The liver plays a major role in maintaining homeostatic, immunological, and synthetic processes. Hence, liver dysfunction and liver failure have significant consequences on overall health.

There are five forms of viral hepatitis (A, B, C, D, and E).

The leading causes of chronic viral hepatitis are chronic hepatitis B and C.

The pathophysiology of all viral hepatitis is an inflammatory-mediated process with active hepatocellular damage and necrosis with a lobular inflammatory response.

Viral hepatitis is considered acute when inflammation lasts 6 months or less.

With chronic viral hepatitis, the longstanding repetition of the inflammation and healing process leads to liver fibrosis.

RNA virus with an average incubation period of 35–70 days.

Typically , it is a self-limiting process leading to acute hepatitis.

Clinical illness manifests as malaise, myalgias, arthralgia, anorexia, nausea, vomiting, diarrhea, low-grade fevers, and/or jaundice.

Clinical features usually subside over 2–3 weeks.

There is no chronic form of hepatitis A.

Mode of transmission: fecal-oral, sewage-contaminated shellfish.

Prevention: pooled gamma globulin, hepatitis A vaccine.

Complications: Hepatitis A can lead to fulminant liver failure. It has <0.2% mortality rate [1].

DNA virus with an average incubation period of 60–110 days that has an insidious onset leading to acute hepatitis.

Chronic hepatitis develops in 1–5% of immunocompetent adults, a substantial proportion of immunocompromised adults and as high as 90% of infected children [2].

After an infection with hepatitis B there are four phases: (1) immune tolerant, (2) immune clearance, (3) inactive HBsAg carrier state, and (4) reactivated chronic hepatitis B.

Mode of transmission: vertical transmission (mother to fetus), percutaneous, and sexual.

Risk factors: IV drug use, unprotected sex with multiple sexual partners, incarceration, needle sticks, tattoos, body piercings, hemodialysis, and blood transfusions.

Prevention: hepatitis B immunoglobulin, hepatitis B vaccine.

The clinical features of acute hepatitis B are similar to that of hepatitis A.

Complications: The clinical course associated with acute hepatitis B ranges from asymptomatic to fulminant disease and death in a few days. If aminotransferase levels remain elevated for more than 6 months, the patient is considered to have chronic hepatitis B.

20% of chronic hepatitis B cases progress to cirrhosis [2].

Hepatocellular carcinoma develops in cirrhotic patients at a rate of 2–4% per year [2].

RNA virus with an average incubation period is 35–70 days.

The clinical illness of acute hepatitis C is often mild and usually asymptomatic. Majority of cases progress to chronic liver disease.

Mode of transmission: percutaneous.

Risk factors: IV drug use, incarceration, needle stick, tattoos, body piercing, hemodialysis, and blood transfusion.

Prevention after exposure: interferon plus ribavirin.

Complications: Chronic hepatitis C is clinically indistinguishable from other causes of chronic hepatitis. Cirrhosis occurs in 20% of affected patients after 20 years [3]. Patients are also at risk for developing hepatocellular carcinoma. Hepatitis C has been shown to be associated with mixed cryoglobulinemia and membranoproliferative glomerulonephritis. HCV infection increases a patient’s risk of developing non-Hodgkin lymphoma.

Excessive alcohol intake leading to a fatty liver, followed by hepatitis and cirrhosis.

The consumption of 50 g daily (5 standard drinks) of alcohol for 10 years or more puts individuals at risk for ALD.

The clinical course of ALD includes a spectrum of disease: alcoholic steatosis, alcoholic steatohepatitis, cirrhosis, and hepatocellular carcinoma.

The pathophysiology of alcoholic liver disease starts with acute or chronic inflammation leading to parenchymal necrosis of the liver. The liver inflammation and hepatocyte degeneration at the level of alcoholic steatosis is reversible with cessation of alcohol use. The dreaded complication of alcoholic liver disease is progression to cirrhosis.