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
hepatitis B
-DNA Virus
-8 Genotypes
-Route:
-Infected blood/blood products, bodily fluids
-Common in homosexual men, IVDU, but greatest number of transmission is via heterosexual contact
-vertical transmission common- mom to child
-Incubation: 1-5 months (average: 3 mos)- LONG
-Treatment of acute Hepatitis B ds: supportive
-Prognosis: Very good but chronic disease depends on when acquired (Child vs adult)
-if you get it as a child -> higher chance of chronic
-Mortality for acute ds: 0.1-1% but higher with superimposed D
-Vaccinate all children and adults
hepatitis B: HBsAg
-First evidence of infection appearing before biochemical evidence of liver disease and persists throughout clinical illness
-YOU ARE INFECTIOUS IF YOU HAVE HBsAg IN YOUR BLOOD
-Implies infectivity
-Persistence=Chronic ds
hepatitis B: anti HBs
-Appears after clearance of HBsAg, or with vaccination
-Recovered and no longer infectious
-recovered or vaccination
-you dont have anti HBs with HBsAg
hepatitis B: anti HBc
-Appears shortly after HBSag detected
-HBcAg DOES NOT APPEAR IN SERUM
-Fills the serologic gap (window period) in patients who have cleared HBSag but not yet made Anti HBs
-fills serologic gap
-no antigen and no antibody -> this HBc fill this gap to show presence of the disease
hepatitis B: HBeAg
-Found only in HBsAg positive serum
-Appears during incubation period
-Indicates viral replication and infectivity**
-Persistence in serum >3mos indicates increased likelihood of chronic HBV
-Disappearance often followed by anti HBe
-lots of replication, very infectious
hepatitis B: HBV DNA
-Sensitive and precise marker of viral replication and infectivity
-Small amounts can persist long after recovery
-sits dormant in liver
-if you are immunosuppressed-> can reactivate
hepatitis D (delta agent)
-Defective RNA virus requiring coinfection with HBV
-D needs B to survive
-Specifically needs HBsAg
-May coinfect or superinfect (worse)
-Usually percutaneous exposure
-Serology: Anti HDV or HDV RNA
hepatitis C
-RNA Virus, 6 genotypes
-Exposure/Risk: Exposure to infected blood:
-Blood transfusions, IVDU, intranasal cocaine, body piercing, hemodialysis, tattoos
-Low risk of sexual and maternal-neonatal transmission
-More than 58 million people infected worldwide
-Estimated 2.5 million cases of chronic Hep C in US
-75% unaware of dx (asymptomatic)
-When infected, high rate of chronic hepatitis -> 14-50%
-Incubation: 14-180 days (average range 14-84 days)
-Anti HCV: DOES NOT MEAN RECOVERY -> simply means you have been exposed *****
-HCV RNA PCR- Must always order this to see if they are infected still
-ALT labs vary- not a marker
acute hepatitis C treatment
-Some clear on own
-Controversial-Treat immediately or at 12 weeks
-see if they clear it -> if not treat at 12 weeks
-Sofosbuvir-velpatasvir for 12 weeks or glecaprevir-pibrentasvir for eight weeks (DONT NEED TO KNOW)
-Can be used for any genotype.
