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Hepatobiliary disorders

Hepatitis

Inflammation of the liver

Viral hepatitis (A, B, C, D, E, G)

Most common cause

Other possible causes

Drugs (alcohol)

Chemicals

Autoimmune liver disease

Bacteria (rarely)

Hepatitis A virus (HAV)

RNA virus

Transmitted fecal-oral route, parenteral (rarely)

Frequently occurs in small outbreaks

Found in feces 2 or more weeks before the onset of symptoms and up to 1 week
after the onset of jaundice

Present in blood briefly

No chronic carrier state

Poor hygiene, improper handling of food, crowded situations, and poor sanitary
conditions are all factors related to hepatitis A.

Transmission occurs between family members, institutionalized individuals, and


children in day-care centers, and as the result of common-source outbreaks.

Serologic Events in HAV Infection

Hepatitis A virus (HAV)

Anti-HAV immune globulin M (IgM)

Appears in the serum as the stool becomes negative for the virus

Detection of IgM anti-HAV indicates acute hepatitis.

Anti-HAV immune globulin G (IgG)

IgG anti-HAV: Indicator of past infection

Presence of IgG antibody provides lifelong immunity.

Hepatitis B virus (HBV)

DNA virus

Transmission of HBV

Perinatally by mothers infected

Percutaneously (IV drug use)

Horizontally by mucosal exposure to infectious blood, blood products, or


other body fluids

Transmission occurs when infected blood or other body fluids enter the body of a
person who is not immune to the virus.

Sexually transmitted disease

Can live on a dry surface for 7 days

Kissing/sharing food items may spread the virus via saliva.

More infectious than HIV

Complex structure with three antigens

Surface antigen (HBsAg)

Core antigen (HBcAg)

E antigen (HBeAg)

Each antigencorresponding antibody may develop in response to acute viral


hepatitis B

Presence of hepatitis B surface antibodies

Indicates immunity from HBV vaccine

Past HBV infection

With chronic infection, liver enzyme values may be normal or

15% to 25% of chronically infected persons die from chronic liver disease.

In North America, approximately 0.5% of the population are HBV carriers; in parts
of Asia, the rate is approximately 8% to 10%.

Hepatitis C virus (HCV)

RNA virus

Transmitted percutaneously

Risk factors

IV drug use

Most common mode of transmission in United States and Canada

Blood transfusions

Transmission <1 per 1 million blood transfusions

High-risk sexual behavior

Hemodialysis

Occupational exposure

P Up to 10% of patients with HCV cannot identify a source.

Additional data needed regarding risk of body piercings, tattooing, and


intranasal drug use in transmission of HCV

perinatal transmission

Pathophysiology

Acute infection

Liver damage mediated by

Cytotoxic cytokines

Natural killer cells

Liver cell damage results in hepatic cell necrosis.

Proliferation and enlargement of Kupffer cells

Inflammation of the periportal areas may interrupt bile flow.

Cholestasis may occur.

Widespread inflammation of the liver tissue

Pathophysiologic changes in the various types of viral hepatitis are similar.

Liver cells can regenerate over time and, if no complications occur, can resume their
normal appearance and function.

Antigen-antibody complexes

Systemic effects of this activation include

Rash

Angioedema

Arthritis

Fever

Malaise

Cryoglobulinemia

Abnormal proteins in blood

Glomerulonephritis

Vasculitis

Clinical Manifestations

30% of patients with HBV are asymptomatic.

80% of patients with acute HCV will be asymptomatic.

In patients who are asymptomatic during the acute phase, the infection may not be
detected.

Acute phase

Lasts from 1 to 4 months

May be icteric (symptomatic) or anicteric

During incubation, symptoms include

Malaise

Anorexia

Fatigue

Nausea

Occasional vomiting

Abdominal discomfort

Headache

The anorexia is sometimes severe and may be due to cytokines or other


chemicals produced by the infected liver. Weight loss may occur.

The patient may find food repugnant and, if a smoker, may have distaste for
cigarettes.

Low-grade fever

Arthralgias

Skin rashes

Physical exam may reveal hepatomegaly, lymphadenopathy, and


splenomegaly.

Maximal infectivity period

Jaundice

Results when bilirubin diffuses into tissues

Urine darkens because excess bilirubin is excreted.

If bilirubin cannot flow out of liver, stool will be light or clay-colored.

Pruritus can accompany jaundice.

Accumulation of bile salts beneath the skin

When jaundice occurs, fever subsides.

Liver is usually enlarged and tender.

After the fever subsides, the GI symptoms usually remain, and some
fatigue may continue.

Clinical manifestations:

Pruritus can accompany jaundice.

Accumulation of bile salts beneath the skin

When jaundice occurs, fever subsides.

Liver is usually enlarged and tender.

Convalescent phase (2 4 months)

Begins as jaundice is disappearing

Lasts weeks to months

Faza de convalescent dureaza cateva saptamani, dau splenomegalia subsides

Major complaints

Malaise

Easy fatigability

Almost all cases of hepatitis A are resolved.

Many HBV and most HCV infections result in lifelong (chronic) infection.

Absence of jaundice does not mean recovery.

Many HBV infections and most HCV infections result in chronic (lifelong) viral
infection.

Some patients may be asymptomatic. Others, however, may have intermittent or


ongoing malaise, fatigue, myalgias, arthralgias, and hepatomegaly.