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Viral Hepatitis

Viral Hepatitis. Objectives 1-to know the method of transmission of hepatitis A,B, and C viruses so can prevent this. 2- to know the features of these infections so diagnosed early, reduce complications, and differentiated from others diseases.

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Viral Hepatitis

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  1. Viral Hepatitis

  2. Objectives 1-to know the method of transmission of hepatitis A,B, and C viruses so can prevent this. 2- to know the features of these infections so diagnosed early, reduce complications, and differentiated from others diseases. 3- to know the main lines of treatment so treated correctly and reduce the morbidity and mortality. 4-to encourage the preventive measures.

  3. Viral Hepatitis is a major health problem in both developing and developed countries. Its caused by five pathogenic hepatotropic viruses : hepatitis A, B, C, D, and E viruses . HEPATITIS A ETIOLOGY. HAV is an RNA virus, a member of the picornavirus family . EPIDEMIOLOGY : 1- Its responsible for most forms of acute and benign hepatitis . 2- Transmission is almost always by person-to-person contact through the fecal-oral route.Parenteral transmission occurs rarely . 3- Infection has been associated with contact with contaminated food or water and after travel to endemic areas.

  4. Also contacts with infected persons, child-care centers, and household contacts . 4- HAV infection during pregnancy or at the time of delivery does not result in clinical disease in the newborn. 5- HAV excreted in the stool from 2 wk before to 7days after the onset of jaundice. The patient is therefore contagious during this period. CLINICAL MANIFESTATIONS : Incubation period is ≈3 wk. The onset is abrupt with systemic symptoms include: fever, malaise, nausea, emesis, anorexia, and abdominal discomfort. Diarrhea often occurs in children. Jaundice, dark-colored urine with pale stool occur, and develop after the systemic symptoms. Right upper quadrant pain.

  5. The typical duration of illness is 7–14 days. Rarely other organ systems can be affected including: 1-Regional lymph nodes and the spleen may be enlarged. 2-The bone marrow moderately hypoplastic, and aplastic anemia 3- Ulceration of the gastrointestinal tract 4- Acute pancreatitis , myocarditis, nephritis, arthritis (rarely). Fulminant hepatitis is uncommon in children; co-infection with HCV increases the risk for fulminant hepatitis. HAV is not associated with chronic liver disease, or an intestinal carrier state. DIAGNOSIS : 1-detection of antibodies to HAV(anti-HAV IgM) in the serum by radioimmunoassay. These antibodies remains positive for 4–6 mo after the acute infection. while anti-HAV (IgG) is usually detected within 8 wk of symptoms onset & continuo for life.

  6. Pattern of response to hepatitis A virus (HAV) infection.

  7. 2- Identification of viral particles in stool . 3- Viral polymerase chain reaction (PCR) assay. 4- Liver function test: Hyperbilirubinemia (mixed or conjugated (direct)),rise in serum levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) & alkaline phosphatase (ALP) . COMPLICATIONS. Most patients achieve full recovery. Acute liver failure (fulminant hepatitis) rare but can occur. Those at risk are adults, with underlying liver disorders or immunocompromised patient . Edema and Ascites due to decrease synthetic activity of liver (decrease albumin ).

  8. TREATMENT : No specific treatment for hepatitis A. Supportive treatment with Intravenous hydration as needed . Hospitalization in : 1-Repeated vomiting and dehydration 2-prolong PT because PT asses the degree of liver injury . PREVENTION 1- Patients should be excluded from school, child care, or work during contagious period . 2- Careful handwashing, particularly after changing diapers and before preparing food. 3-Vaccine : two inactivated, HAV vaccines are approved for children >2 yr of age. They are administered intramuscularly in a two-dose schedule, with the 2nd dose given 6–12 mo after the 1st dose .

  9. 4- Hepatitis A Virus (HAV) Prophylaxis : - pre-exposure prophylaxis : Immunoglobulin (Ig) is recommended for all travelers to endemic countries . - postexposure prophylaxis : 1- household and sexual contacts of HAV cases 2- newborn infants of HAV-infected mothers 3- child-care center staff, children, and their household contacts during an outbreak 4- outbreaks in institutions and hospitals.

  10. HEPATITIS B ETIOLOGY : HBV which is double-stranded DNA virus .The surface of the virus includes particles designated hepatitis B surface antigen (HBsAg) . The inner portion of the virion contains hepatitis B core antigen (HBcAg), the nucleocapsid that encodes the viral DNA, called hepatitis B e antigen (HBeAg), whichserves as a marker of active viral replication . EPIDEMIOLOGY : 1- Transmission occurs through blood & blood products exposure,sexual contact, intravenous drugs(addict), tattoos, and intimate contact with carriers. 2- Transplacental transmission from HBsAg-positive mother .The risk of transmission is greatest if the mother is also HBeAg positive . Transmission also can occurr at the time of delivery from amniotic fluid, maternal feces or blood that contained the virus.

  11. 3- HBsAg is recovered in breast milk of infected mothers. CLINICAL MANIFESTATIONS : Incubation period ranges from 45 to 160 days . Many cases in children are asymptomatic . Acute symptomatic episode is similar to that of HAV infection but more severe. The first clinical evidence is elevation of ALT levels, which begin to rise just before development of lethargy, anorexia, and malaise, which occurs about 6-7 wk after exposure. The illness may be preceded in a few children by arthralgia or skin lesions, including urticarial, purpuric, or maculopapular rashes. Papularacrodermatitis, the Gianotti-Crosti syndrome, may also occur. Extrahepatic conditions include polyarteritis, glomerulonephritis, and aplastic anemia.

  12. Jaundice, usually begins ≈8 wk after exposure and lasts for ≈4 wk. Most patients do recover, but the “chronic carrier state”defined as being positive for HBsAg for >6 mo, complicates up to 10% of cases. Chronic hepatitis cirrhosis and hepatocellular carcinoma are seen with chronic infection. On physical examination : icteric skin and mucous membranes. The liver is usually enlarged and tender. Splenomegaly and lymphadenopathy are common. Clinical signs of altered sensorium and hyper-reflexivity indicate encephalopathy and ALF. DIAGNOSIS Diagnosis of acute HBV infection requires A- assay of serologic markers: 1-HBsAg is the 1st serologic marker of infection to appear and is found in almost all infected persons.

  13. 2- Antibody to HBcAg (anti-HBcIgM) :is the most valuable serologic marker of acute HBV infection because it rises early after infection and remains positive for many months before being replaced by anti-HBcIgG, which persists for years. 3- Anti-HBs and anti-HBc antibodies are detected in persons with resolved infection . While persons immunized with hepatitis B vaccine have only anti-HBs antibodies . 4- HBeAg is present in active acute or chronic infections and is a marker of infectivity. B- HBV DNA can be detected in the serum of acutely infected patients and chronic carriers. C- Liver function test :The 1st biochemical evidence of HBV infection is elevation of ALT levels .

  14. COMPLICATIONS : 1- ALF with coagulopathy, encephalopathy, and cerebral edema occurs more frequently with HBV than with the other hepatotropic viruses. The risk of ALF is further increased when there is co-infection or super-infection with HDV. 2- chronic hepatitis, which can lead to cirrhosis, end-stage liver disease, and primary hepatocellular carcinoma. 3- Membranous glomerulonephritis due to circulating immune complexes is a rare complication . TREATMENT. Treatment of the acute infection is supportive. Chronic hepatitis B treated with Interferon-αwhich have immunomodulatory and antiviral effects .

  15. PREVENTION 1- Hepatitis B vaccine : at birth, 2 , & 6mo. of age . 2-Infants born to HBsAg-positive women should receive vaccine at birth accompanied by administration of Hepatitis B Immunoglobulin(HBIG) as soon after delivery as possible (within 12 hr) . 3- postexposure prophylaxis : Hepatitis B vaccine and HBIG given for household, sexual, and needle-sharing contacts, those with blood exposure & Immunocompromised patients.

  16. HEPATITIS C previously known as “transfusion-related non-A, non-B hepatitis . ETIOLOGY HCV is a single- stranded RNA virus . EPIDEMIOLOGY. 1- Its the most common cause of chronic liver disease in adults . 2- Risk factors for transmission include: *blood transfusion *Illegal drug use with exposure to blood or blood products from HCV-infected individuals . *Sexual transmission . *occupational exposure . *perinatal transmission from mother to her infant .

  17. CLINICAL MANIFESTATIONS : The incubation period is 7–9 wk . Acute HCV infection is mild and insidious in onset. Acute liver failure rarely occurs. HCV is the most likely hepatotropic virus to cause chronic infection . Chronic HCV infection is defined by persistently elevated levels of ALT in the presence of hepatic fibrosis and by the presence of HCV RNA in blood. Chronic hepatitis C is clinically silent until a complication develops.About 25% of infected patients progress to cirrhosis, liver failure, and primary hepatocellular carcinoma (HCC) within 20–30 yr of the acute infection . Chronic HCV infection can be associated with small vessel vasculitis, peripheral neuropathy, membranoproliferative glomerulonephritis, and nephrotic syndrome . DIAGNOSIS. 1- serologic test which is enzyme immunoassay (EIA) to detect theantibodies to HCV antigens (anti-HCV) . 2- PCR assay for detection of small amounts of HCV RNA .

  18. 3-Aminotransferase levels typically fluctuate during HCV infection . 4- liver biopsy to assess the presence and extent of hepatic fibrosis . 5-Children born to HCV-infected women should be tested for anti-HCV after 12 mo of age but PCR can be done in infancy. COMPLICATIONS. 1- chronic hepatitis(60-80%) . 2- cirrhosis or HCC 3- acute liver failure (rarely) TREATMENT. Interferon-α and ribavirin use for children >3 yr of age with HCV hepatitis. PREVENTION. No vaccine is available to prevent HCV. Immunoglobulin preparations are not beneficial .

  19. HEPATITIS D HDV cannot produce infection without HBV. Its either cause an infection at the same time as the initial HBV infection (co-infection), or infect a person who is already infected with HBV (super-infection). HDV must be considered in all cases of ALF .

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