Vous êtes sur la page 1sur 16

Gastrointestinal Hepatobiliary System


Mouth-Buccal/Oral Cavity

1. Lips and Cheeks

• made up of skeletal muscles covered by a skin
• keep food in mouth while chewing
2. Palate
a. Hard
• Covers bone and provides hard surface against which the tongue forces food
b. Soft
• Ends at uvula
• When food is swallowed, soft palate rises as a reflex to close oropharynx
3. Tongue
• Contains mucus and serous glands, taste buds
• Mixes food and saliva during chewing, forms the food into a mass (bolus)
• Initiates swallowing

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

4. Teeth
• Used to chew (masticate)
• 32 permanent
• embedded at the gingiva

• 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

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

1. Epiglottis
• A flap of cartilage over the top of larynx
• Keeps food out of larynx during swallowing

2. Gastroesophageal sphincter- between esophagus and stomach

• Located high on the left side of the abdominal cavity
• A distensible organ – can hold up to 4 liters
• Regions:
a. cardiac region
b. fundus
c. body
d. pylorus

Pyloric sphincter- controls emptying of the stomach into the duodenum

1. Storage reservoir for food
2. Mechanical digestion
Page 1 of 16
3. Gastric glands has 4 cells:
a. Mucous
• Alkaline mucus
• Serves as protection against gastric juice
b. Zymogemic cells
• Pepsinogen (inactive pepsin-protein digesting enzyme)
c. Parietal
• Increases the activity of protein digesting cells
Intrinsic factor
• Absorption of vitamin B12
d. Enteroendocrine
• Gastrin, histamine, endorphirs, serotonin and sonatoslatin
• Gastrin- regulates secretion and motility of the stomach

Small Intestine
• Starts at pyloric sphincter and ends at ileocecal junction
• About 20 feet, one inch by diameter
• Divisions:
a. Duodenum
• Begins at the pyloric sphincter up to around the head of the pancreas
• Pancreatic enzymes and bile from the liver enter the small intestine
b. Jejunum - middle part
c. Ileum - terminal end of small intestine
• Site of chemical digestion and absorption through
a. microvilli
b. villi
c. circular folds
• Breaks carbohydrates and proteins
• Enzymes
a. Pancreatic amylase
• acts on starchy
b. Pancreatic enzymes
• breaks protein peptides
c. Pancreatic lipase
• breaks lipids
d. Triglycirides
• Enters as fat globules
• Coated by bile salts and emulsified

Large Intestine (Colon)

• Divisions
a. Cerum - first part
b. Colon
o Ascending
o Transverse
o Descending
o Sigmoid

1. Eliminates indigestible food residue
a. Goblet cells produce mucus- facilitates lubrication
b. Defecation reflex
• stretching of the rectal wall
• can be suppressed voluntarily
• expulsion can be attained by Valsalva maneuver
2. Absorbs water, salts and vitamins formed by the bacteria

• Largest gland

Page 2 of 16
• Approximately 3 pounds (1.4 kg)
• Located at the right side
• Made up of lobules (composed of plates of hepatocytes)
• Sinusoids
- blood filled spaces
- lined with Kaupffer cells (phagocytic cells)

1. Secretes bile
2. Stores fat-soluble vitamins
3. Conjugates bilirubin
4. Stores blood and releases during hemorrhage
5. Synthesizes protein  albumin
6. Synthesizes Prothrombin, Fibrinogen and factors I, II, VII, IX and X
7. Synthesizes fats from carbohydrates and protein  energy or adipose tissue
8. Synthesizes cholesterol  production of bile salts, steroid hormones and plasma membranes
9. Deamination (Amino acid  carbohydrates)
10. Releases during hypoglycemia
11. Takes up glucose during hyperglycemia
12. Detoxification
13. Stores iron as ferritin (necessary for RBC production)

• Triangular gland extending across the abdomen

1. Produces 1-1.5 L of pancreatic juice everyday
2. Pancreatic juice
- clear with high bicarbonate content
- can digest all categories of food




1. Mechanical = trauma
2. Chemical = irritants, drugs, toxins
3. Biological = infections
 HS virus I & II
 Spirochete
 Bacteria - Staphylococcus, Streptococcus

1. Stomatitis = Mouth inflammation & erosions

 Etiology: trauma, irritants as tobacco and alcohol, chemotherapy, renal, liver and blood
 S/S: halitosis, soreness of mouth, excessive salivation

2. Glossitis = Tongue inflammation & ulcers

 Etiology: trauma, irritants

3. Gingivitis = Gum inflammation & ulcers

 Etiology: poor dental care, malocclusion, irregular teeth, low fiber diet
 S/S: Bleeding esp. with brushing, pain, swelling, redness; Periodontitis (pus, abscess,
loose teeth)

4. Herpes Simplex:
 Etiology: HS virus I & II
 Also called “cold sore or Fever blisters”
 Classified as STD

Page 3 of 16
 S/S: Vesicles on an erythematous base; lesions @ junction of lips & face
 Activated by: sunlight, heat, fever, menses, digestive disturbances, food allergies.

5. Vincent’s Angina
 Known as “ Trench Mouth” / Acute necrotizing ulcerative gingivitis
 Etiol: Fusiform bacteria, Spirochetes (Borrelia vincentii)
 Purple-red gums with pseudomembrane
 S/S: fever, anorexia, foul breath, cervical lymphadenopathy
 Maybe acute, sub-acute or chronic

6. Aphthous Ulcer
 Very painful, (1cm)
 shallow erosions of called “canker sores”
 circumscribe with white or yellow center, encircle by a red ring

7. Parotitis = inflammation of parotid glands

 Etiology: Staphylococcus (usual)/ Streptococcus
 S/S: Pain at ear and area of gland; No salivation Pus exudates

8. Oral Candidiasis
 Moniliasis or thrush
 Etiol: prolonged high-dose antibiotic tx or steroids
 S/S: Pearly, bluish-white milk curd membranous lesion at oral mucosa/larynx; sore mouth
yeasty halitosis

NCP: Oral Inflammations

NDx1 = Pain:
 Topical Xylocaine
 Analgesics
 Bland, Soft/liquid diet
 Mild antiseptic mouthwash

NDx2: Nutrition, < BR

 At least 1,500 cal/d
 Fluid intake at least 2l/d

NDx3: Imp. Oral M. M.

 Oral care q 4h
 Gingival massage (gingivitis)
 Antibiotics for infections; Acyclovir; Steroids
 Mild oral antiseptics
 Prof’l dental care
 Fibrous rather than soft diet
 Adequate fluid intake
 Conscientious brushings habits with flossing


A. Description: inflammation of the esophagus; may be acute or chronic.

B. Etiology:
• Commonly caused by gastroesophageal reflux disease (GERD) - a syndrome caused by a
reflux of gastric contents into the esophagus:
a. Lower esophageal sphincter (LES) tone is decreased or relaxed.
b. Hiatal hernia
c. Emesis
d. Delayed gastric emptying time (eg, gastroparesis), common in diabetics.
e. Ingestion of hot or corrosive substances
f. infectious process (eg, herpes or monilial invasion)

A. Pathophysiology and manifestations

Page 4 of 16
Backflow of HCl / intake of corrosive agents

Damage of the epithelial cells of esophagus

Frequent exposure to chemicals


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

B. 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


• Refers to herniation or displacement of a portion of the lower esophagus or the stomach into the
thoracic cavity.


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 due to the aging process (more than
• Trauma
• Hereditary factors
• Symptoms are associated with gastro-esophageal reflux:
1. Dysphagia
2. Pyrosis
3. Regurgitation
4. Bloating
Page 5 of 16
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 because 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 Fuldoplicaion


A. Description: Inflammation of the stomach mucosa.

B. Etiology
1. Acute (transient intermittent inflammation)
• Caused by:

Page 6 of 16
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)

C. Pathophysiology processes and manifestations

Prolonged exposure to irritants / HCl

Irritation of gastric mucosa



S/Sx may include:

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

D. 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


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)  mucosal breakdown

Page 7 of 16
 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)

2. Duodenal ulcers are thought to occur more prevalent than gastric ulcers and usually occur between
the 2nd and 5th decades of life.

C. Pathophysiology and manifestations

1. Gastric ulcers

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 or secondary to
vagal stimulation, 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 – relieved by eating
b. Duodenal – aggravated by eating
6. Pain may be associated with:
a. ingestion of specific foods (spicy or fried)
b. Alcohol
c. medications

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
• Magnesium-based  diarrhea
• Aluminum-based  constipation

b. H2 receptor antagonists
• Reduces HCl secretion
• Taken with meals
• Examples: Tagamet (Cimetidine), Zantac (Ranitidine)

Page 8 of 16
• 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  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

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


A. Description
1. Is an inflammation of the GI; it most commonly affects the small intestine.
2. A.K.A Traveler’s diarrhea, dysentery.
3. History – will differentiate from other conditions

B. Etiology and Incidence

1. Bacterial
• E. Coli – Traveler’s Diarrhea
• Shigellosis – Bacillary Dysentery
• By way of fecal-oral
Page 9 of 16
• Affects all ages
• Affects in warm climates
2. Viral gastroenteretits
• rotavirus and parvovirus-type
• by way of the respiratory system.
• Affects primarily infants and the aged
• Crowded living conditions

C. Pathophysiology and manifestations.

1. Symptoms common to all types of gastroenteritis include:
• Nausea
• Vomiting
• Diarrhea
2. Bacterial – stool specimens with high WBC, possibly high RBC
3. Viral - high WBC and the presence of pus
4. Fever depends on microorganism, bacterial usually causes higher temp.
5. S/Sx of viral gastroenteritis include
• Headache
• Weakness
• muscle aches and pains
• abdominal distention and tenderness (but no rebound tenderness)
6. Infection can last anywhere from 2 to 7 days.
7. In diarrhea and vomiting become severe  FVD

D. Nursing Intervention
1. Drugs – anti-infective agents, analgesics, and electrolyte replacement medications (eg,
potassium). No drugs to suppress gastric motility.
2. Monitor I & O
3. Watch out for F & E imbalances
4. Dietary changes
• intake of clear liquids initially
• lactose-free foods for 1 to 2 weeks (after symptoms subside)
5. Parenteral therapy for severe cases.
6. Collect stool specimen.
7. Provide meticulous perianal skin care.
8. Provide patient teaching covering:
• Adherence to medication regimen
• Appropriate sanitary methods for cooking and personal hygiene

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:
a. Bloody diarrhea (15-20 times daily) – with or without pus
b. Abdominal tenderness
c. N/V
d. Fever
e. Anorexia
f. Weight loss

Page 10 of 16
D. Overview of Nursing Interventions
1. Administer medications, as ordered.
a. Antimicrobial c. Antidiarrheal
b. Antispasmodics
2. Institute dietary management:
a. Low-residue c. Elemental type (fast GI absorption)
b. Lactose-free d. TPN if needed
3. Monitor I & O
4. Collect stool specimen
5. Monitor weight
6. Prepare for surgery and institute postoperative care.


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

B. Etiology
1. Exact cause unknown; usually associated with:
a. Infectious process
b. Allergy or autoimmune disorders
c. 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

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.


A. Description: An inflammation of the diverticula 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)

Page 11 of 16
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:
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.

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

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
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.


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.

Page 12 of 16
C. Pathophysiology and manifestations

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

D. Overview of Nursing Interventions

1. Avoid excessive food intake to prevent autodigestion.
2. Demerol for pain. Avoid morphine as it stimulates release of pancreatic juice
3. Monitor for signs of shock.


• 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
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

Page 13 of 16
• 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


 Irreversible chronic inflammatory disease characterized by massive degeneration and destruction of


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 and Manifestations

1. Laennec’s Cirrhosis
 Alcohol causes changes  fatty infiltration of the hepatocytes  liver cell necrosis and scarring
 as it progresses, inflammation decreases but fibrosis increases  liver distortion  structural
(biliary channel) and vascular changes.
 Scar tissue formation and irregular hepatocyte regeneration  compression of portal vein 
obstruction  portal hypertension
 Decreased Vitamin ADEK absorption
1. bleeding tendencies
2. poor calcium transport
3. poor skin turgor
4. visual disturbances
 Depletion of glycogen  hypoglycemia
 Decreased albumin  decreased COP  anasarca
 Increased HP  ascites
 Decreased bilirubin metabolism  hyperbilirubinemia  jaundice
2. Manifestations postnecrotic - same as Laennec’s cirrhosis.
3. Biliary cirrhosis
 Chronic obstruction  increased pressure in the hepatic bile duct  accumulation of bile 
areas of necrosis  edema, fibrosis and hepatocellular destruction  scar tissue destruction 
1. Hyperbilirubenemia
2. Jaundice
3. Pruritus
4. clay-colored stools
5. RUQ pain.
4. Cardiac cirrhosis

Page 14 of 16
 Enlarged liver  congested venous blood flow  failure of the heart to pump blood to different
areas of the body.
 Congestion causes anoxia to the liver  necrosis and fibrosis

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

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.


• Cholelithiasis is stone formation in the GB

• Cholecystitis is inflammation of the GB
• Cause: unknown
• Predisposing factors
female fat
forty fair complexion
• Theories
• Metabolic factors
• Biliary stasis
• Inflammation
• Composition of Gall stone
cholesterol bile salts
Ca bilirubin

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

Page 15 of 16
• poor absorption of fat soluble vitamins
4. Increased serum bilirubin
• Jaundice
• Pruritus
• Tea-colored urine
5. Infection
• Cholecystitis
• Pancreatitis

1. Relief of pain
• Meperidine HCL, not 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
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

Page 16 of 16

Centres d'intérêt liés