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Hepatitis
HEPATITIS
Acute Hepatitis
Viral hepatitis
Drug induced hepatitis
Chronic Hepatitis
Chronic persistent hepatitis
Chronic lobular hepatitis
Chronic active hepatitis
CIRRHOSIS
General
Causes
Clinical Manifestations
-usually results from viral infection, drug reaction, or hepatotoxin exposure
-acute hepatocellular injury associated with variable amounts of cellular necrosis
-clinical manifestations generally related to the severity of inflammation and amount of necrosis
-amount of cellular necrosis appears to be a more important factor in clinical manifestations
mild inflammation: may appear in asymptomatic elevations in serum transaminases
severe inflammation: may occur in massive hepatic necrosis ex. acute fulminant hepatic failure
-most commonly from hepatitis A, hepatitis B, or hepatitis C
-also caused by hepatitis D and hepatitis E
-hepatitis A and hepatitis E: transmitted by oral-fecal route
-hepatitis B and hepatitis C: transmitted by contact with bodily fluids and percutaneously
-usually have a mild prodromal illness lasing 1- 2 wks
-prodromal illness may consist of: fatigue, maliase, low grade fever, nausea and vomitting
-may be associated with jaundice which typically can last from 2 -12 wks
-clinical course may be more complicated with hepatitis B and hepatitis C
-hepatitis B leads to chronic hepatitis in about 3 -10% incidence of chronic hepatitis
-hepatitis C leads to chronic hepatitis in about 50% incidence of chronic hepatitis
May be caused by:
-toxic substances ex. alcohol, acetaminophen, salicylates, tetracyclines, vinyl chloride)
-idiosyncratic ex. volatile anesthetics(halothane), phenytoin, sulfonamides, rifampin,
-toxic and idiosyncratic ex. methyldopa, isonazid, sodium valproate, amiodarone
-primarily cholestatic ex. chlorpromazine, cyclosporine, oral contraceptives, anabolic steroids
-alcoholic hepatitis may be the most common cause of drug induced hepatitis
-acetaminophen ingestion > 25 grams may result in fatal fulminant hepatic disease
General
-persistant hepatic inflammation > 6 months
-associated elevated serum transaminases
Three distinct syndromes of chronic hepatitis determined by biopsy
-chronic persistent hepatitis
-chronic lobular hepatitis
-chronic active hepatitis
-chronic inflammation of portal tracts with preservation of cellular architecture
-usually does not progress into cirrhosis
-usually present with acute hepatitis but eventually resolves
-often from hepatitis B and hepatitis C
-variant of chronic persistent hepatitis
-acute hepatitis that resolves but associated with recurrent exaccerbations
-foci of inflammation and cellular necrosis is present in hepatic lobules
-usually does not progress into cirrhosis
-chronic active inflammation with destruction to the normal cellular architecture on biopsy: piecemeal necrosis
-cirrhosis is evidenced in about 20 - 50 % of patients initially or develops eventually
-most commonly occurs as a sequela of hepatitis B and hepatitis C
-other possible causes may include drugs (ex. methyldopa, isoniazid) and autoimmune conditions
-pts often present with a history of fatigue and recurrent jaundice
Laboratory findings
-usually show only mild elevations in serum transaminases
-mild elevated serum transaminase levels usually correlates poorly with the severity of disease
Treatment
-is usually with long term corticosteroid therapy +/- azathiopine
-patients usually respond well to immunosuppresants unless the cause is from hepatitis B or hepatitis C
-progressive disease of the liver that eventually results in hepatic failure
-hepatocyte necrosis followed fibrosis and hepatic nodular regeneration
-portal hypertension develops as the normal cellular architecture is detroyed and obstructs portal venous flow
-abnormal hepatic synthetic and metabolic functions results in multisystemic disease
-alcohol is the most common cause of cirrhosis in the US: Laennec's cirrhosis
-alcohol is the most common cause of cirrhosis (Laennec's cirrhosis)
-chronic active hepatitis (postnecrotic cirrhosis)
-chronic biliary inflammation or obstruction (biliary cirrhosis)
-chronic right sided heart failure (cardiac cirrhosis)
-hemochromatosis
-wilson's disease
-alpha1 anti-trypsin deficiency
-signs and symptoms generally do not correlate with the severity of hepatic disease
-clinical manifestations are initially absent but eventually usually develop jaundice and ascites
-other signs include: spider angiomas, palmar erthyema, splenomegaly and gynecomastia
-close to 10% of cirrhotic patients have at least one episode of spontaneous bacterial peritonitis
-some cirrhotic patients may develop hepatocellular carcinoma
CNS:
-encephalopathy
CVS:
-hyperdynamic state ex.high cardiac output
Resp:
-increased intrapulomonay shunting
-decreased FRC
-pleural effusion
-restrictive ventilation
-respiratory alkalosis
Liver/Metabolic:
-hyponatremia
-hypokalemia
-hypomagnesemia
-hypoalbuminemia
-hypoglycemia
GI
-portal hypertension ex. ascites, esophageal varices, hemorrhoids, bleeding
Renal:
-increased proximal sodium reabsorption
-increased distal sodium reabsorption
-impaired clearance of free water (perhaps from decreased renal perfusion, or hepatorenal syndrome)
Hematology:
-anemia
-coagulopathy (hypersplenism, thrombocytopenia, and leukopenia)
Three major associated complications with cirrhosis
-variceal hemorrhage from portal hypertension
-intractable fluid retention ex. ascites, hepatorenal syndrom
-hepatic encephalopathy, coma