Cirrhosis, Hepatic Coma PDF

CLASSIFICATION OF CIRRHOSIS: CIRRHOSIS remains. Early indicators of this stage: signs of 1. Laennec’s/Alcoholic/Portal cirrhosis...

CLASSIFICATION OF CIRRHOSIS: CIRRHOSIS remains. Early indicators of this stage: signs of 1. Laennec’s/Alcoholic/Portal cirrhosis portal hypertension, impaired digestion  or micronodular cirrhosis caused by chronic and absorption. alcoholism, nutritional deficiencies or both.  is the most frequent cause of death related to long-term, high-risk alcohol consumption.  is the end result of alcoholic liver disease. PATHOPHYSIOLOGY: The functional liver tissue is gradually destroyed and 2. Biliary cirrhosis replaced by fibrous scar tissue  bile flow is obstructed within the liver or in the biliary system, retained bile damages and destroys Abnormal nodules encircled by connective tissue liver cells close to the interlobular bile ducts forming a constricting bands.  Early in the disease: jaundice, pruritus and steatorhea PATHOPHYSIOLOGIC EFFECT OF CIRRHOSIS:  Fibrosis, ductul cell destruction and inflammation 1. Loss of liver function makes the liver enlarged, firm and green. 2. Interference with blood, lymph and bile flow in the liver. 3. Post-hepatic cirrhosis  or macronodular cirrhosis CLINICAL MANIFESTATIONS:  Advanced progressive liver disease resulting from chronic hepatitis B or C or from an unknown 1. Onset is insidious; may take years to develop cause.  The liver is shrunken and nodular, with extensive 2. Early Stage: liver cell loss and fibrosis.  liver usually is enlarged and may be tender  Vague symptoms such as a dull, aching pain 4. Cardiac cirrhosis in the RUQ along with fever, nausea, vomiting, diarrhoea, anorexia and malaise  can stem from liver congestion caused by severe chronic right sided heart failure, mitral or tricuspid 3. Later complaints: valvular diseases. a. Edema, ascites - Impaired plasma protein  The liver becomes congested with blood and synthesis (hypoalbuminaemia), Disrupted hepatic cells become anoxic and die causing hormone balance and fluid retention, fibrotic scarring. Increased pressure in portal venous system b. Bleeding, bruising - due to Decreased clotting STAGES OF LAENNAEC’S CIRRHOSIS: Alcohol factor synthesis ,Increased platelet destruction causes metabolic changes in the liver: by enlarged spleen ,Impaired vitamin K absorption and storage triglyceride and fatty acid synthesis c. Esophageal varices, haemorrhoids - Due to increases and the formation and Increased pressure in portal venous system release of lipoproteins decrease, with collateral vessel development leading to fatty infiltration of d. Gastritis, anorexia, diarrhea - due to Engorged 1st STAGE hepatocytes (causing fatty liver). veins in gastrointestinal system ,Alcohol ingestion , Impaired bile synthesis and fat At this stage, abstinence from alcohol absorption can allow the liver to heal. e. Abdominal wall vein distension (caput medusae) - due Portal hypertension f. Jaundice - due to Impaired bilirubin 2nd STAGE Inflammatory cells infiltrate the liver, metabolism and excretion causing necrosis, fibrosis and g. Malnutrition, muscle wasting - due to Impaired ALCOHOLIC nutrient metabolism, Impaired fat absorption , destruction of functional liver tissue. HEPATITIS Impaired hormone metabolism h. Anemia, leucopenia, increased risk of infection 3rd STAGE - due to Bleeding , Increased blood cell fibrotic tissue replaces normal tissue, destruction by spleen ALCOHOLIC significantly altering basic liver structure (END STAGE) to the extent that little normal function Abigail marie Midterms | Medical Surgical 3 17  i. Asterixis, encephalopathy - due to Asterixis (liver flap) is an early sign of Accumulated metabolic toxins , Impaired portal systemic encephalopathy. ammonia metabolism and excretion j. Gynecomastia, infertility, impotence - due to STAGE III: Dramatic confusion, somnolence Altered sex hormone metabolism STAGE IV: Coma, unresponsiveness MAJOR COMPLICATIONS: 1. PORTAL HYPERTENSION: DIAGNOSTIC TEST:  is a result of impaired blood flow caused by tissue damage and fibrosis - Increased 1. Liver function studies - may be elevated in cirrhosis pressure within the portal circulation; impaired blood flow to the liver; and slowed, congested 2. FBC with platelets circulation from the portal vein.  A low RBC count, hemoglobin and hematocrit  The veins are easily torn by passage of food –  Platelets are low massive hemorrhage – the first sign of the  Leucopenia major complication.  Characterized by: bleeding esophageal varices, 3. Coagulation studies hemorrhoids, collateral veins on the abdominal  show a prolonged prothrombin time wall (caput medusa), peripheral edema (feet, ankle, pre-sacral area), ascites. 4. Serum electrolytes  Hyponatremia - common. 2. FLUID RETENTION:  Hypokalemia, hypophosphatemia and  in the form of ascites and edema hypomagnesemia  Ascites may result from disturbances in both the local and systemic mechanism that govern the 5. Bilirubin levels movement of fluid and electrolytes.  are elevated in severe cirrhosis a. Local factors: 6. Serum albumin levels - hypoalbuminemia a.1. Portal hypertension a.2. Increased hepatic lymph flow 7. Serum ammonia levels - Elevated b. Systemic factors: 8. Serum glucose and cholesterol levels frequently b.1. Decreased colloid oncotic pressure are abnormal in people with cirrhosis. b.2. Hyperaldosteronism b.3. Impaired water excretion 9. Abdominal ultrasound is to evaluate liver size  detect ascites and identify liver nodules. 3. HEPATIC ENCEPHALOPATHY:  Liver biopsy under ultrasound is useful to aid  a metabolic disorder of the nervous system that diagnosis may occur as cirrhosis progresses, resulting from the inability of the liver to convert ammonia 10. Endoscopy may be done to determine the presence to urea. of esophageal varices.  results from accumulation of neurotoxins in the blood and cerebral edema.  Cerebral edema that leads to increased MEDICAL MANAGEMENT: Cirrhosis intracranial pressure and cerebral hypoxia is the leading cause of death in people with portal systemic encephalopathy and liver failure. a. Nutritional measures: a.1. Diet modification – encourage client to eat high-calorie moderate protein meals and to have CLINICAL SIGNS OF HEPATIC ENCEPHALOPATHY: supplementary feedings  Abstinence from alcohol STAGES OF HEPATIC ENCEPHALOPATHY:  2000-3000 kcal/day, low protein at least 10-20 Tremors, slurred speech, impaired g/day, low Na