ch44 part 2: Cirrhosis

  1. Define cirrhosis.
    • Chronic progressive liver disease characterized by replacement of liver tissue with fibrosis, scar tissue, and regenerative nodules, resulting in progressive liver deformation and decreased function
    • Signs & symptoms - ascites (most common), spider hemangiomata, palmar erythema, gynecomastia, hypogonadism, splenomegaly, hepatic encephalopathy
  2. Define nonalcoholic fatty liver disease (NAFLD).
    • Group of disorders characterized by hepatic steatosis (fat buildup in liver), not associated with other diseases, disorders, or hepatotoxins
    • Accumulation of fat can lead to inflammation and scarring called nonalcoholic steatohepatitis (NASH)
    • Risk factors - obesity, diabetes, hypertriglyceridemia, severe weight loss; poor diet, tuberculosis, intestinal bypass, and corticosteroids can lead to NAFDL
    • Labs - persistently elevated ALT levels with no other cause
  3. Define primary biliary cirrhosis.
    • Chronic inflammatory condition of liver
    • T-cell mediated attack of small bile duct epithelial cells resulting in loss of bile ducts and cholestasis, leading to liver necrosis and cirrhosis
    • Increased risk for hepatocellular cancer
    • 95% of patients are female
    • Associated with autoimmune disorders including rheumatoid arthritis, Sjogren's, and scleroderma
    • Early symptoms - fatigue and pruritis; hypoprothrombinemia related bleeding may occur
    • Late sign - jaundice
    • Other signs - fat malabsorption and low levels of fat-soluble vitamins r/t decreased bile secretion; xanthomas, hyperlipidemia, anemia
    • Treatment goals - suppress ongoing liver damage, prevent complications, symptom management; med = ursodiol (Actigall)
  4. Define Wilson's disease.
    • Autosomal recessive - progressive, familial, terminal neurologic disease accompanied by chronic liver disease leading to cirrhosis
    • Copper storage - decreased hepatocellular excretion of copper into bile, increased hepatic copper accumulation and cell injury
    • Hallmark sign - Kayser-Fleischer rings, brownish red colored rings seen in the cornea near limbus on eye exam
    • Other neurologic dysfunctions include tremor, involuntary movements, drooling, dysarthria, rigid dystonia, seizures, migraine headaches, and insomnia
    • Labs - elevated serum ALT & AST, low serum ceruloplasmin, low serum uric acid, elevated urinary copper
    • Treatment - chelating agents such as D-penicillamine or trientine (Syprine), promote excretion of urinary copper
  5. Define hemochromatosis (HH).
    • Iron disorder - increased and inappropriate storage of dietary iron
    • Systemic disease, affects liver, heart, pancreas, endocrine system
    • Progressive, slow disease
    • Major causes of death - decompensated cirrhosis, hepatocellular carcinoma, diabetes mellitus, cardiomyopathy
  6. Four types of cirrhosis.
    • Alcoholic (a.k.a. portal or nutritional) cirrhosis: Fatty deposits in liver due to excess alcohol intake; with continued alcohol abuse, widespread scar formation
    • Postnecrotic cirrhosis: Complications of viral, toxic, or idiopathic (autoimmune) hepatitis; broad bands of scar tissue formation
    • Biliary cirrhosis: Chronic biliary obstruction and infection leading to diffuse fibrosis; jaundice is main feature
    • Cardiac cirrhosis: Longstanding, severe right-sided heart failure causing chronic hepatic congestion, resulting in fibrosis
  7. Early manifestations of cirrhosis.
    • Usually insidious onset
    • Liver has altered ability to metabolize carbs, fats, and proteins
    • Abdominal pain - dull, heavy feeling in RUQ or epigastrium
    • GI disturbances are common - Anorexia, dyspepsia, flatulence, nausea and vomiting, and changes in bowel habits (diarrhea or constipation)
    • Other symptoms - Fever, lassitude, slight weight loss, hepatosplenomegaly (enlarged liver & spleen)
  8. Later manifestations of cirrhosis.
    • Symptoms may be severe r/t liver failure and portal hypertension
    • Jaundice, peripheral edema, and ascites
    • Advanced stage, liver becomes small and nodular
    • Jaundice - liver unable to conjugate and excrete bilirubin (hepatocellular jaundice)
    • Pruritis - bile salts accumulate under skin
    • Skin lesions - spider angiomas (nose, cheek, upper trunk, neck, shoulders) and palmar erythema; r/t liver's decreased ability to metabolize estrogen
    • Thrombocytopenia, leukopenia, and anemia - splenomegaly (caused by backup of blood from portal vein into spleen) causes overactive spleen, increasing removal of blood cells from circulation
    • Bleeding disorders - liver incapable of producing prothrombin and other clotting factors, causing decreased coagulation ability
    • Endocrine - liver incapable of metabolizing adrenocortical hormones, estrogen, and testosterone; in men, gynecomastia, alopecia (axillary/pubic), testicular atrophy, loss of libido; in women, amenorrhea in menopausal women or vaginal bleeding in postmenopausal women; hyperaldosteronism causes sodium and water retention and potassium loss
    • Lab values - high sodium, low potassium
    • Peripheral neuropathy - dietary deficiency in thiamine, folic acid, and cobalamin
  9. Complications of cirrhosis.
    Portal hypertension resulting in esophageal varices, peripheral edema and ascites, hepatic encephalopathy (coma), and hepatorenal syndrome.
  10. Define portal hypertension.
    • Hypertension in the portal vein and its tributaries (veins from intestines to liver)
    • Symptoms caused by blood being forced down alternate channels rather than into the portal system
    • Symptoms include ascites, hepatic encephalopathy, bacterial peritonitis, hepatorenal syndrome, splenomegaly, caput medusae (distended paraumbilical veins), and esophageal, gastric, and anorectal varices
  11. Define esophageal varices.
    • Distention of esophageal veins; bleed easily
    • Most life-threatening complication of cirrhosis
    • Risk factors - ingesting poorly masticated or coarse foods or alcohol, acid reflux, increased pressure r/t nausea, vomiting, straining at stool, coughing, sneezing, lifting heavy object
  12. Treatment of esophageal varices.
    • No aspirin, alcohol, or irritating foods; chew food 28 times or eat mechanical soft diet
    • Avoid coughing, treat URI
    • Prophylactic propanolol (Inderal) - lowers portal hypertension, prevents recurrent GI bleed
    • Endoscopic sclerotherapy - endoscopic injection of sclerosing agent (e.g., morrhuate/Scleromate) into veins; NPO, conscious sedation; post procedure, check gag reflex, bleeding
    • Balloon tamponade - tube-ballon down esophagus, inflate to put pressure against esophageal wall; keep scissors in reach if ballon slips to grab, cut, and pull tube to remove airway blockage
    • Banding/ligation - tie off vessels to stop bleeding
    • Shunt - shunting blood away from liver reduces pressure in esophageal veins
    • Fresh frozen plasma and packed RBCs - for blood loss
    • Vitamin K - blood clotting
    • H2 histamine blockers and proton pump inhibitors - reduce reflux, reduce acidity and irritation
    • Vasopresin (Pitressin) - potent vasoconstrictor
    • Octreotide (Sandostatin) - decreases bleeding and pressure
    • Nitroglycerine - vasodilator, lowers blood pressure, acts on heart to dilate heart arteries
    • Neomycin and Lactulose - decease bacterial flora in the colon, which decreases ammonia production
  13. Transjugular intrahepatic portosystemic shunt (TIPS).
    • A&P: Some of the esophageal veins drain into the portal vein (esophageal veins -> left gastric vein -> portal vein)
    • Problem: Hepatitis causes blood to congest in liver, back up into portal vein and cause venous distention and esophageal varices
    • Solution: Create a bypass from the portal vein to the hepatic vein so that some blood is routed past the liver, relieving pressure in portal vein
    • How: Using the jugular vein as an entrance, a shunt is guided down the superior to inferior vena cava and into the hepatic vein, punctured out the hepatic vein, and directed towards and anchored into the portal vein
    • Contraindications: Severe hepatic encephalopathy, hepatic carcinoma, and portal vein thrombosis
    • Complications: Increased levels of serum ammonia and resultant encephalopathy (ammonia is filtered by the liver, bypassing liver decreases filtering)
  14. Hepatic encephalopathy - define and treat.
    • Define: Neuropsychiatric manifestation of liver damage, caused by excess ammonia in systemic circulation (liver filters ammonia)
    • How: Disorder of protein metabolism and excretion with nitrogenous
    • Problem: Considered terminal complication of liver disease
    • "Stop a Bus" Test: Put hands straight out, palms out, like hand signal to stop a bus, if high ammonia, hands will flap
    • Nursing considerations: Seizure precautions, suction in room, lactulose for life (3-4x daily), neomycin to bring down bacterial load in gut
    • Resolution: When ammonia levels decrease, mental state clears
  15. Ascites - define and treat.
    • Define: Accumulation of serous fluid in the peritoneal or abdominal cavity causing increased weight, increased girth, striae, dehydration, decreased potassium, and decreased urine output
    • How: Proteins move from blood vessels into capillaries and into lymph space; lymphatic system unable to carry off excess proteins and water; osmotic pressure of proteins pulls additional fluid into peritoneal cavity
    • Treat: Paracentesis, shunting, salt restriction, diuretics, water restriction
  16. Fulminant hepatic failure - define and treat.
    • Define: Acute liver failure, severe impairment of liver function associated with hepatic encephalopathy
    • Cause: Most commonly drug use, usually acetaminophen with alcohol; second most common is HBV; also mushroom poisoning ("death cap" mushroom)
    • How: Drug disrupts essential intracellular processes or causes buildup of toxic metabolic products
    • Treat: Liver transplant
    • Nursing Considerations: Frequent mental status checks for decline in LOC; quiet environment to minimize agitation; seizure precautions; I&O for renal function; oral and skin care to avoid breakdown and infection; monitor renal function, glucose, F&E; watch for increased ICP; HOB at 30 degrees
  17. Liver cancer.
    • Metastatic carcinoma of the liver is more common than primary carcinoma
    • 80% of liver cancer patients also have cirrhosis of liver
    • Hep C responsible for 50-60% of liver cancers
    • Hep B responsible for 20% of liver cancers
    • Clinical manifestation similar to cirrhosis
    • Liver biopsy is definitive test
    • Management similar to cirrhosis; lobectomy or liver transplant
    • If no signs of metastasis, treatment options may include radiofrequency ablation, cryoablation, percutaneous ethanol injection or percutaneous acetic acid injection
    • Prognosis is poor; cancer grows rapidly, death within 4-7 months from hepatic encephalopathy or massive blood loss from GI bleed
Card Set
ch44 part 2: Cirrhosis
Chapter 44 Cirrhosis and Complications