Jaundice and Acute Viral Hepatitis Flashcards
Jaundice (icterus)
-increased serum bilirubin
-Yellow appearance due to deposition of bile pigment in the skin and mucous membranes
-Bilirubin is a waste product of hgb metabolism
-Interruption of the breakdown pathway
-Marked increase in load due to RBC destruction
-Results in increased serum bilirubin and (if high enough) clinical jaundice
-sclera and conjunctiva
causes of jaundice
-classified as:
(1) hemolysis
(2) genetic defects in bilirubin handling
(3) hepatocellular disease*
(4) obstruction
Functional or anatomic obstruction at any level in pathway results in increase in serum bili—->jaundice
pathways:
-hemoglobin breakdown
-uptake by the hepatocellular membrane
-excretion into biliary system
unconjugated bilirubinemia (indirect)
-Breakdown products of hemoglobin (e.g., hemolytic anemia)
-Impaired uptake and storage (Gilberts, Crigler Najjar, drug reactions)
-Hemolysis, genetic ds, drug rx
-Stool and urine color are normal
-Indirect bilirubin increased
conjugated bilirubin (direct)
-Hereditary cholestatic syndromes
-Hepatocellular dysfunction (hepatitis, cirrhosis, biliary cirrhosis, infections, etc)*
-Biliary obstruction (choledocholithiasis, biliary atresia, pancreatic ds, ca)
-Hepatocellular ds, biliary obstruction or impaired flow
-Urine dark, stool light
-Direct bilirubin increased
liver labs
-total bilirubin labs can be broken down into unconjugated and conjugated
-ALT/AST- show liver injury
-AST- alcohol injury
-ALT- viral liver disease
-alkaline phosphatase
-albumin and total protein- liver function
-bilirubin-
-GGT- alcohol injury
-prothrombin time- time to blood clot
-AMA, ANA, anti smooth muscle antibodies, alpha 1 antitrypsin- chronic
acute hepatitis: prodromal phase
-Onset: abrupt or insidious
-Malaise, myalgias, arthralgias, fatigability , URI symptoms, anorexia
-Nausea, vomiting, diarrhea, or constipation
-RUQ or epigastric pain
acute hepatitis: icteric phase
-Jaundice occurs after 5-10 days if at all
-not everyone gets jaundice
-Acholic stools (light stools)
-May occur with prodromal symptoms
acute hepatitis: convalescent phase
-Increasing sense of well being
-Appetite returns
-Jaundice, fatigue and pain resolve
general signs of acute hepatitis
-Hepatomegaly >50%
-Liver tenderness
-Splenomegaly-15%
-Lymphadenopathy- Cervical and epitrochlear
acute hepatitis labs
-WBC normal to low- Large atypical lymphocytes
-Mild proteinuria (some liver illness affect kidney as well)
-Bilirubinuria often precedes jaundice
-Strikingly elevated AST/ALT ***
-PT/INR may be prolonged and correlates with increased mortality
general supportive tx for acute hepatitis
-Bed rest
-IV fluids if hospitalized otherwise oral
-If encephalopathic or severe coagulopathy hospitalize
-Avoid strenuous exercise, alcohol and hepatotoxic agents
-No morphine
course and complications of acute hepatitis
-Acute illness usually subsides over 2-3 weeks
-Complete clinical and laboratory recovery by:
-6-9 weeks in HAV
-16 weeks in HBV
-5-10% of cases may take longer
-1% will have a fulminant course
-Hepatitis B, D, C, G may become chronic**
viral hepatitis types
-Hepatitis A Virus (HAV)
-Hepatitis B Virus (HBV)
-Hepatitis C Virus (HCV)
-Hepatitis D Virus (HDV)
-Hepatitis E Virus (HEV)
-Hepatitis G Virus (HGV)
hepatitis A
-RNA Hepativirus
-Route: Fecal-oral
-Common Source: Water/food
-Incubation: Average 28 days-excreted in feces 2 weeks prior
-Mortality rate is low
-No chronic carrier state**
-Serology: Anti HAV IgM and IgG
-Treatment: Supportive
-Prognosis: Excellent: DOES NOT CAUSE CHRONIC LIVER DISEASE!
-Vaccination: Children and at risk adults
-Usually subsides over 2-3 weeks
-Complete resolution by 9ish
-Can relapse but recovery is the rule