks with fluorouracil (5-FU)
either continuously or every three
weeks.Chemotherapy may be given after
surgery (adjuvant, i.e. to reduce risk of
recurrence), before surgery (neoadjuvant)
or if surgery is not possible; in this case,and
5-FU are used.
Nursing Management.
 Nutritional therapy.
 Improve physical condition.
 Care of NGT.
 Care of parental lines and fluid therapy.
 Post operative care like any other patient

done thoracic surgery.

 Position-fowler’s position.
 Vital signs monitoring.
 Manage pain.
 Patient education.
Prognosis
 In general, the prognosis of esophageal
cancer is quite poor, because most patients
present with advanced disease. By the time
the first symptoms such as dysphagia start
manifesting themselves, the cancer has
already well progressed. The overall five-
year survival rate (5YSR) is less than 20%,
with most patients dying within the first
year of diagnosis.
OesophagealVarices
 Tortuous, distended vessels of the
esophagus
◦ may rupture and bleed
 causes: Portal hypertension caused by
cirrhosis of the liver
 S/S Hematemesis, hemorrhage from UGI,

black tarry stools, pain, shock.

Treatment
◦Iced saline lavage
◦Medications( Vasopressin,
antibiotics, analgesics)
◦Surgeries: ligation, injection
sclerotherapy-Repair of malformed
vessels.
◦Blood transfusions.
Interventions

◦Administer meds
◦Provide pre/post op care
◦Administer blood transfusions
◦Monitor tube placement
◦Assess vital signs, bleeding
Stomach conditions
4. GASTRITIS
 An inflammation of the gastric mucosa.
Gastritis is a condition in which the stomach
lining—known as the mucosa—is inflamed, or
swollen. The stomach lining contains glands
that produce stomach acid and an enzyme
called pepsin. The stomach acid breaks down
food and pepsin digests protein. Acute
causes include:
o Excessive alcohol use.
o Major surgeries and traumatic injuries
o Burns, severe infections.
Cont.
 A thick layer of mucus coats the stomach lining and
helps prevent the acidic digestive juice from dissolving
the stomach tissue. When the stomach lining is
inflamed, it produces less acid and fewer enzymes.
 Causes are classified as acute causes or chronic.
 Acute gastritis is often caused by; dietary indiscretion-
eats food that is contaminated with disease-causing
microorganisms or that is irritating or too highly
seasoned. Overuse of aspirin and other nonsteroidal
anti-inflammatory drugs , excessive alcohol intake,
bile reflux, and radiation therapy, ingestion of strong
acid or alkali, which may cause the mucosa to become
gangrenous or to perforate.
Chronic causes include:
 H. pylori infection
 Chronic bile reflux.
 Stress
 Crohn's disease.
 Metaplasia- mucus glands metaplasia and

intestinal metaplasia
Signs and symptoms
 Many patients experience no symptoms at
all
 Central abdominal pain is the most common

sign
 Nausea
 Vomiting (if present, may be clear, green or

yellow, blood-streaked, or completely

bloody, depending on the severity of the
stomach inflammation.
Signs and symptom cont.
 Feeling full after only a few bites of food
 Loss of appetite
 Unexplained weight loss
 Belching (if present, usually does not relieve

the pain much)

 Bloating
An erosive Gastritis
Diagnosis
 Often, a diagnosis can be made based on
the patient's description of his or her
symptoms, but other methods which may
be used to verify gastritis include:
 Blood tests:

◦ Blood cell count

◦ Presence of H. pylori
 Liver, kidney, gallbladder, or pancreas
functions
 Urinalysis
 Stool sample, to look for blood in the stool
 X-rays
 ECGs
 Endoscopy, to check for stomach lining

inflammation and mucous erosion

 Stomach biopsy, to test for gastritis and

other conditions.
Management
 Modify diet
 Promote rest
 Reduce stress
 Refrain from alcohol and food until symptoms Subsides.
 Non irritating diet.
 I.V fluids parenteral.
 Incase of ingestion of strong acids and alkalosis RX by
diluting and neutralizing the offending substance .
 Sedatives.
 Analgesics agents.
 Anti acids
 Extreme cases of gangrenous and perforated tissues
surgery is indicated-Gastrojejunostomy/Gastric resection
5 PEPTIC ULCER
 Also known as ulcer pepticum or PUD
 Denotes mucosal erosion of the GIT usually

by the acid.
 Peptic ulcers most commonly occurs on the

duodenum rather than in the stomach.

 4% of stomach ulcers are caused by

malignant tumors while duodenal ulcers are

generally benign.
PUD
Classification
 By Region/Location
 Stomach (called gastric ulcer)
 Duodenum (called duodenal ulcer)
 Esophagus (called Esophageal ulcer)
 Meckel's Diverticulum (called Meckel's

Diverticulum ulcer)
 Modified Johnson Classification of
peptic ulcers:
 Type I: Ulcer along the body of the stomach,

most often along the lesser curve

 Type II: two ulcers present; 1 gastric, 1

duodenal.
 Type III: In the pyloric channel within 3 cm of

pylorus. Associated with acid over secretion.

 Type IV: Proximal gastroesophageal ulcer
 Type V:can occur anywhere
PUD
Pathophysiology
a. Ulcers or breaks in mucosa of GI tract occur
with
i. H. pylori infection (spread by oral to oral,
fecal-oral routes) damages gastric epithelial
cells reducing effectiveness of gastric mucus
ii. Use of NSAIDS: interrupts prostaglandin
synthesis which maintains mucous barrier of
gastric mucosa
b. Chronic with spontaneous remissions and
exacerbations associated with trauma, infection,
physical or psychological stress
Symptoms
 Abdominal pain, classically epigastric. Pain
due to duodenal ulcer is relieved by food
while gastric ulcers are exacerbated by
food.
 Bloating and abdominal fullness.
 Nausea and copious vomiting.
 Water brash (rush of saliva after an episode

of regurgitation to dilute the acid in

esophagus.
 Loss of weight and appetite.
Symptoms cont.
 Hematemesis.
 Melena stool.
 Rarely, can lead to gastric or duodenal

perforation resulting to acute peritonitis.

This is extremely painful and requires
immediate surgery.
Causes
 H. pylori (60% of gastric and up to 90%
duodenal ulcers)
 Use of NSAIDS- blocks COX 1, essential for

the synthesis of prostagladins which

stimulates production of mucus.
 Smoking.
 Zollinger-Ellison’s syndrome (gastrinomas)
 Stress.
Diagnosis
 Based on characteristic
symptoms.
 Barium contrast x-rays and

endoscopy confirm the

diagnosis.
 Blood tests for antibodies against

H. pylori.
 OGD
PUD NURSING DIAGNOSIS
 Pain R/T Increased Secretion of Gastric Acid
 Diarrhea R/T Gastrointestinal Bleeding
 Altered Nutrition: Less Than Body
Requirements R/T Nausea, Vomiting or Pain
or more than body requirements R/T……..
 Fluid Volume Deficit R/T Gastrointestinal
Bleeding
 Knowledge Deficit R/T Management and
Treatment of Peptic Ulcer Disease
Nursing Interventions
 Three meals a day – decreases acid
production
 Decrease foods that stimulate acid

secretions and cause discomfort

 Treat pain with rest, diet and drug therapy
 Educate on stress management and

relaxation
Treatment
• Goals- relieve symptoms, promote healing,
prevent complications and recurrence
– Rest and stress reduction
– Nutritional management
– Avoid stimulants such as nicotine and caffeine
– Avoid carbonated drinks e.g. sodas
– Pharmacological management
• Antacids (MgSO4), Neutralizes acids
• Proton pump inhibitors; Block gastric
acid secretion.
• H2 receptors antagonist.
Cont..
 Pharmacological management
◦ Histamine blockers (ranitidine, cimetidine)
 Blocks gastric acid secretion
◦ Sucralfate/Carafate
 Forms protective layer over the site
◦ Mucosal barrier enhancers (colloidal bismuth,
prostaglandins)
 Protect mucosa from injury
◦ Antibiotics (Amoxicillin, Ampicillin, clindamycin)
 Treat H. Pylori infection
Cont..
• NG suction
• Surgical intervention
– Minimally invasive gastrectomy
• Partial gastric removal with laparoscopic
surgery
– Billroth I -Gastroduodenostomy
– Billroth II-Gastrojejunostomy
– Vagotomy
• Cutting of the vagus nerve to decrease acid
secretion
– Pyloroplasty
• Widens the pyloric sphincter
Complications
 GI bleeding
 Perforation.
 Penetration.
 Gastric outlet obstruction.
 Increases the risk of developing

gastric cancer.
Comparison between gastric
ulcer and duodenal ulcer
Gastric Ulcers
 burning pain 1-2 hrs. after meals, upper

left abd/back,relieved by food

 N/V, anorexia, wt loss

 Shallow/ gastric secretions decreased

 Older men, working class, bld type A, under

stress
Cont..
Duodenal Ulcers
 Burning/ cramping pain 2-4hrs. P meal,

beneath xiphoid and back, relieved by

antacids/food
 Increased gastric acid

 Young men, all social classes, blood type O,

chronic illnesses
UPPER GIT BLEEDING
 Predisposing factors include:
◦Drugs,
◦Esophageal varicosities
◦Esophagitis
◦PUD
◦Gastritis
◦Carcinoma
Signs and symptoms

◦ Coffee ground vomitus

◦ Black, tarry stools
◦ Melena
◦ Decreased B/P
◦ Vertigo
◦ Drop in Hct, Hgb
◦ Confusion
◦ syncope
Diagnosis
 History
Blood, stool, vomitus studies
Endoscopy
Treatment of Upper GI
Bleeding
• Treatments
– Volume replacement
• Crystalloids- normal saline
• Plasma expanders
• Blood transfusions
– NG lavage
– OGD
• Endoscopic treatment of bleeding ulcer
• Sclerotheraphy-injecting bleeding ulcer
with necrotizing agent to stop bleeding
RX.
 Treatments
◦ Surgical intervention
 Removal of part of the stomach
Irritable Bowel Syndrome (IBS)
(spastic bowel, functional colitis)

Definition
a. Functional GI tract disorder without
identifiable cause characterized by
abdominal pain and constipation, diarrhea,
or both
b. Affects up to 20% of people
c. More common in females
Cont..
Pathophysiology
a. Appears there is altered CNS
regulation of motor and sensory functions
of bowel
1.↑ bowel activity in response to food intake,
hormones, stress
2. ↑ sensations of chyme movement through gut
3.Hypersecretion of colonic mucus
b. Lower visceral pain threshold causing
abdominal pain and bloating with normal
levels of gas
c. Some linkage of depression and
anxiety
Cont..
5. Diagnostic Tests: Find a cause for client’s
abdominal pain, changes in feces elimination
a. Stool examination for occult blood, O&C, culture
b. CBC with differential, (ESR): to determine if
anemia, bacterial infection, or inflammatory process
c. Sigmoidoscopy or colonoscopy
1.Visualize bowel mucosa, measure intra-luminal
pressures, obtain biopsies if indicated
2.Findings with IBS: normal appearance increased
mucus, intra-luminal pressures, marked spasms,
possible hyperemia without lesions
d. Small bowel series (Upper GI series with small
bowel-follow through) and barium enema:
examination of entire GI tract; IBS: increased
motility
Cont..
Medications
a. Purpose: to manage symptoms
b. Bulk-forming laxatives: reduce bowel spasm,
normalize bowel movement in number and form
c. Anticholinergic drugs (dicyclomine (Bentyl),
hyoscyamine) to inhibit bowel motility and
prevent spasms; given before meals
d. Antidiarrheal medications (loperamide
(Imodium), diphenoxylate (Lomotil): prevent
diarrhea prophylactically
e. Antidepressant medications
f. Research: medications altering serotonin
receptors in GI tract to stimulate peristalsis of the
GI tract
Cont..
Dietary Management
a. Often benefit from additional dietary fiber:
adds bulk and water content to stool reducing
diarrhea and constipation
b. Some benefit from elimination of lactose,
fructose, sorbitol
c. Limiting intake of gas-forming foods,
caffeinated beverages
8. Nursing Care
a. Contact in health environments outside
acute care
b. Home care focus on improving symptoms
with changes of diet, stress management,
medications; seek medical attention if serious
changes occur
6. PERITONITIS
 This is the inflammation of the peritoneum, the serous
membrane that lines the abdominal cavity and the
abdominal viscera.
 It may be localized or generalized.
 May occur due to bacteria infection or result from non
infectious process.
 May occur due to gunshot wounds, stab wounds
 May occur due to inflammation that extends from
organs out the peritoneal area eg kidney.
 May occur due to other infections like appendicitis,
perforated ulcer,diverticulitis,bowel perforation.
 Abdominal surgical procedures.
 Peritoneal dialysis.
Signs and symptoms
 The main signs are acute abdominal pain,
abdominal tenderness and guarding which
are exacerbated by moving the peritoneum
e.g by coughing
 Blumberg(rebound tenderness) sign is

positive
 Temperature and pulse rate increases.
 Peristalsis diminishes.
 Elevation of the leukocytes.
 Diffuse abdominal rigidity (washboard

abdomen)
Causes
 infected peritonitis.
 Perforation of part of gastrointestinal tract
 Disruption of peritoneum
 Spontaneous bacterial peritonitis. Occurs in

patients with ascites especially children in

absence of any contamination
 Intraperitoneal dialysis
 Systemic infections eg, TB
 Non infected peritonitis
 Leakage of sterile body fluids into the

peritoneum eg. Blood

 Sterile abdominal surgery
 Much rare non-infectious causes include

familiar Mediterranean fever, porphyria-

chemicals, and systemic lupus
erythmatosus.
Assessment and diagnosis
 Primarily based on clinical features-
 Laboratory invest-Elevated wbc,Low

HB,Hematocrit level is low.

 Abdominal x rays may reveal dilated,

edematous intestines
 Ultrasound examination
 Exploratory peritoneal lavage or

laparascopy.
 Paracentensis if ascites is present
 Culture of the peritoneal fluid.
Treatment
 Fluid, colloid, and electrolyte replacement is the
major focus of medical Mngmt.
 Assessment of pain, vital signs, GI function,
 Intake and output and central venous pressure
assists in calculating fluid replacement
 Antibiotics iv or infused into the peritoneum.
 Analgesics are prescribed for pain.
 Antiemetic's,
 Intestinal intubation and suction assist in relieving
abdominal distention
 Surgery (laparotomy) to perform a full exploration
and lavage.
Complications
 Shock and renal failure due to
sequestration(loss of fluids) of fluid and
electrolytes.
 Peritoneal abscess
 Sepsis
 Splinting and difficult in breathing because of
fluid pressing on the diaphragm.
 Post operative complication like wound
evisceration,abcess formation.
 Intestinal Obstruction due to bowel
adhesions.
CA STOMACH
1. Incidence
a. Older adults of lower socioeconomic
groups higher risk
2. Pathophysiology
a. Adenocarcinoma most common form
involving mucus-producing cells of stomach
in distal portion
b. Begins as localized lesion (in situ)
progresses to mucosa; spreads to lymph
nodes and metastasizes early in disease to
liver, lungs, ovaries, peritoneum
Cont..
Risk Factors
a. H. pylori infection
b. Genetic predisposition
c. Chronic gastritis, pernicious anemia,
gastric polyps
d. Achlorhydria (lack of hydrochloric
acid)
e. Diet high in smoked foods and nitrates
f. Cigarette smoking
g. diet high in starch, salt, salted meat,
pickled foods, nitrates
Manifestations
a. Disease often advanced with
metastasis when diagnosed
b. Early symptoms are vague: early
satiety, anorexia, indigestion, vomiting, pain
after meals not responding to antacids
c. Later symptoms weight loss, cachexia
(wasted away appearance), abdominal
mass, stool positive for occult blood
Cont..
Collaborative Care
a. Support client through testing
b. Assist client to maintain adequate
nutrition
Diagnostic Tests
a.CBC indicates anemia
b.Upper GI series, ultrasound identifies
a mass
c.Upper endoscopy: visualization and
tissue biopsy of lesion
Cont..
Treatment
a. Surgery, if diagnosis made prior to metastasis
1. Partial gastrectomy with anastomosis to duodenum:
Bilroth I or gastroduodenostomy
2. Partial gastrectomy with anastomosis to jejunum:
Bilroth II or gastrojejunostomy
3. Total gastrectomy (if cancer diffuse but limited to
stomach) with esophagojejunostomy
Assignment, read on Dumping syndrome
Cont..
Treatment: dietary pattern to delay gastric
emptying and allow smaller amounts of
chyme to enter intestine
1. Liquids and solids taken separately
2. Increased amounts of fat and protein
3. Carbohydrates, especially simple
sugars, reduced
4. Client to rest recumbent or semi-
recumbent 30 – 60 minutes after eating
5. Anticholinergics, sedatives,
antispasmodic medications may be added
6. Limit amount of food taken at one time
Cont..
Nutritional problems
1 Anemia: iron deficiency and/or pernicious
2 Folic acid deficiency
3. Poor absorption of calcium, vitamin D
c. Radiation/chemotherapy to control
metastasis spread
d. Palliative treatment including surgery,
chemotherapy; client may have
gastrostomy or jejunostomy tube inserted
Nursing Diagnoses
a. Imbalanced Nutrition: ??? PEM
b. Anticipatory Grieving
7. APPENDICITIS
 Is a condition characterized by inflammation of the
appendix.
 Appendixis a small, finger-like appendage about 10 cm
(4 inch) long that is attached to the cecum just below
the ileocecal valve.
 The appendix fills with food and empties regularly into
the cecum. Because it empties inefficiently and its
lumen is small, the appendix is prone to obstruction and
is particularly vulnerable to infection (i.e, appendicitis).
 Its a medical emergency and many cases require
removal of the inflamed appendix, either by laparotomy
or laparoscopy Untreated, mortality is high, mainly
because of peritonitis and shock.
Pathophysiology
It becomes inflamed and edematous as a
result of either becoming kinked or occluded
by a fecalith (ie, hardened mass of stool),
tumor, or foreign body. The inflammatory
process increases intraluminal pressure,
initiating a progressively severe,
generalized or upper abdominal pain that
becomes localized in the right lower quadrant
of the abdomen within a few hours, the
inflamed appendix fills with pus.
Causes
 It is caused by obstruction of the
appendiceal lumen. This can be caused by:-
 Impacted feaces
 Parasites or growths that clog appendiceal

lumen.
 Inflammatory bowel disease eg. Chron’s
 Trauma to the abdomen
Signs and symptoms
The main symptom is pain which usually:-
 Occurs suddenly
 Occurs before other symptoms
 Begins at the belly button and then radiates

to the lower abdomen and to the right.

 Is new and unlike any other pain felt before.
 Gets worse in matter of hours
 Worsens when walking, breathing and

coughing
Signs and symptoms cont.
 Loss of appetite
 Nausea and vomiting
 Constipation or diarrhea
 Bloating
 Low grade fever
 Abdominal swelling
 A feeling that passing stool will relieve

discomfort
Diagnosis
 Good history particularly about the symptoms
 Blood tests for infection.

 Imaging tests.

Rovsing's sign
 Continuous deep palpation starting from the

left iliac fossa upwards (anti clockwise along

the colon) may cause pain in the right iliac
fossa, by pushing bowel contents towards the
ileocaecal valve and thus increasing pressure
around the appendix. This is the Rovsing's
sign.
Cont.
Psoas sign
 Psoas sign or "Obraztsova's sign" is right

lower-quadrant pain that is produced with

the patient extending the hip due to
inflammation of the peritoneum overlying
the iliopsoas muscles and inflammation of
the psoas muscles themselves.
Straightening out the leg causes the pain
because it stretches the muscles, and
flexing the hip into the "fetal position"
relieves the pain
Cont.
Obturator sign
 If an inflamed appendix is in contact with

the obturator internus, spasm of the muscle

can be demonstrated by flexing and internal
rotation of the hip. This maneuver will cause
pain in the hypogastrium.
Dunphy's sign
 Increased pain in the right lower quadrant

with coughing
Cont.
Volkovich-Kocher (Kosher)'s sign
 During anamnesis, the appearance of pain in the

epigastric region or around the stomach at the

beginning of disease with a subsequent shift to
the right iliac region.
Sitkovskiy (Rosenstein)'s sign
 Increased pain in the right iliac region as patient

lies on his/her left side.

Bartomier-Michelson's sign
 Increased pain on palpation at the right iliac

region as patient lies on his/her left side

compared to when patient was on supine position
Management

 Appendicectomy-prepare for surgery. Pre and Post

 Antibiotics where surgery is indicated.
 Correct fluid and electrolyte imbalance and
dehydration.
 I.V fluids.
 Analgesics can be administered after the
diagnosis is made.
 Reduce anxiety.
 Maintain skin integrity.
 Attain optimal nutrition.
8. INTESTINAL OBSTRUCTION
 This is mechanical or functional obstruction of
the intestines, preventing normal transit of the
products of digestion.
 It can occur at any level distal to the duodenum
and it is a medical emergency.
 Mechanical obstruction-An intraluminal
obstruction or a mural obstruction from pressure
on the intestinal walls occur.
 Functional obstruction-Intestinal musculature
cannot propel the content along the bowel.-
muscular dystrophy, endocrine disorders,
neurological disorders.
Causes of small bowel
obstruction
 Adhesions from the previous abdominal surgeries
 Hernias containing bowels
 Crohn’s disease
 Neoplasms, benign or malignant
 Intussusception in children
 Volvulus
 Superior mesenteric artery syndrome- compression of
duodenum by the artery and abdominal aorta.
 Paralytic ileus.
 Carcinoma.
 Diverticular.
 I.B.D
 Benign tumors.
Pathophysiology
 Intestinal contents, fluid, and gas accumulate
above the intestinal obstruction. Abdominal
distention and retention of fluid reduce the
absorption of fluids and stimulate more
gastric secretion.
 With increasing distention, pressure within the
intestinal lumen increases, causing a
decrease in venous and arteriolar capillary
pressure. This causes edema, congestion,
necrosis, and eventual rupture or perforation
of the intestinal wall, with resultant peritonitis.
 Reflux vomiting may be caused by
abdominal distention.
 Vomiting results in a loss of hydrogen ions

and potassium from

 Dehydration and acidosis develop from loss

of water and sodium. With acute fluid

losses,
hypovolemic shock may occur.
Signs and symptoms
 Crampy pain that is wavelike and colicky.
 Patient may pass blood and mucus, but no

fecal matter and no flatus.

 Vomiting occurs.
 The abdomen becomes distended.
 Abdominal pain.
 Fecal vomiting.
 Constipation.
Small Bowel vs Large Bowel

 Small:
abdominal pain
vomiting
pass blood and mucous, no stool, no gas
over time signs of dehydration
Large
symptoms develop slowly
constipation
distended abdomen
crampy lower abdominal pain
fecal vomiting
Diagnosis
 Blood tests
 X ray will show distended gut
 CT scanning/ ultrasound
 Biopsy if masses are detected
 Colonoscopy and laparascopy
Treatment
 Decompression of the bowel through a
nasogastric or small bowel tube is
successful in most cases.
 Intravenous therapy is necessary to replace

the depleted water, sodium, chloride, and

potassium.
 Some cases resolve spontaneously
 The surgical treatment of intestinal

obstruction depends largely on the cause of

the obstruction.
Nursing management
 Maintaining the function of the nasogastric
 tube,
 Assessing and measuring the nasogastric

output,
 Assessing for fluid and electrolyte

imbalance, monitoring nutritional status and

assessing improvement.
 Input output monitoring.
Inflammatory Bowel
Disease
 The term inflammatory bowel disease refers
to two chronic inflammatory G.I disorders:
regional enteritis (i.e, Crohn’s disease or
granulomatous colitis) and ulcerative colitis.
Both disorders have striking similarities but
also several differences.
Crohn’s disease

• Regional enteritis commonly occurs in

adolescents or young adults but can appear
at any time of life.
 It can occur anywhere along the GI tract,

but the most common areas are the distal

ileum and colon.
Pathophysiology
 Is a sub acute and chronic inflammation that
extends through all layers (i.e., transmural
lesion) of the bowel wall from the intestinal
mucosa.
 It is characterized by periods of remissions and
exacerbations. The disease process begins with
edema and thickening of the mucosa. Ulcers
begin to appear on the inflamed mucosa. These
lesions are not in continuous contact with one
another and are separated by normal tissue.
Fistulas, fissures, and abscesses form as the
inflammation extends into the peritoneum.
As the disease advances, the bowel walls
thickens and becomes fibrotic and the
intestinal lumen narrows.
Signs and Symptoms
 lower right quadrant abdominal pain and
diarrhea unrelieved by defecation.
 Abdominal tenderness and spasm.
 Crampy abdominal pains.
 Patient tends to limit food intake.
 Weight loss, malnutrition, and secondary
anemia.
 Nutritional deficits.
 Thin and emaciated from inadequate food intake
and constant fluid loss.
 Abscesses, fistulas, and fissures are common.
Assessment and Diagnostic Findings

A proctosigmoidoscopic examination - inflamed.

A stool examination is also performed; the result may
be positive for occult
 blood and steatorrhea (i.e, excessive fat in the feces)

 Barium study of the upper GI tract.

 A CT scan may show bowel wall thickening and

fistula tracts.
 C.B.C is performed to assess HCT and HB levels

(decreased) and the WBC-elevated

 The sedimentation rate is elevated.

 Albumin and protein levels may be decreased,

indicating malnutrition
Complications
 Intestinal obstruction.
 Perianal disease,
 Fluid and electrolyte imbalances,
 Malnutrition from malabsorption,
 Fistula and abscess formation.
 Stricture formation.
ULCERATIVE COLITIS

 Ulcerative colitis is a recurrent ulcerative

and inflammatory disease of the mucosal
and submucosal layers of the colon and
rectum.
 The structures may ulcerate and become

infected.
 It is most common in young adults and

mostly starts at the rectum or sigmoid

colon.
Causes
Unknown, but several factors have been
suggested
 Genetic factors
 Multiple autoimmunity
 Environmental factors
 Diet with low fermentable fibers
Pathophysiology
 Affects the superficial mucosa of the colon and is
characterized by multiple ulcerations, diffuse
inflammations, and desquamation or shedding of
the colonic epithelium.
 Bleeding occurs as a result of the ulcerations. The
mucosa becomes edematous and inflamed. The
lesions are contiguous, occurring one after the other.
 Disease process usually begins in the rectum and
spreads proximal to involve the entire colon.
 Eventually the bowel narrows, shortens and thickens
because of muscular hypertrophy and fat deposits
 Abscess formation
Signs and symptoms
 Diarrhea mixed with blood and mucus
 Weight loss
 Blood on rectal examination
 lower left quadrant abdominal pain,

intermittent tenesmus.
 Anorexia, weight loss, fever, vomiting,

and dehydration, as well as cramping.

Classification
 Colitis is normally continuous from the
rectum to the colon. The disease can be
classified based on the extent, or severity.
 By extent:-
 Distal colitis
 Extensive colitis.
By severity:-
 Mild colitis- less than four stools in a day, no

systemic signs of toxicity

 Moderate disease- more than 4 stools in a

day, mild signs of toxicity eg anemia, mild

pain and low grade fevers
 Severe-more than 6 bloody stools, fever,

tachycardia, anemia, ↑ESR

 Fulminating disease-more than ten stools,

continuous bleeding, toxicity, abdominal

tenderness and distension
Assessment and Diagnostic
Findings
 Assesse for tachycardia, hypotension,
tachypnea, fever, and pallor, hydration
nutritional status, abdomen should be
examined for characteristics of bowel
sounds, distention, and tenderness.
 Stool is positive for blood,
 low HCT and HB.
 Elevated WBC.
 Sigmoidoscopy or colonoscopy.
Management
Medical
 Aminosalycylates such as sulfasalizine.

 Corticosteroids such as cortisone, predinisolone,

beclomethasone.
 Immunosupressive drugs e.g mercaptopurine,

azathioprine, methotrexate.
 Antibiotic for secondary infection.

 Antidiarrheal.

 Sedatives.

Surgery:
Removal of large intestines indicated when there is
exsanguinating hemorrhage, frank perforation or strongly
suspected carcinoma –Total colectomy- ileostomy.
Management Cont.
 Dietary modifications- high fiber diet especially
from brassica that has been shown to heal ulcers.
 Nutritional therapy-oral fluids, low residue high
protein, high calorie diet, supplemental vitamin
therapy.
 Physical care.
 Emotional support.
 Reduce anxiety.
 Relieve pain.
 Maintain normal elimination patterns.
 Maintain fluid intake.
10. PANCREATITIS
Inflammation of the pancreas, and this is a serious
condition.
Can either be acute or chronic.
 Acute pancreatitis is sudden while the chronic type is

characterized by recurring abdominal pain with or

without steatorrhea or DM.
 Acute pancreatitis can be medical emergency

associated with a high risk for life threatening

complication and mortality.
 Chronic pancreatitis often goes undetected until 80% to

90% of the exocrine and endocrine tissue is destroyed.

 Acute pancreatitis does not usually lead to chronic

pancreatitis unless complication develops.

Acute pancreatitis
The disease ranges from mild self limiting disorder to a
severe ,rapidly fatal disease that does not respond to any
treatment.
Characterized by;
 Edema
 Inflammation confined to the pancreases.
 Minimal organ dysfunction is present.
 Patient is acutely ill.
 Risk for hypovolemic shock.
 Fluid and electrolyte disturbance.
 Sepsis

Note that this condition affects people of all ages but

mortality rate increases with advancing age.
Pathophysiology
 Self digestion of the pancreas by its own
proteolytic enzymes principally trypsin causes
pancreatitis.
 Other biliary tract diseases like gallstones which
block flow of pancreatic juice as well as causing a
reflux of bile duct into the pancreatic duct.
 Long term use of alcohol leads to pancreatitis.
 Bacterial or viral infection causes pancreatitis.
 Blunt abdominal trauma ,PUD,Ischaemic vascular
diseases,hyperlipidemia,hypercalcemia,use of
drugs like streroids,diuretics(Thiazides) oral
contraceptives have also ben associated with A.P
Patho.Cont.
Acute pancreatitis may follow surgery of
biliary track or any form of biliary
instrumentation.
Mortality rate occurs due
shock,anoxia,hypotension or fluid and
electrolyte imbalance.
Clinical Manifestation
 Severe abdominal pain and tenderness(Mid epigastic
region)-due to irritation and edema of the inflamed
pancreas that stimulate the nerve ending.
 Abdominal distention –poorly defined palpable
abdominal mass.
 Decreased peristalsis.
 Nausea ad vomiting.
 Patient is acutely ill.
 Fever,Jaundice,mental confusion, and agitation may
occur.
 Hypotension-hypovolemic shock occurs as a result of
loss of protein rich fluid into the tissue and peritoneal
cavity.
Diagnosis
 From HX.-Presence of risk factors.
 Physical examination.
 Lab investigation-serum amylase and lipase

levels are high.(3 times high).

 Elevated W.B.C
 Hypocalcaemia.
 Ultrasound /CT Scan- used to identify an

increase in the size of the pancreas.

 Stool of patient with pancreatic disease is

bulky, pale and foul smelling.

Management
 Directed toward relieving symptoms and
preventing or treating complications.
 Histamine 2/H2 antagonist are prescribed to
decrease pancreatic activity by inhibiting HCL
secretion.
 Nasogastric sanction to relieve nausea, vomiting,
abdominal distention,gastic content.
 Avoid oral intake.
 Parenteral nutrition is usually an important part of
therapy.
 Manage pain.
 Anti emetic agent.
Mx Cont.
 Correction of fluid and blood loss and low
albumin levels is necessary to maintain fluid
volume and prevent renal failure.
 Antibiotic if infection is present.
 Insulin therapy.
 Respiratory care.
 Biliary drainage in case of obstruction.
 Surgical intervention-if in case of necrotic
pancreas or gall stones.
 Improve skin integrity due to risk of skin
breakdown
Chronic Pancreatitis
Inflammatory disorder xrised by progressive anatomic
and functional destruction of the pancreas.
All cells are replaced by fibrous tissue with repeated
attacks of pancreatitis.
The end result is mechanical obstruction of the
pancreatic and common bile ducts and the duodenum.
This follows atrophy of the epithelium of the ducts,
inflammation and destruction of the secreting cells of
the pancreas.
Alcohol consumption and malnutrition are the major
cause.
Clinical Manifestation
 Recurrent attacks of severe upper
abdominal and back pain,occasionaly by
vomiting.
 Severe weight loss.
 Malabsorption occurs in late stage.
 Impaired digestion of fats and proteins-

steatorrhea-high fat content.

 Calcification of the gland occurs-leading to

calcium stones within the ducts.

Diagnosis
 M.R.I
 Computed Tomography.
 Ultrasounds.
 Endoscopic Retrograde

Cholangiopancreatography.(E.R.C.P)This is
to visualize biliary structures and pancreas
via endoscopy.
 Glucose tolerance test-pancreatic islet cell

function.
Medical MX.
 Depends with probable cause in each
patient.
 Aim at preventing and managing acute

attacks.
 Relieve pain and discomfort.
 Manage exocrine and endocrine

insufficiency of pancreas.
 Non surgical management- Endoscopy to

remove pancreatic ducts stones and stent

stricture –this is to relieve obstruction.
Surgical management
 Done to relieve abdominal pain and
discomfort, restore drainage of pancreatic
secretions and reduce the frequency of
acute attacks of pancreatitis.
 Surgical intervention depends with the

degree of the disease, location and type of

the disease.
 E.g. Pancreaticojejunostomy.

Pancreaticoduoderectomy.
CANCER OF THE PANCREAS
 A malignant neoplasm of the pancreas
 About 95% of exocrine pancreatic cancers

are adenocarcinomas . The remaining 5%

include adenosquamous carcinomas, signet
ring cell carcinomas, hepatoid carcinomas,
colloid carcinomas, undifferentiated
carcinomas, and undifferentiated
carcinomas with osteoclast-like giant cells.
Exocrine pancreatic tumors are far more
common than pancreatic endocrine tumors,
which make up about 1% of total cases.
 Hereditary, 5–10% of pancreatic cancer
patients have a family history of pancreatic
cancer. Pancreatic cancer has been
associated with the following syndromes;
autosomal recessive ataxia-telangiectasia
and autosomal dominantly inherited
mutations in the tumor suppressor gene,
hereditary non-polyposis colon cancer (Lynch
syndrome), familial adenomatous polyposis,
and the familial atypical multiple mole
melanoma-pancreatic cancer syndrome.
Cigarette smoking, exposure to industrial chemicals
or toxins in the environment, and a diet high in fat
meat or both are associated with pancreatic cancer.
Other risk factors
• Cigarette smoking.

• Diabetes mellitus.

• Chronic pancreatic.

• Hereditary pancreatitis.
 Age (particularly over 60).

 Male sex (likelihood up to 30% greater than

females)
 Diets low in vegetables and fruits, high in red meat.
Risk factors cont.
 Diets high in sugar-sweetened drinks (soft
drinks).
 Obesity.
 Diabetes mellitus is both risk factor for
pancreatic cancer, and, new onset diabetes
can be an early sign of the disease.
 Helicobacter pylori infection.

Cancer can arise from any portion of the

pancreas but 75% originate from the head of
the pancreas.
Signs and symptoms
 Pain in the upper abdomen that typically
radiates to the back.
 Loss of appetite and/or nausea and vomiting
 Significant weight loss.
 Painless jaundice (yellow skin/eyes, dark
urine).
 steatorrhea.
 itching as the yellow pigment irritates the
skin.
 Ascitis.
Diagnosis
 Abdominal ultrasound
 CT SCAN
 Percutaneous fine needle aspirate biopsy-

Cell for cytology.

 Endoscopic biopsy-ERCP.
 Liver function tests.
 MRI
Treatment
 Surgery- the Whipple procedure (pancreato-
duodenectomy) for tumors of the head of
the pancreas,
 Cancers of the tail of the pancreas can be

resected using a procedure known as a

distal pancreatectomy
 Chemotherapy using gemcitabine,

Fluorouracil.
 Radiation therapy.
Nursing MX.
 Manage pain.
 Attend to nutritional requirement.
 Skin care.
 Promote patient comfort.
 Input output monitoring.
 Vitals.
12. HEPATITIS
 An inflammation of the liver characterized by the
presence of inflammatory cells in the tissue of
the organ.
 Systemic viral infection in which necrosis and
inflammation of liver cells produce a
characteristic cluster of chemical biochemical
and cellular changes.
 Hepatitis is acute when it lasts less than six
months and chronic when it persists longer.
 We have type A,B,C,D & E Hepatitis.
 It is estimated that 60% to 90% of cases of viral
hepatitis go unreported.
Signs and symptoms of acute
hepatitis.
 Malaise, muscle and joint aches, fever,
nausea or vomiting, diarrhea, and
headache. More specific symptoms,
 loss of appetite,
 Dark urine,
 Jaundice
 Abdominal discomfort. hepatomegaly
 Lymphadenopathy or splenomegaly
Signs and symptoms of chronic
hepatitis.
 Weight loss, easy bruising and bleeding
tendencies, peripheral edema and ascites
 Cirrhosis may lead to various complications:

esophageal varices that can cause life-

threatening bleeding.
 Hepatic encephalopathy and hepatorenal

syndrome.
 Acne, abnormal menstruation, lung scarring,

inflammation of the thyroid gland and

kidneys may be present in women with
autoimmune hepatitis.
Causes
a) Acute hepatitis
 Viral hepatitis:
 Hepatitis A, B, C, D, and E.
 Herpes simplex
 Cytomegalovirus
 Epstein-Barr
 Yellow fever
 Adenoviruses
Non viral infection

 toxoplasma
 Leptospira
Q fever
 rocky mountain spotted fever
 Alcohol
 Toxins:
 Amanita toxin in mushrooms,
 carbon tetrachloride,
 Drugs:
 Paracetamol,
 amoxycillin,
 antituberculosis medicines, minocycline
 Ischemic hepatitis (circulatory insufficiency)
 Pregnancy
 Auto immune conditions, e.g., Systemic

Lupus Erythromatosus (SLE)

 Metabolic diseases, e.g., Wilson's disease
Chronic hepatitis, causes
 Viral hepatitis: Hepatitis B with or without
hepatitis D, hepatitis C
 Autoimmune hepatitis
 Alcohol
 Drugs :- methyldopa
 nitrofurantoin
 isoniazid
 ketoconazole
 Non-alcoholic steatohepatitis
 Heredity
 Wilson's disease
 alpha 1-antitrypsin deficiency
 Primary biliary cirrhosis and primary

sclerosing cholangitis occasionally mimic

chronic hepatitis
Diagnoses
 Liver function tests- AST and ALT
 Blood tests
 Based on signs and symptoms
 Liver biopsy.
 Hepatitis Antigen test.
Treatment
 Based on etiology.
 Anti viral drugs are used.TDF/3TC
 In acute stage –bed rest.
 Frequent small feeding-supplemented if
necessary by I.V fluids with glucose.
 Follow up blood work.
 Avoid alcohol.
 Sanitation and hygiene measures.
 Environmental sanitation.
 Health education to the community about the
disease.
Hepatitis A Virus.
 Accounts for 20%-25% of cases of clinical
hepatitis.
 Caused by DNA Virus of the enterovirus
family.
 Mode of transmission of this disease is fecal –
oral route-ingestion of food or liquid infected
by the virus.
 More prevalent in developing countries or in
areas with overcrowding ad poor sanitation.
 Can as well be transmitted during sexual
activity.
Hepatitis B Virus.
 Transmitted primarily through blood
(Percutaneous and per mucosal routes.)
 HBV have been found in
blood,saliva,semen,and vaginal secretion and
can be transmitted through mucous
membranes and breaks in the skin.
 Mothers to child at time of birth transmission.
 HBV has a long incubation period and it
replicates in the liver and remains in the
serum for relatively long periods allowing
transmission of the virus.
Hepatitis c Virus.
 A significant proportion of cases of viral hepatitis are
neither hepatitis A, hepatitis B, nor hepatitis D; as a
result, they are classified
as hepatitis C.
 Modes of transmission is by; blood transfusions, sexual
contact, sharing contaminated needles by,IV/injection
drug users and unintentional needle sticks and other
injuries in health care workers, The incubation period is
variable and may range from 15 to 160 days. The
clinical course of acute hepatitis C is similar to that of
hepatitis B; symptoms are usually mild.
 Following Hep C.infection,there is increased risk of
chronic liver disease,cirrhossis of liver and cancer.
Hepatitis D Virus.
 Hepatitis D occurs in some cases of hepatitis B.
because the virus requires hepatitis B surface
antigen for its replication, only individuals with
hepatitis B are at risk for hepatitis D.
 Hepatitis D antibodies in the presence of HBAg on
testing confirm the diagnosis. It is common
among IV/injection drug users, hemodialysis
patients, and recipients of multiple blood
transfusions.
 Sexual contact with those with hepatitis B is
considered to be an important mode of
transmission of hepatitis B and D.
Cont.
 The incubation period varies between 21
and 140 days.
 The symptoms of hepatitis D are similar to

those of hepatitis B,except that patients

are more likely to develop fulminant
hepatitis and to progress to chronic active
hepatitis and cirrhosis.
 Treatment is similar to that of other forms

of hepatitis.
13. LIVER CIRRHOSIS
 A consequence of chronic liver disease
characterized by replacement of liver tissue
by fibrosis, scar tissue and regenerative
nodules (lumps that occur as a result of a
process in which damaged tissue is
regenerated), leading to loss of liver
function.
Causes
 Alcoholism
 Chronic hepatitis c
 Non-alcoholic steatohepatitis
 Primary billiary cirrhosis
 Primary schelerosing cholangitis
 Autoimmunity
 Hereditary hemochromatosis
 Wilson’s disease
 Alpha 1-antitrypsin deficiency
 Cardiac cirrhosis due to right sided heart

failure
 Galactosemia
 Glycogen storage disease type IV
 Cystic fibrosis
 Hepatotoxins
 Scistosomiasis
Signs and symptoms
 Spider angiomata or spider nevi. Vascular
lesions consisting of a central arteriole
surrounded by many smaller vessels
because of an increase in estradiol
 Palmar erythema.
 Nail changes. Muehrcke's lines - paired

horizontal bands separated by normal color

resulting from hypoalbuminemia
 Terry's nails - proximal two-thirds of the nail
plate appears white with distal one-third
red, also due to hypoalbuminemia
 Clubbing - angle between the nail plate and

proximal nail fold > 180 degrees

 Hypertrophic osteoarthropathy. Chronic

proliferative periostitis of the long bones

that can cause considerable pain.
 Dupuytren's contracture. Thickening and
shortening of palmar fascia that leads to
flexion deformities of the fingers.
 Gynecomastia.
 Hypogonadism.
 Splenomegally
 Caput medusa due to opening of umbilical

vein
 Jaudice
 Ascites
 Asterixis. Bilateral asynchronous flapping of

outstretched, dorsiflexed hands seen in

patients with hepatic encephalopathy
 Fetor hepaticus. Musty odor in breath as a

result of increased dimethyl sulfide.

Diagnosis
 The gold standard for diagnosis of cirrhosis
is a liver biopsy, through a percutaneous,
transjugular, laparoscopic, or fine-needle
approach. A biopsy is not necessary if the
clinical, laboratory, and radiologic data
suggests cirrhosis.
Lab findings
 Aminotransferases - AST and ALT are
moderately elevated, with AST > ALT.
However, normal aminotransferases do not
preclude cirrhosis.
 Alkaline phosphatase - usually slightly

elevated.
 Gamma-glutamyl transferase – correlates

with AP levels.
 Bilirubin - may elevate as cirrhosis

progresses.
 Albumin - levels fall
 Prothrombin time - increases since the liver

synthesizes clotting factors.

 Globulins - increased due to shunting of

bacterial antigens away from the liver to

lymphoid tissue.
 hyponatremia due to inability to excrete

free water resulting from high levels of ADH

and aldosteron
 Thrombocytopenia - due to both congestive
splenomegaly as well as decreased
thrombopoietin from the liver. However, this
rarely results in platelet count < 50,000/mL.
Leukopenia and neutropenia - due to
splenomegaly with splenic margination.
Coagulation defects - the liver produces
most of the coagulation factors and thus
coagulopathy correlates with worsening
liver disease.
Treatment
 Liver cirrhosis can not be reversed once it
has taken place
 Treat the underlying cause.
 If alcohol, abstain
 If wilson’s disease, use chelating

compounds such as penicillamine

 Dietary support
 Prevent complications by :-
 Restricting salt intake
 Giving propranolol to lower BP over portal

system
 Antibiotics
 Give laxatives e.g lactulose to prevent

constipation
 Liver transplant.
Complications
 Hepatocellular carcinoma
 Bruising and bleeding
 Hepatic encephalopathy
 Portal hypertension
 Hepatorenal syndrome
 Hepatopulmonary syndrome
 Portal hypertension gastropathy
14. JAUDICE
 Is a yellowish pigmentation of the skin, the
conjunctival membranes over the sclerae
and other mucous membranes caused by
hyperbilirubinemia. Typically, the
concentration of bilirubin in the plasma
must exceed 1.5 mg/dL ( > 35
micromoles/L), three times the usual value
of approximately 0.5 mg/dL, for the
coloration to be easily visible.
Signs and symptoms
 Yellowing of the conjuctiva of the eyes
 Kernicterus in neonates
 Yellow pigmentation of mucous membranes
Types of Jaudice
 Jaudice is categorized as pre-hepatic,
hepatic and post hepatic depending on
where the physiology of bilirubin
metabolism is disrupted
 In pre-hepatic jaundice, the pathology is

occurring prior to the liver. Eg in hemolytic

anemia. Lab findings here include no
bilirubin in urine, increased unconjugated
serum bilirubin
 in hepatic jaundice, the pathology is within
the liver. The causes include
 Hepatitis
 Hepatotoxicity
 Alcohol liver disease
 Primary billiary cirrhosis
 Gilbert’s syndrome
 Crigler-Najjar syndrome
Causes Cont.
 The lab findings here include presence of
conjugated bilirubin in urine with
urobilirubin levels greater than 2 units and
variable
 Post hepatic jaundice is also called

obstructive jaundice and is due to

interruption of the flow of the bile in the
biliary system.
 Causes include:-
 Gallstones
 Pancreatic cancer
 Liverflukes
 Strictures of the common bile duct
 Biliary atresia
 Ductal carcinoma
 Pancreatitis
 Pancreatic pseudocysts
 The presence of pale stools and dark urine
suggests an obstructive or post-hepatic
cause as normal feces get their color from
bile pigments.
 Patients also can present with elevated

serum cholesterol, and often complain of

severe itching or "pruritus" because of the
deposition of bile salts.
 Not one test can differentiate between

various classifications of jaundice

Diagnosis
Pre-hepatic Hepatic Post-hepatic
Function test
Jaundice Jaundice Jaundice
Normal /
Total bilirubin Increased
Increased
Conjugated
Normal Increased Increased
bilirubin
Unconjugated Normal /
Increased Normal
bilirubin Increased
Normal / Decreased /
Urobilinogen Increased
Increased Negative
Dark
Dark
Normal (urobilinogen +
Urine Color (conjugated
(urobilinogen) conjugated
bilirubin)
bilirubin)
Stool Color Normal
Alkaline
phosphatase Increased
Treatment
 Surgery to relieve obstruction
 Phototherapy in neonates
 Treatment of the underlying cause e.g

liverflukes
15. CHOLECYSTITIS
 Means inflammation of the gall bladder
 The cause is normally the presence of

choleliths or gallstones the causes

inflammation and infection with bacteria
especially E.coli
Signs
 Pain in the right upper quadrant
 This pain may present after eating fatty

greasy food
 Low grade fevers
 Nausea and vomiting
 High fevers, shock and jaundice indicate

complications such as formation of abscess,

perforation or ascending cholangitis
Diagnosis
 fever (usually low grade in uncomplicated
cases)
 tender right upper quadrant +/- Murphy's sign
 Ortner's sign - tenderness when hand taps the
edge of right costal arch.
 Georgievskiy-Myussi's sign (phrenic nerve sign)
- pain when press between edges of
sternocleidomastoid
 Boas' sign-Increased sensitivity below the right
scapula.(also due to phrenic nerve irritation)
 Blood tests- elevated alkaline phosphatase,
↑bilirubin, ↑WBC
 Sonography
 CT scan
 Scintigraphy with tectinium-99m
Treatment
 Surgical removal of gallbladder
 Fluid resuscitation and antibiotics
 Complications of cholecystitis
 Perforation or rupture
 Ascending cholangitis
 Rokitansky-Aschoff sinuses
 bile leak ("biloma")
 bile duct injury (about 5-7 out of 1000

operations.
 abscess
 wound infection
 bleeding (liver surface and cystic artery are

most common sites)

 hernia
16. Cholelithiasis
 Gallstones are hard, pebble-like deposits
that form inside the gallbladder. Gallstones
may be as small as a grain of sand or as
large as a golf ball.
Causes
 Stones made out of cholesterol. Gallstones
made out of cholesterol are by far the most
common type. Cholesterol gallstones have
nothing to do with the cholesterol levels in
the blood.
 Stones made from too much bilirubin in the

bile. Such stones are called pigment stones.

 Failure of the gallbladder to empty bile
properly
 hemolytic anemia, including sickle cell

anemia
 Liver cirrhosis and biliary tract infections
 Diabetes
 Bone marrow or solid organ transplant
 Rapid weight loss, particularly eating a very

low-calorie diet
 Prolonged intravenous feeding
Symptoms
 Pain in the right upper or middle upper
abdomen:
◦ May go away and come back
◦ May be sharp, cramping, or dull
◦ May spread to the back or below the right
shoulder blade
◦ Occurs within minutes of a meal
 Fever
 jaundice
 Abdominal fullness
 Clay-colored stools
 Nausea and vomiting
Diagnosis
 Abdominal ultrasound
 Abdominal CT scan
 Endoscopic retrograde

cholangiopancreatography
 Gallbladder radionuclide scan
 Endoscopic ultrasound
 Magnetic resonance

cholangiopancreatography
 Percutaneous transhepatic cholangiogram
 The doctor may order the following blood
tests:
o Bilirubin
o Liver function tests
o Pancreatic enzymes
Treatment
 In the past, open cholecystectomy was the
usual procedure for uncomplicated cases.
However, this is done less often now.
 laparoscopic cholecystectomy is most

commonly used now.

 Endoscopic retrograde

cholangiopancreatography (ERCP) and a

procedure called a sphincterotomy may be
done to locate or treat gallstones in the
common bile duct.
 chenodeoxycholic acids (CDCA) or
ursodeoxycholic acid (UDCA, ursodiol) may
be given in pill form to dissolve cholesterol
gallstones
 Electrohydraulic shock wave lithotripsy

(ESWL) of the gallbladder has also been

used for selected patients who cannot have
surgery.
17. CHOLANGITIS
 Cholangitis is an infection of the common
bile duct, the tube that carries bile from the
liver to the gallbladder and intestines.
 Risk factors include a previous history of

gallstones, sclerosing cholangitis, HIV,

narrowing of the common bile duct, and
parasitic infections.
Symptoms
 Abdominal pain
 In the right upper side or middle of the

upper abdomen
 May come and go
 Pain is sharp, crampy, or dull
 Pain may move to the back or below the

right shoulder blade.

 Chills
 Fever Clay-colored stools
 Dark urine
 Nausea and vomiting
 Jaudice that may be on and off
Ascending cholangitis
 Caused by bacteria, and causes pain,

jaundice, and fever. The bacteria usually

originate from a preceding
choledocholithiasis and is ascending from
the intestines. Typical bacteria is; - Aerobic:
E. coli, Klebsiella, Pseudomonas (post
ERCP), streptococcus faecalis and
Enterobacter - Anaerobic: Bacteroides
fragilis, Clostridium perfringens.
Types of cholangitis
 Primary sclerosing cholangitis
 Primary sclerosing cholangitis is a

cholangitis with autoimmune origin.

 Secondary sclerosing cholangitis
 Secondary sclerosing cholangitis is a

cholangitis with other causes.

 Recurrent pyogenic cholangitis
Diagnosis
 Abdominal ultrasound
 Endoscopic retrograde

cholangiopancreatography (ERCP)
 Magnetic resonance

cholangiopancreatography (MRCP)
 Percutaneous transhepatic cholangiogram

(PTCA)
 Blood test for:-
 Bilirubin level
 Liver enzyme levels
 Liver function tests
 White blood count (WBC)
Treatment
 Bed rest
 Antibiotics
 Pain medications
 Hospitalization
 Gallstone treatments
18. HAEMORROIDS
 Hemorrhoids are dilated portions of veins in
the anal canal.
 Increased pressure in the hemorrhoidal

tissue due to pregnancy may initiate

hemorrhoids or aggravate existing ones.
Classification

 External hemorrhoids are those that occur

outside the anal verge (the distal end of the
anal canal). Specifically they are varicosities
of the veins draining the territory of the
inferior rectal arteries.
 They are those appearing outside the

external sphincter.
Internal
 Internal hemorrhoids are those that occur

inside the rectum. Specifically they are

varicosities of veins draining the territory of
branches of the superior rectal arteries. As
this area lacks pain receptors, internal
hemorrhoids are usually not painful and
most people are not aware that they have
them.
 They appear above the internal sphincter.
Signs and symptoms
 Itching,
 Rectal pain,
 Rectal bleeding
 The common sign of internal hemorrhoids is

bright red blood covering the stool, a

condition known as hematochezia,
Causes of Hemorrhoids.
 Constipation or diarrhea
 Sedentary life.
 Nutrition (low-fiber diet),
 Increased intra-abdominal pressure.
 Pregnancy,
 Genetics,
 Absence of valves within the hemorrhoid veins,
 Aging
 Obesity
 Sitting for long periods of time
Treatment
 Increasing dietary fiber,
 Oral fluids to maintain hydration,
 Non-steroidal anti-inflammatory drugs.
 Sitz baths, and rest.
 Increased fiber intake has been shown to

improve outcomes and may be achieved by

dietary alterations or the consumption of
fiber supplements.
 Good personal hygiene and avoiding

excessive straining during defaecation.

 Hemorrhoidectomy is a surgical excision of
the hemorrhoid used primary only in severe
cases.
 Doppler guided transanal hemorrhoidal

dearterialization
 Rubber band ligation
 Sclerotherapy involves the injection of a

sclerosing agent (such as phenol) into the

hemorrhoid.