Hepatitis
- 3rd among reported diseases in incidence (STDs and chicken pox – #1 & #2)
- 1-2 million deaths worldwide
- 1.2 million Hep B carriers in the U.S.
- 300 million carriers worldwide
Acute Hepatitis
Asymptomatic Hepatitis
- inapparent disease unless the patient somehow gets liver function tests
- HAV is especially at risk for being asymptomatic
Symptomatic Hepatitis
- Icteric
- Anicteric – insufficient elevation of bilirubin to produce jaundice. Hard diagnosis
- Extrahepatic manifestations – HBV and HCV – due to circulating Ag-Ab complexes rash, arthritis, vasculitis, glomerulonephritis
Relative Frequency of Acute Hepatitis
Sporadic Cases
- HAV> HCV> HBV> rest
- Difficult to assess because HCV and HAV may be unrecognized blood transfusion related cases
INCUBATION PERIODS
HAV 15-60 days
HEV 15-64 days
HBV 45-160 days
HDV 45-180 days
HCV 14-180 days
HGV unknown
Epidemiology and Transmission
HAV
- ssRNA
- Human is only reservoir
- Fecal-Oral Transmission
- Lower socio-economic class gets it more
- In 3rd world countries most cases are asymptomatic and in children
- NO CARRIER STATE, NO CHRONIC DISEASE
HBV
- ONLY ONE THAT IS DNA VIRUS
- Human is principal reservoir
- Parental, perinatal, and venereal transmission
- Increasing in incidence in U.S.
- HbsAg – 5-10% of U.S. population
- Anti-HBs = immune
- Anti-HBc = not immune
- HbeAg = active replication in serum
- Incidence very high in Asia, Pacific Islands, Africa, and Middle East (75-90% of population)
- Pathognomonic – ground glass cell (pink eosinophilic)
- Pathophysiology – CD8 cells trying to destroy the virus cause hepatocyte damage also.
- Risk factor for hepatocellular CA
HDV
- PATIENT MUST HAVE HBV; SYMBIOTIC WITH HBV
- Superinfections have worse prognosis than when coinfected at the same time.
- Usu. IV drug use or sexual contact
- Up to 70% of patients develop cirrhosis
HCV
- ssRNA
- 1-2% carrier rate in U.S.
- ONLY ONE THAT HAS BILE DUCT INFLAMATION
- 80-95% or majorityof patients get chronic liver disease
- Even more of a risk factor for Hepatocellular CA than HBV
HEV
- clinically similar to HAV, no relation
- fecal-oral
- high mortality rate among pregnant women
- no chronic disease reported
HGV
- new RNA virus
- some of the cases of transfusio related hepatitis
- does have a dhronic state and can also be present with HCV or HBV
Non A-E viruses
- goes to the other cases of transfusion and sporadic related hepatitis
Clinical Manifestations
- Non-specific and flu-like
- Lassitude, loss of appetite, nausea, weakness, fever, vomiting, headache, chills, abdominal discomfort, myalgia, drowsiness.
Morphology of Acute Viral Hepatitis
- entire liver is involved
- histologic picture is the sum of hepatocyte necrosis, hepatocyte regeneration, inflammation and repair.
Classic Pattern
- patchy necrosis in lobule (more in zone 3 than in zone 1)
- Lobular architectural disarray
- Predominance of lymphocytes
- Hyperplasia and hypertrophy of Kupffer Cells
- Cholestasis may or may not be present
Bridging (Submassive) Necrosis
- necrosis bridging between portal tracts and central veins
- young patients – bridging necrosis has no effect on prognosis
- older patients – bad prognosis and many will eventually go on the cirrhosis or die acutely
Massive Necrosis
- multilobular necrosis with few or no surviving hepatocytes
- liver small, soft and very flexible
- only the fibrous and reticulin structure of the liver is left
- poor survival rate
- if patients survive, liver regenerates back to normal without cirrhosis.
Sequelae of Acute Hepatitis Infection
HAV HAB HCV
Complete Recovery 99% 80-85% 0-20%
Fulminant Hepatitis rare yes yes
Carrier State no yes yes
Chronic Hepatitis no 5-10% 80-100%
Cirrhosis no 10-30% 20%
Hepatocellular CA no yes yes
Chronic Hepatitis
- evidence of continuing or relapsing hepatic disease for at least 6 mths.
- May be benign or progress to cirrhosis
Etiology of Chronic Hepatitis
- HCV, HBV, HDV, HGV, No-A-E viruses
- Autoimmune diseases
- Drug related ( Ex. Isoniazid )
Chronic Hepatitis – Clinical
- Common: fatigue, lethargy, increased need for sleep, lack of energy
- Less Common: poor appetite, intermittent nausea, pain over liver, muscle aches, mental depression
- CORRELATION IS POOR SYMPTOMS AND SEVERITY OF DISEASE
Chronic Hepatitis – Types
- Chronic persistent hepatitis
- Chronic Active Hepatitis
- Chronic Lobular Hepatitis
- Other liver disease other than chronic hepatitis that can cause piecemeal necrosis
Ø Primary biliary cirrhosis, primary sclerosing cholangitis, Wilson’s disease, Alpha-1-antitrypsin disease, Alcoholic liver disease.
Acute Alcoholic Liver Disease
Fatty Metamorphosis
- universal, immediate, reversible
- metabolism of EtOH is culprit
- mild to none – clinical complications
- no cirrhosis
- Benign except for “sudden death syndrome”
Acute Alcoholic Hepatitis
- not very well understood
- can be reversed if early; patient must stop alcohol intake
- can lead to cirrhosis
- manifestations vary greatly – asymptomatic to jaundiced to critically ill
- Most common physical finding – hepatomegaly (ascites, jaundice, splenomegaly, and encephalopathy also found
- NOT benign
- Only prevention – stop alcohol intake
- Morphological changes
Ø Mallory’s Hyaline is Hallmark
Ø Neutrophilic inflammatory infiltrate
Ø Must have these two
- other entities assoc. with centrilobular Mallory’s hyaline: jejunoileal bypass, drugs, non-alcoholic steatohepatitis, rarely obesity, rarely diabetes mellitus
- other entities assoc. with peripheral lobular Mallory’s hyaline: cholestasis, 1o biliary cirrhosis, 1o sclerosing cholangitis, indian childhood cirrhosis, Wilson’s disease, pulmonary asbestosis, cryptogenic cirrhosis
Tags: Acute Hepatitis, Alcoholic Liver Disease, Autoimmune diseases, bile duct inflamation, Cholestasis, HBV HDV, hepatocellular CA, HEV, HGV, Hyperplasia, hypertrophy of Kupffer Cells, Lymphocytes, Mallory's Hyaline, myalgia, Necrosis, Non A-E viruses, Symptomatic Hepatitis
