• Benign , self-limited, rare fatalities 
• spread by ingestion of contaminated food and water 
• blood borne transmission rare 
• No carrier state, does not produce chronic hepatitis 
• not a/w hepatocellular ca 
• IgM first then IgG 

Hepatitis B 

• Without vaccine -> 30% chance getting it when stick with needle 
• Active hepatitis 
• Chronic non-progressive hepatitis 
• Cirrhosis 
• massive liver necrosis 
• Asymptomatic carrier state 
• Vaccine abaliable to protect against this 
• Transmission 
• Transfusion 
• IVDA
• Needle sticks
• Sexual activity 
• DNA virus 
• 4-26 week incubation period 
• Acute disease lasting months: jaundice, taste abnormalities 
• Acute disease can be followed by serum markers over the course of months to see what state they are in and prognosis of developing more serious complications 
• Hazy ground glass appearance 
• IgM and then  IgG

• appears before symptoms , peaks during overt disease,3-6 months undetecable 
• HBeAG, HBV- DNA , DNA polymerase appears in serum soon after HBsAg signifies acute viral replication 
• Perisistence of HBeAG = probable chronic hepatatis 
• IgM anti-HBc in serum shortly before symptoms 
• IgG anti-HBC replaces IgM anti-HB over months 

• Acute infection has peaked and is on the wane 
• IgG anti-HBs rises after acute phase is over 
• Anti-HBs may persist for life, basis for vaccination 

• 3% chance of getting when stuck with a needle 
• most imp. cause of transfusion associated hepatitis 
• High rate of progression to cirrhosis and chronic disease 
• incubation 2-26 weeks 
• Clinical course milder than HBV 
• RNA virus 
• No vaccine for this 
• .3 % chance of getting HIV when stuck with a needle 

• Replication Defective - causes infection only if encapsulted with HBsAg 
• Coinfection- exposure to serum with HBV and HDV (most people will recover)
• Superinfection: chronic carrier of HBV and HDV 
• HDV does not seem to be directly pathogenic 
• IgM anti-HDV ; most relaible indicator of recent exposure 

• High mortality in pregnant women 
• Not assoicated with chronic disease or viremia 
• Water borne infection 
• Seen in travelers 

• Similar to HCV 
• A/w transfusions 
• Seen in cirrhotic patients 

• Carrier State 
• Asymptomatic Infection 
• Acute Hepatitis 
• Chronic Hepatitis 
• Fulminant Hepatitis 

• No symptoms 
• Harbors and transmits virus 
• Best characterized by HBV 

• Identified incidentally 
• Minimally elevated serum transaminases 
• Antiviral antibodies 

• Incubation period 
• Symptomatic preicteris phase: Malaise, wt loss, fever 
• Symptomatic Icteric Phase: Jaundice 
• Convalescene 
• why Hep C is a public concern 
• Many people may or may not seek txt during acute hepatitis presentation and then go into convalescene 
• Then pass to other people 

• HBV - ground glass hepatocytes sanded nuclei 
• HCV  - fatty change 
• Hepatocyte injury 
• Hepatocyte necrosis : necrotic tissue next to healthy tissue 
• Regenerative changes 
• Sinusoidal cell reactive changes 
• Microscopically
• Disrupted lobular architecture 
• inflammatory cells in the sinusoids 
• Hepatocyte apoptosis 

Chronic Hepatitis 

• symptomatic, biochemical or serologic evidence of hepatic disease for 6 months
• Histologically documented inflammation and necrosis 
• HCV is a common cause 
• Fatugue, mild jaundice, loss of appetite 
• Clinical course highly variable 

• Similar changes as seen in acute hepatitis 
• Inflammation 
• Fibrosis ( lacks band-like, organized, firm deposition of collagen of cirrhosis)->  can progress to cirrhosis 
• HBV: ground glass hepatocytes sanded nuclei 
• HCV: fatty change 
• Microscopically: 
• Portal tract expansion by lymphoid nodule 
• Cirrhosis from chronic viral hepatitis  
• coarse larger nodules compared to micronodules seen in alcoholic cirrhosis 

• Hepatic insuffiency progressing from onset to hepatic encephalopathy in 2-3 weeks 
• Common cause is HBV 
• Drugs and chemicals are other causes 
• Random areas or entire liver involved 
• Mortality rate can be high 

• Viral is more common than autoimmune 
• Chronic hep in pts with immune problems 
• Females 
• autoantibodies 
• No serologic markers of virus 
• High titers of autoantibodies 
• Increased frequency of HLA B8 or HLADRW3

• Parasites, bacteria, fungus 
• Multiple or solitary 
• Surgical drainage is often necessary 
• Diagnosis often delayed 

• Liver subject to damage from various chemicals 
• Drug induced chronic hepatitis is indistinguisable from  chronic viral hepatitis 
• Must check serologic markers of viral infection to r/o viral 
• Tylenol overdose