Bullets
Disorders of the Liver
A. Hepatitis
1. Definition/etiology - acute inflammatory disease of the liver caused by viral, bacterial, or toxic ingestion
2. Pathophysiology
a. inflammation of liver, enlargement of Kupffer cells, bile stasis
b. regeneration of cells with no residual damage
c. types
i. hepatitis A
• transmitted from infected food, water, milk, shellfish
• fecal-oral route of infection common in poor sanitation/overcrowding
• higher incidence in fall and winter
• new vaccine available
ii. hepatitis B
• blood-borne and sexually transmitted
• may become a carrier
iii. hepatitis C
• transmitted parenterally (post-transfusion hepatitis) and possibly fecal-oral route
• may become a carrier
iv. hepatitis D
• blood borne
• coexists with hepatitis B
v. hepatitis E
• water borne
• contaminated food or water; rare in the United States
B. Hepatitis B
1. Risk factors/infection route
a. homosexuality
b. iv drug use
c. health professionals
d. hemodialysis
e. transmission routes
i. sexual
ii. fecal-oral route: incubation 12 to 14 weeks or longer
f. pathophysiology
i. hepatitis B has three distinct antigens
• HBsAg - surface antigen
• HBcAg - core antigen
• HBeAg - e antigen
ii. damage to the hepatocytes causes inflammation and necrosis
iii. liver function decreased in proportion to damage
iv. healing takes three - four months
3. Findings
a. jaundice if liver fails to conjugate bilirubin or excrete it
b. clay-colored stools from lack of urobilin
c. urine is dark from urobilin excreted in urine rather than stool
d. urine foams when shaken
e. pruritus from bile salts excreted through skin
f. right upper quadrant pain from edema and inflammation of liver
g. anorexia, nausea, vomiting, malaise, weight loss
h. prolonged bleeding from impaired absorption of vitamin K
i. anemia from decreased RBC lifespan
4. Diagnostics - serologic markers of HBV
a. HBsAg - hepatitis B surface antigen
b. anti-Hbc - antibodies to B core antigens
c. elevated alanine aminotransferase (ALT previously SGPT)
d. elevated bilirubin
e. elevated aspartate aminotransferase (AST; previously SGOT)
f. elevated alkaline phosphatase
g. prolonged prothrombin time
5. Management - nonspecific and supportive
a. symptomatic treatment of pain
b. antiemetics as needed
6. Nursing interventions
a. fatigue - provide rest periods; may require bed rest initially
b. maintain skin integrity
c. client will tolerate less activity
d. nutrition needs:
i. increase carbohydrates and proteins; decrease fat
ii. avoid alcohol
iii. eat frequent, small meals
e. remedy knowledge deficit
f. arrange for home care needs
g. teach infection control
i. use disposable utensils and dishes or keep separate from others
ii. good handwashing
iii. do not share razors, toothbrush, etc.
7. Prevention
a. hepatitis B vaccine provides active immunity
b. hepatitis B immune globulin provides passive immunity
c. observe Standard and Enteric Precautions
d. good handwashing
C. Cirrhosis
1. Definition/etiology - irreversible, chronic, progressive degeneration of the liver, with fibrosis and areas of nodular regeneration
a. types
i. Laennec's cirrhosis - related to alcohol abuse
ii. post-necrotic - associated with viral hepatitis or exposure to hepatotoxin
iii. biliary cirrhosis - associated with inflammation or obstruction of gallbladder or bile duct
iv. cardiac cirrhosis - associated with congestive heart failure
2. Pathophysiology
a. nodular liver with fibrosis and scar tissue
b. destroys hepatocytes and kills tissue (necrosis)
c. necrosis, nodules, and scar tissue obstruct flow of blood, lymph, and bile
d. impaired bilirubin metabolism
3. Findings
a. weakness, fatigue, weight loss, hepatomegaly
b. right upper quadrant pain (illustration )
c. jaundice, pruritus, steatorrhea (decreased absorption of fat and fat-soluble vitamins)
d. clay-colored stools
e. increased bilirubin in urine, producing dark colored urine
f. impaired aldosterone metabolism resulting in edema
g. impaired estrogen metabolism: gynecomastia, menstrual changes, changes in distribution of body hair, vascular changes - spider angiomas, palmar erythema
h. impaired metabolism of protein, carbohydrate, and fat
i. produces less plasma protein, resulting in edema and ascites
ii. produces less of proteins needed for clotting (fibrinogen and prothrombin)
iii. absorbs less vitamin K, resulting in prolonged bleeding
iv. liver fails to convert glycogen to glucose, resulting in hypoglycemia
4. Diagnostics
a. liver function studies - ALT, AST, alkaline phosphatase
b. prothrombin time, CBC
c. decreased cholesterol because liver synthesis impaired
d. elevated serum bilirubin and urine bilirubin
e. ERCP to examine bile duct
f. CTscan of liver
g. liver biopsy
5. Management
a. steroids for post-necrotic cirrhosis
b. replace B vitamins and fat-soluble vitamins
c. diet
i. increased carbohydrates
ii. protein may be restricted, depending on amount of damage and symptoms
iii. no alcohol
6. Nursing interventions
a. monitor for bleeding
b. alteration in nutrition
i. 2,000-3,000 calories daily
ii. low fat
c. provide rest periods; client will not tolerate strenuous activities
d. remedy any knowledge deficit about cirrhosis and its therapies
e. changes in LOC
i. confusion
ii. avoid sedation
f. impaired skin integrity, from edema and pruritus
g. monitor fluid balance
h. measure abdominal girth daily
i. weigh daily
j. measure I & O
7. Complications
a. portal hypertension
b. ascites
c. hepatic encephalopathy
D. Portal hypertension
1. Definition/etiology - increased pressure in the portal
2. Pathophysiology: normal blood flow is altered producing an increased resistance to flow through the liver. Congestion in the portal system dilates veins, especially in esophagus and rectum.
3. Findings
a. prominent abdominal-wall veins (caput medusa)
b. hemorrhoids
c. enlarged spleen
d. anemia from increased destruction of RBCs
e. esophageal varices and GI bleeding
4. Diagnostics: endoscopy
5. Management
a. sclerotherapy - injection of a sclerosing agent into varices
b. balloon tamponade
i. sangstaken-Blakemore tube is inserted into the stomach
ii. gastric balloon is inflated and presses on lower esophagus while allowing suctioning
iii. esophageal balloon places pressure on varices
iv. pressure is released as ordered to prevent necrosis
v. traction for increased pressure added by attaching tube to football helmet
vi. assess for bleeding and signs of shock
vii. assess for respiratory distress - aspiration or displacement of tube, suction PRN
viii. keep head of bed elevated
c. medications
i. vasopressin
• constricts veins and decreases portal blood flow
• given IV or into superior mesenteric artery
• side effects include hypothermia, myocardial ischemia, acute renal failure
ii. nitroglycerin will decrease myocardial effects
iii. beta-adrenergic neuron-blocking agents may decrease risk of recurrent bleeding by decreasing pressure in portal system
iv. cathartics to remove blood from GI tract and decrease absorption of ammonia
d. surgical intervention
i. shunt to decrease blood flow to liver and therefore pressure Splenorenal shunt
• mesocaval shunt
• portacaval shunt
ii. TIPS (transjugular intrahepatic portosytsemic shunt) - shunt placed between hepatic and portal vein
6. Nursing interventions
a. prevent bleeding
b. avoid intake of alcohol, irritating or rough food
c. avoid increased pressure in abdomen
d. if bleeding occurs - administer transfusions, fresh frozen plasma, vitamin K
e. monitor for infection
E. Ascites
1. Definition/etiology - accumulation of fluid in the peritoneum
2. Pathophysiology
a. portal hypertension causes increased plasma and lymphatic hydrostatic pressure in portal system
b. hypoalbuminemia causes decreased colloid osmotic pressure
c. hyperaldosteronism due to liver's inability to metabolize aldosterone causes body to retain sodium and water
3. Findings
a. abdominal distention, protruding umbilicus, dull sound on percussion of abdomen, fluid wave
b. bulging flank
c. dyspnea
4. Diagnostics
a. abdominal x-ray
b. CT scan
c. ultrasound
ASCITES - PARACENTESIS
• Paracentesis - aspiration of abdominal ascites, usually 1000-1500cc removed
• Before paracentesis: empty client's bladder
• During procedure: client sits upright
• After procedure: take frequent vital signs; monitor urine output; and monitor for drainage from puncture site
5. Medical management
a. diuretics - spirnolactone (Aldactone) - aldosterone antagonist, spares potassium
b. iv albumin
c. paracentesis to remove fluid
d. diet low in sodium
e. peritoneal venous shunt - allows drainage of fluid from the peritoneum to superior vena cava
6. Nursing interventions
a. abdomen will have excess fluid, blood vessels too little
b. measure I & O, daily weight, abdominal girth, skin turgor
c. restrict fluids
d. monitor for ineffective breathing patterns
e. semi-Fowler's position
f. monitor for impaired skin integrity
g. remedy knowledge deficit
F. Hepatic encephalopathy - mental dysfunction associated with severe liver disease
1. Definition/etiology
a. impaired ammonia metabolism in liver poisons brain tissue
b. ammonia produced in bowel from action of bacteria on protein
2. Findings
a. changes in LOC from confusion to coma
b. changes in sleep pattern
c. memory loss
d. asterixis - flapping tremor
e. impaired handwriting
f. hyperventilation with respiratory alkalosis
g. fetor hepaticus - musty, sweet odor to breath
3. Diagnostics - serum ammonia level
4. Management
a. neomycin sulfate (Mycifradin) - inhibits action of intestinal bacteria
b. lactulose (Cephulac) - absorbs ammonia and produces evacuation of the bowel
c. low protein diet
5. Nursing interventions
a. tremor, confusion can lead to injury: maintain safety
b. ascites and low intake decrease fluid volume
c. diarrhea from medications
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