[

GASTROINTESTINAL SYSTEM
REVIEW OF SYSTEMS

(Image taken from Medical-Surgical Nursing, M. Hogan & T. Madayag)

MOUTH (BUCCAL/ORAL CAVITY)

Lips and Cheeks

 made up of skeletal muscles covered by a skin
 keep food in mouth while chewing

Palate

Hard
 Covers bone and provides hard surface against which the tongue forces food

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Soft
 Ends at uvula
 When food is swallowed, soft palate rises as a reflex to close oropharynx

Tongue
 Contains mucous and serous glands, taste buds
 Mixes food and saliva during chewing, forms the food into a mass (bolus)
 Initiates swallowing

Saliva
 Produced by the salivary gland
 Moistens food to form bolus
 Dissolves food substances that begin chemical breakdown of starches

Teeth
 Used to chew (masticate)
 32 permanent
 embedded at the gingiva

PHARYNX
 Nasopharynx and oropharynx
 Provide passageway for food, fluids and air
 Its skeletal muscles move food to the esophagus (peristalsis)
 It has mucus producing glands that provide fluid for easy swallowing

ESOPHAGUS
 A muscular tube about 10 inches (25 cm)
 Serves as passageway of food
 Descends through the thorax and diaphragm

Epiglottis
 A flap of cartilage over the top of larynx
 Keeps food out of larynx during swallowing

Gastroesophageal sphincter
 Between esophagus and stomach
 Prevents reflux of food

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STOMACH
 Located high on the left side of the abdominal cavity
 A distensible organ – can hold up to 4 liters
 Regions:
o cardiac region
o fundus
o body
o Pylorus

Pyloric sphincter- controls emptying of the stomach into the duodenum

Functions:
 Storage reservoir for food
 Mechanical digestion
 Gastric glands has 4 cells:

1. Mucous
 Secretes alkaline mucus
 Serves as protection against gastric juice

2. Zymogemic cells
 Pepsinogen (inactive pepsin-protein digesting enzyme)

3. Parietal
 HCI - increases the activity of protein digesting cells
 Intrinsic factor – aids in the absorption of vitamin B12

4. Enteroendocrine
 Gastrin, histamine, endorphins, serotonin and somatostatin
 Gastrin - regulates secretion and motility of the stomach

Phases of gastric juice secretion

1. Cephalic Phase
 Preparation
 Triggered by sight, odor, taste/thought
 Impulse - vagus nerve - mucous cells

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2. Gastric Phase
Starts with the “full” stimulation of Vagus nerve

Stimulation of vagus nerve

↓
Stimulation of enteroendocrine cells

↓ ↓ ↓
Gastrin Histamine 2 Serotonin
↓ ↓ ↓
Gastric motility Stimulation of Parietal Cells Activates tryptophan
↓ (a natural sedative)

HCl Intrinsic factor

3. Intestinal Phase
 Food enters small intestine
 Zymogemic cells activate

SMALL INTESTINES
 Starts at pyloric sphincter and ends at ileocecal junction
 About 20 feet, one inch by diameter
 Divisions:
 Duodenum
o Begins at the pyloric sphincter up to around the head of the pancreas
o Pancreatic enzymes and bile from the liver enter the small intestine
 Jejunum - middle part
 Ileum - terminal end of small intestine
 Site of chemical digestion and absorption through
 Microvilli
o Villi
o circular folds
 Breaks carbohydrates and proteins

Enzymes
 Pancreatic amylase - acts on starchy foods
 Pancreatic enzymes - breaks protein peptides
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 Pancreatic lipase - breaks lipids

 Triglycerides
o Enters as fat globules
o Coated by bile salts and emulsified

LARGE INTESTINE (COLON)

Divisions:
 Cecum - first part
 Colon
o Ascending
o Transverse
o Descending
o Sigmoid

Functions:
 Eliminates indigestible food residue
 Absorbs water, salts and vitamins formed by the bacteria
 Goblet cells produce mucus- facilitates lubrication
 Defecation reflex
o stretching of the rectal wall
o can be suppressed voluntarily
o expulsion can be attained by Valsalva maneuver

LIVER
 Largest gland
 Approximately 3 pounds (1.4 kg)
 Located at the right side of the abdomen
 Made up of lobules (composed of plates of hepatocytes)
 Sinusoids:
o blood filled spaces
o lined with Kaupffer cells (phagocytic cells)

Functions:
 Serves as the detoxification center of the body
 Secretes bile
 Stores fat-soluble vitamins
 Conjugates bilirubin
 Stores blood and releases during hemorrhage
 Synthesizes protein  albumin, globulin, amino acid
 Synthesizes Prothrombin, Fibrinogen and factors I, II, VII, IX and X
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 Synthesizes fats from carbohydrates and protein  energy or adipose tissue

PANCREAS
 Triangular gland extending across the abdomen
 Functions:
 Produces 1-1.5 L of pancreatic juice
o clear with high bicarbonate content
o can digest all categories of food

DIAGNOSTIC TESTS

Laboratory Tests

CEA ( Carcinoembryonic Antigen)

 (+) colorectal Ca
 X heparin for 2 days
 Specimen by venipuncture

Exfoliative Cytology
 Detect malignant cells
 Written consent
 Liquid diet
 UGI : NGT insertion
 LGI : laxative; enema
o Cells are obtained from saline Lavage – NGT / Proctoscope

Fecal Analysis

Stool for Occult Blood (Guaiac Stool Exam)

 Detect G.I. Bleeding
 Increase fiber (48 – 72 hours)
 No red meats, poultry, fish, turnips, horseradish
 Withold for 48 hrs: Iron, Steroids, Indomethacine, Colchicine
 3 stool specimen ( 3 successive days)

Stool for Ova and Parasites

 Send fresh, warm stool specimen

Stool Culture
 Sterile test tube / cotton – tipped applicator

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Stool for Lipids

 Assess steatorrhea
 No fat diet, no alcohol (3 days )
 72 hour stool specimen (store on ice)
 No mineral oil, neomycin SO4

Gastric Analysis
 Measures secretion of HCI and pepsin
 NPO for 12 hours
 NGT is inserted , connected to suction
 Gastric contents collected every 15 minutes to 1 hour

Radiographic Tests

Scout Film / Flat Plate of the Abdomen

 Plain X – ray of the abdomen
 X belts / jewelries

UGIS ( Barium Swallow)

 To visualize the esophagus, stomach, duodenum and jejunum
 NPO for 6 – 8 hours
 Barium Sulfate (BaSO4) per orem
 X – rays taken on standing, lying position
 After the procedure:
o Laxative
o Increase fluid intake
o Inform client that the stool is white for 24 – 72 hours
o Observe for Ba impaction : distended abdomen, constipation

LGIS (Ba Enema)

 To visualize the colon
 Low residue / clear liquid diet for 2 days
 Laxative for cleansing the bowel
 Suppository / cleansing enema in A.M.
 BaSO4 per rectum
 Care after the procedure – same as UGIS

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Endoscopic Procedures

UGI Endoscopy
 Direct visualization of esophagus, stomach, and duodenum
 Obtain written consent
 NPO for 6 – 8 hours
 Anticholinergic (AtSO4) as ordered
 Sedatives, narcotics, tranquilizers
o E.g. Diazepam, Meperidine HCl
 Remove dentures, bridges
 Local spray anesthetic on posterior pharynx – instruct : X swallow saliva

After the procedure

 Side – lying position
 NPO until gag reflex (2 – 4 hrs)
 NSS gargle; throat lozenges
 Monitor VS
 Assess : bleeding, fever, dyspnea, dysphagia, back / shoulder pain
 Advise to avoid driving for 12 hours if sedative was used.

LGI Endoscopy

Proctosigmoidoscopy (sigmoid, rectum)

 Clear liquid diet 24 hours before
 Administer cathartic / laxative as ordered
 Cleansing enema
 Knee – chest / lateral position

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After the procedure

 Supine position for few minutes
 Assess for signs of perforation
o Bleeding
o Pain
o Fever
o Hot sitz bath for discomfort

Colonoscopy
 Sedation
 Position : left side, knees flexed

After the procedure:

 Monitor VS (note for vasovagal response)
 Assess for s and sx of perforation.

Ultrasonography
 NPO for 8 – 12 HOURS
 Laxative as ordered ( bowel gas)

Liver biopsy
 Determine hepatic malignancies
 Assess results of coagulation tests
 Place on the right side with pillow under costal margin
 Avoid heavy lifting and strenuous activities for a week
 Maintain bed rest for several hours

ALTERATIONS

ESOPHAGITIS
Description: inflammation of the esophagus; may be acute or chronic.
Etiology:
 Commonly caused by gastroesophageal reflux disease (GERD) - a syndrome caused
by a reflux of gastric contents into the esophagus and is due to:
o Decreased or relaxed LES
o Hiatal hernia
o Emesis
o Delayed gastric emptying time (eg, gastroparesis), common in diabetics.
o Ingestion of hot or corrosive substances
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o infectious process (eg, herpes or monilial invasion)

Signs and Symptoms:

1. N/V
2. Pyrosis (hallmark symptom); may radiate to the back, neck, or jaw.
3. Pain after eating and at night when in a supine position.
4. Pain aggravated by an increase in intraabdominal pressure (eg, straining, lifting).
5. Bleeding
6. Strictures may also occur

Overview of nursing interventions:

1. Medications
 Antacids
 H2-receptor antagonists – Tagamet (Cimetidine)
2. Diet
 Low-fat
 Small frequent feedings
 no alcohol, no caffeine, no spices
 high-Fowler’s during and 1 hour eating
3. Weight reduction
4. Avoid activities that increase intraabdominal pressure.
5. Encourage the patient to:
 stop smoking, if applicable.
 avoid wearing tight, restrictive clothing

ESOPHAGEAL HIATAL HERNIA

 Refers to herniation or displacement of a portion of the lower esophagus or the

stomach into the thoracic cavity.

Types:

1. Sliding esophageal hernia (90% of occurrences): herniated portion of the stomach

slides back and forth upward through the hiatus secondary to positional changes.
 weakening of the muscles of the esophageal hiatus (aging process - more than
60%)
 Trauma
 Hereditary factors
 Symptoms are associated with gastro-esophageal reflux:
1. Dysphagia

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2. Pyrosis
3. Regurgitation
4. Bloating

2. Rolling / paraesophageal esophageal hernia: fundus and possibly the greater

curvature of the stomach herniated alongside the esophagus into the thorax
 Occurs less commonly
 Complications are high and include gastric volvulus, strangulations or
obstruction.
 Symptoms are related to increased intrathoracic pressure:
1. Chest pain
2. Shortness of breath
3. Tachycardia with subsequent impaired gas exchange.
 Chest pain is characteristic - it mimics anginal pain and usually is not relieved
when the patient is recumbent.

Nursing Interventions:
1. Medications
 Antacids
 H2-receptor antagonists – Tagamet (Cimetidine)
 Analgesics
2. Diet
 Low-fat
 Small frequent feedings
 no alcohol, no caffeine, no spices
 high-Fowler’s during and 1 hour eating
3. Advise patient to:
 Reduce weight, if indicated
 Avoid wearing tight-fitting or restricted clothing.
 Alcohol and cigarette use.
4. Prepare for herniorrhapy / hernioplasty (Nissen Fundoplication)

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GASTRITIS

Description: Inflammation of the stomach mucosa.

Etiology
1. Acute (transient intermittent inflammation)
 Caused by:
a. Local irritants (eg, drugs, alcohol, corrosive substances),
b. Allergy and bacterial endotoxin invasion (eg, Salmonella, Escherichia coli).
 Associated with mucosal hemorrhages and erosions.
2. Chronic gastritis
 Secondary to bile acid reflux or to peptic ulcer disease.
 Related to chronic use of local irritants (eg, alcohol, drugs)

Pathophysiology processes and manifestations

Prolonged exposure to irritants / HCl


Irritation of gastric mucosa

Erosion  pain

S/Sx

S/Sx may include:

a. Mild to severe abdominal discomfort or pain (may or may not be accompanied by
N/V and diarrhea.)
b. Intolerance to spicy or high-fat food.
c. Diarrhea à FVD if unabated
d. May lead to PUD if not relieved
e. Hemorrhage (as hematemesis or melena) à anemia

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A. Nursing Interventions
1. Correct fluid and electrolyte disorders.
2. Diet therapy.
3. Avoid oral feeding until emesis subsides.
4. Avoid foods contributing to gastric distress.
5. Parenteral therapy
6. Teach the patient about diet and lifestyle changes to prevent exacerbation.
7. Avoid cigarette smoking and alcohol consumption.
8. Medications:
a. Antacids
b. H2-receptor antagonist

PEPTIC ULCER DISEASE

A. Description
1. A chronic condition characterized by an ulceration of the gastric mucosa,
duodenum, or less frequently, of the lower esophagus and jejunum.
2. It is an acute response to medical or surgical stress.

B. Etiology and incidence

1. Unknown
 Infection (H. pylori) à mucosal breakdown
 Genetic predisposition
 Tobacco use
 Ingestion of food or drugs that:
a. injure or alter gastric mucosa
b. increase hydrochloric acid production Stress
 Diseases that alter gastric secretion (eg, pancreatitis, Crohn’s disease)
 Stress

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2. Duodenal ulcers
 more prevalent than gastric ulcers
 usually occur between 20-50 years.

C. Pathophysiology and manifestations

1. Gastric ulcers
Injury

Histamine release

Production of HCl by the parietal cells

More injury
 
Erosion of gastric mucosa Stricture
 
Hematemesis and Melena Pyloric obstruction and perforation

Gastric ulcers are slow to heal, in part because of poor circulation to the ulcerative site.

2. Duodenal ulcers.
1. Increased rate of gastric acid secretion
 increased number of parietal cells
 vagal stimulation that affects gastric release
2. Dumping syndrome reduces the buffering effects of food.
3. Complications include hemorrhage, obstruction, or perforation.
3. Stress ulcers
1. Coffee ground aspirate - hallmark sign
2. Multiple ulcerations felt to be erosions develop secondary to gastric ischemia.
4. S/Sx common to all PUDs:
1. Bloating
2. Belching
3. Nausea
4. Vomiting
5. Pain (usually described as burning or aching)
a. Gastric – aggravated by eating
b. Duodenal – relieved by eating
6. Pain may be associated with:
a. ingestion of specific foods (spicy or fried)
b. alcohol
c. medications

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D. Medical Management
1. Medications
a. Antacids
 Neutralizes HCl
 Taken 1-2 hours pc
 Examples: Amphogel (AL-OH), Basaljel (AL-Carbonate), Milk of Magnesia (Mg-
PH), Maalox (AL-MG-OH)
 Magnesium-based à diarrhea
 Aluminum-based à constipation
b. H2 receptor antagonists
 Reduces HCl secretion
 Taken with meals
 Examples: Tagamet (Cimetidine), Zantac (Ranitidine)
 Side effects:
 Diarrhea
 Abdominal cramps
 Confusion
 Dizziness
 Weakness
c. Cytoprotective drugs
 Coats ulcer
 Taken on an empty stomach (30-60 mins ac)
 Example: Carafate (Sucralfate)
d. H. Pylori Drug Treatment
 Pepto-Bismul
 Amoxicillin/Tetracycline
 Flagyl

2. Surgeries
b. Vagotomy
 Resection of the vagus nerve
 Decreases cholinergic stimulation à decreases HCL secretion
c. Pyroplasty – surgical dilatation of the pyloric sphincter
d. Antrectomy
 Billroth I
 Billroth II
 Subtotal Gastrectomy
o Removal of 75% of the distal stomach

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E. Nursing Interventions
1. Relieve pain: Take prescribed medications as ordered
2. Promote a healthy lifestyle
a. Diet
1. Liberal bland diet during exacerbation
2. Eat slowly and chew food properly
3. Small, frequent feedings during exacerbation
4. Avoid the following:
a. Fatty foods
b. Coffee, tea, cola drinks, chocolate
c. Spices, red /black pepper
d. Alcohol
e. Bedtime snacks
f. Binge eating
g. Large quantities of milk (400 mls/day is allowed)
b. Quit smoking
c. Coping
 Stress Therapy
(a)Recreation and hobbies
(b) Regular pattern of exercise
(c)Stress reduction at home and at work

INFLAMMATORY BOWEL DISORDERS

ULCERATIVE COLITIS

A. Description: Is an inflammatory process affecting the mucosa of the colon and

rectum.

B. Etiology and Incidence:

1. Exact cause unknown but closely associated with:
a. Infection
b. Autoimmune dysfunction
c. Genetic predisposition
d. Psychological stressor
2. Incidence is higher in young adults (15 to 20 years old)

C. Pathophysiologic Processes and Manifestations

1. Diffuse inflammation of intestinal mucosa  swelling of epithelial cells  necrosis
 crypt formation  site of abscess  ulceration
2. Chronic  narrowing of lumen
3. Symptoms include:
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a. Bloody diarrhea (15-20 times daily) – with or without pus

b. Abdominal tenderness
c. N/V
d. Fever
e. Anorexia
f. Weight loss

REGIONAL ENTERITIS (CROHN’S DISEASE)

A. Description
1. Chronic inflammatory bowel disease affecting segmental areas along the entire
wall of the GI tract.

B. Etiology
1. Exact cause unknown; usually associated with:
g. Infectious process
h. Allergy or autoimmune disorders
i. Genetic predispositions

C. Pathophysiologic Processes and Manifestations

1. Thickening and inflammation is present (Telescoping)
2. Healing lesions result in scar tissue formation  obstruction of GI tract
3. Diarrhea, 3-5 / day without blood.
4. Other symptoms:
a. Weakness d. Malaise
b. Nutritional deficits e. Weight loss
c. Fever with leukocytosis

D. Overview of Nursing Interventions (for IBD’s)

1. Administer medications, as ordered.
a. Antimicrobial c. Antidiarrheal
b. Antispasmodics
2. Institute dietary management:
a. Low-residue, lactose-free
b. Elemental type
c. TPN if necessary
3. Observe for fluid and nutritional status
4. Monitor bowel movement consistency, frequency and volume.

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DIVERTICULITIS

A. Description: An inflammation of the diverticula (diverticulosis) or herniations within

the wall of the intestinal tract.

B. Etiology and Incidence:

1. Chronic constipation
2. Increased incidence associated with ulcerative colitis and Crohn’s disease.
3. Diverticula occurs more in adult.

C. Pathophysiology and Manifestations

1. Commonly affects the sigmoid colon.
2. Increased luminal pressure (chronic constipation)  formation of diverticula /
herniation through a weak structure  bacteria formation through a weak
muscular structure  local abscess  intraabdominal perforation and peritonitis.
3. Symptoms include:
a. Pain on LUQ
b. Intermittent rectal bleeding
c. Constipation
d. Fever (with leukocytosis)

D. Overview of Nursing Interventions

During an acute phase:

1. Bed rest
2. NPO, later on clear liquids
3. Low fiber
4. Analgesics, antibiotics, anticholinergics

Everyday life: (Diverticulosis)

1. Administer antimicrobial agents as ordered.
2. Bulk-forming laxatives
3. Dietary regimen:
a. Low fiber diet
b. Eliminate foods with seeds and nuts.
4. Encourage fluid intake
5. Observe fluid status and bowel movement.
6. Prepare for colostomy; institute postoperative care.

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APPENDICITIS
A. Description: Is the inflammation of the vermiform appendix.

B. Etiology:
1. Exact cause is unknown. Factors may include:
a. Fecal impaction
b. Kinking of the appendix
c. Parasites
d. Infections

C. Pathophysiologic processes and manifestations

Concurrent infection
↓
Mucosal ulceration
↓
Bacterial invasion
↓
Abscess formation
↓
Necrosis
↓
Rupture (24-36 hours)
↓
Peritonitis

1. Psoas sign (lateral position with right hip flexion)

2. Severe abdominal pain with rebound tenderness at Mcburney’s point (RLQ) –
Blumberg Sign
3. Other symptoms:
 Rigid abdomen, guarding
 Anorexia
 N/V
 Fever (38-38.5 oC)
 Leukocytosis (more than 10,000 / cu mm)

D. Overview of Nursing Interventions

1. Bed rest
2. NPO
3. Avoid enemas, heat application and laxatives - prevent rupture.
4. IVF therapy
5. Antibiotic therapy
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6. Appendectomy to avoid peritonitis.

 Done under spinal anesthesia
 Flat on bed (6-8 hours)
 NPO until peristalsis returns
 Institute postoperative care.
 Activities can be resumed within 2-4 weeks.
7. If the diagnosis is not definitive, prepare for exploratory laparotomy.

HEMORRHOIDS

• Dilated blood vessels beneath the lining of the skin in the anal canal
• Two Types of Hemorrhoids
– External hemorrhoids – occur below the anal sphincter
– Internal hemorrhoids – occur above the anal sphincter
• Causes
– Chronic constipation
– Pregnancy
– Obesity
– Prolonged sitting or standing
– Wearing constricting clothings
– Disease conditions like liver cirrhosis, RSCHF

Signs and Symptoms:

1. Constipation ( in an effort to prevent pain or bleeding associated with defecation.)
2. Anal pain
3. Rectal bleeding
4. Anal itchiness
5. Mucous secretion from the anus
6. Sensation of incomplete evacuation of the rectum

Collaborative Management:
1. High fiber diet, liberal fluid intake
2. Bulk laxatives
3. Hot Sitz bath, warm compress
4. Local anesthetic application – Nupercaine
5. Surgery
 Hemorrhoidectomy
 Sclerotherapy (5% phenol in oil)
 Cryosurgery
 Rubber – band ligation
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6. Preop Care
 Low residue diet to reduce the bulk of stool
 Stool softeners
7. Postop Care
a. Promotion of comfort
 Analgesics as prescribed
 Side – lying position
 Hot Sitz bath 12 to 24 hrs. postop
b. Promotion of elimination
 Stool softener as prescribed
 Encourage the client to defecate as soon as the urge occurs
 Analgesic before initial defecation
 Enema as prescribed, using a small – bore rectal tube
c. Patient Teaching
 Clean rectal area thoroughly after each defecation
 Sitz bath at home especially after defecation
 Avoid constipation:
o High – fiber diet
o High fluid intake
o Regular exercise
o Regular time for defecation
 Use stool softener until healing is complete
 Notify physician for the following:
o Rectal bleeding
o Continued pain on defecation
o Continued constipation

PANCREATITIS

A. Description: Is acute / chronic inflammation of the pancreas.

B. Etiology: Results from alterations in the structure or function of the pancreas,

commonly caused by chronic alcohol abuse.

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C. Pathophysiology
D.
Disruptions of pancreatic ducts

Pancreatic enzymes spill out the pancreatic tissues

Autodigestion (hallmark sign)

Incapacitating pain Hemorrhage Spill out to the

peritoneum

Neurogenic shock Necrosis Peritonitis

E. Overview of Nursing Interventions

Assess:
o abdominal, cardiac, and respiratory status
o fluid balance
Monitor and record:
o vital signs
o intake and output
o laboratory studies
o central venous pressure (CVP)
o daily weight
o urine and stool for color
o blood glucose level
Administer the following, as ordered:
o Drug of choice: Morphine Sulfate
o IVF
Diet: NPO
o to rest the pancreas
o prevent nausea and vomiting.
Keep the patient in Semi-Fowler’s position
Environment:
o Quiet
o Restful

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LIVER CIRRHOSIS

 Irreversible chronic inflammatory disease characterized by massive degeneration and

destruction of hepatocytes.

Types:
1. Laennec’s cirrhosis – the most common
1. Caused by the liver’s toxic to alcohol
2. Occurs primarily in middle-aged men
2. Postnecrotic cirrhosis
1. Results from severe liver disease
2. Post - acute viral or chemical hepatitis
3. Primary biliary cirrhosis: inflammation and intrahepatic bile duct destruction.
4. Secondary biliary cirrhosis: chronic partial or complete common bile duct
obstruction due to gall stones, pancreatitis or tumor.
5. Cardiac cirrhosis results from right-sided CHF.

Pathohysiology:

Laennec’s Cirrhosis
 Alcohol causes changes à fatty infiltration of the hepatocytes à liver cell necrosis
and scarring à as it progresses, inflammation decreases but fibrosis increases à
liver distortion à structural (biliary channel) and vascular changes.
 Scar tissue formation and irregular hepatocyte regeneration à compression of
portal vein à obstruction à portal hypertension
 Decreased Vitamin ADEK absorption
1. bleeding tendencies
2. poor calcium transport
3. poor skin turgor
4. visual disturbances
 Depletion of glycogen à hypoglycemia
 Decreased albumin à decreased COP à anasarca
 Increased HP à ascites
 Decreased bilirubin metabolism à hyperbilirubinemia à jaundice

Biliary cirrhosis
 Chronic obstruction à increased pressure in the hepatic bile duct à accumulation of
bile à necrosis à fibrosis and hepatocellular destruction à scar tissue
1. Hyperbilirubenemia
2. Jaundice
3. Pruritus
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4. clay-colored stools
5. RUQ pain.

Cardiac cirrhosis
 Cor plumionale  congested venous blood flow  backflow of blood to the liver
 congestion  anoxia necrosis and fibrosis

Hepatorenal syndrome
 A major complication of cirrhosis
 characterized by renal failure in an anatomically normal kidneys à progressive
oliguria and azotemia.

Nursing Interventions:
1. Assess for signs of bleeding
2. Monitor V/S and laboratory results (platelets, creatininine)
3. Monitor I/O.
4. Monitor daily weight and abdominal girth to detect ascites.
5. Administer the following as ordered to combat symptoms:
1. Vitamin K
2. Stool softeners
3. Diuretics
6. Assess for changes in cardiac output, decreased renal function and electrolyte
imbalances.
7. Assess for impaired skin integrity related to edema, ascites and pruritus.
8. Use preventive measures to keep skin intact.
9. Assess the patient for signs of impaired breathing related to congestion or infection.
10. Relieve breathing difficulty.
11. Observe for signs of encephalopathy (lethargy, confusion, personality changes,
motor changes, depression, irritability).
12. Teach ways to decrease bleeding tendencies.
14. Patient teaching:
a. Nutritional needs
b. Avoidance of alcohol
c. Drug interactions related to decreased liver function.
d. Enough rest
e. Signs and symptoms needing medical intervention.
15. Provide counseling for the patient and family.

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CHOLELITHIASIS/CHOLECYSTITIS

• Cholelithiasis is stone formation in the GB

• Cholecystitis is inflammation of the GB
• Cause: unknown
• Predisposing factors
female fat
forty fair complexion
fertile

• Theories
• Metabolic factors
• Biliary stasis
• Inflammation
• Composition of Gall stone
cholesterol bile salts
Ca bilirubin
protein

Signs and Symptoms:

1. Decreased fat emulsification
• fat intolerance
• anorexia, N/V
• flatulence
• steatorrhea
2. Inflammation
• pain (RUQ)
• fever
• leukocytosis
3. Decreased bile flow in colon
• acholic stool
• poor absorption of fat soluble vitamins
4. Increased serum bilirubin
• Jaundice
• Pruritus
• Tea-colored urine
5. Infection
• Cholecystitis
• Pancreatitis

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Management:
1. Relief of pain
• MorphineSO4
2. Diet: low fat diet
3. Bile salts: chenodeoxycholic acid, ursodioxycholic acid given after meals
4. Surgery: cholecystectomy

Preop care:
1. IVF to replace loss in vomiting
2. DBCT
3. Vit K injection

Postop Care
1. Low or semi-fowler’s position
2. NGT for decompression
3. Diet: low fat for 2-3 months
4. Ambulation after 24 hrs post op
5. T tube if with CBD exploration
 Purpose is to drain bile
 Drainage:
o Brownish red for 1st 24 hrs
o 300-500 ml of bile drainage for 1st 24 hrs
o Drainage bottle should be placed in bed at level of incision to drain excess
but not all of the bile

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