Viral hepatitis. Supervised by: Dr.Gaith. presented by: Shaima a & Anas & Ala a

Transcription

1 Viral hepatitis Supervised by: Dr.Gaith presented by: Shaima a & Anas & Ala a

2 Etiology Common: Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E Less common: Cytomegalovirus EBV Rare: Herpes simplex

3 Epidemiology: HAV is the major cause of viral hepatitis among children in U.S. about 70%-80% of all new cases are related to viral hepatitis A, 5%-30% related to HBV, 5%-15 are related to HCV. The major risk factors for HBV and HCV are injection drug use, frequent exposure to blood products (hemophilia, organ transplant, CRF) and maternal infection. HEV follows travel to endemic area out side USA. HGV is prevalent in HIV infected persons.

4 Hepatitis A: -RNA virus -Incubation period : days -Rout of transmission : fecal oral and rarely parentral -Children most commonly affected. Hepatitis B: -DNA virus -Incubation period : days -Rout of transmission : transfusion of blood and its products, sexual, vertical and inoculation

5 Hepatitis C: -RNA virus -Incubation period : days -Rout of transmission : transfusion, parentral and vertical Hepatitis D: -RNA virus -Rout of transmission : similar to HBV -Usually co infection with HBV Hepatitis E: -RNA virus -Incubation period : days -Rout of transmission : fecal oral

6 Clinical Forms Of Viral Hepatitis: 1.Ictric hepatitis: the most common form and it is divided in to 3 stages, stage 1:preictric phase: it is the prodromal stage and characterized by mild fever, anorexia, vomiting, abdominal pain, this stage last for 4-6 days. stage 2:icteric phase: jaundice will appear, the liver start to enlarge and become tender and this stage last 2-4 weeks. stage 3:convalcent phase: after complete resolution some children may suffer from fatigue and weakness for several weeks.

7 2.Anicteric hepatitis: this type is common in infant usually characterized by mild gastrointestinal symptoms like vomiting, diarrhea, abdominal colic. 3.Fulminant hepatitis: it is the least common, but most serious form ; clinically there is progressive jaundice, bleeding, acute liver failure, the mortality rate is high up to 70%.

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10 Investigations: 1- ALT and AST 2- Alkaline phosphatase 3- total and direct bilirubine 4- prothrombine time (indicate severe disease) 5-serological tests is required to confirm the diagnosis Serum markers: HAV IgM HBV HB sag (acute and chronic) HB eag (acute) HB cag anti HBc (in window period) HCV ELISA HCV and HCV RNA by PCR the test is sensitive for active infection.

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13 -the clearance of HB sag from the serum precedes a variable period followed by antibody formation to surface antigen which indicate life long immunity ( window period ) here I depend on antibody to core antigen. -the presence of HB sag and HB eag in the absence of anti-hbe indicate high risk of transmissibility and associated with ongoing viral replication

14 Differential diagnosis: Viral infections: EBV, CMV, VZV, adenovirus Bacterial infections: E.coli sepsis, leptospirosis Cholecyctitis, cholengitis Drugs: INH, phenytoin, carbamazepine, OCP Mushroom poisoning Wilson disease Metabolic disease: galactosemia

15 Treatment: Acute hepatitis Usually supportive -rest -hydration -adequate nutrition -prevent close contact, good hygiene When to hospitalize: 1. severe vomiting and dehydration 2. Prolonged prothrombine time 3. sings of hepatic encephalopathy

16 -Chronic HBV infection treated by interferon alfa-2b or lamivudine. -Chronic HCV infection treated by interferon alone or in combination with oral ribavirin

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18 Complication : 1. Acute liver failure 2. Aplastic anemia 3. Chronic liver disease and cirrhosis 4. Relapsing hepatitis

19 Prevention: because treatment has limited efficacy,prevantion of viral hepatitis is very important. Good personal hygiene helps prevent transmission, especially fecal-oral transmission as occurs with HAV and HEV. Blood and other body fluids (saliva, semen) Of pt. with acute HBV and HCV and stool of pt. with HAV are consider infectious. Barrier protection is recommended, but isolation has no value in spread of HAV,HBV,HCV. Post transfusion infection is minimized by avoiding unnecessary transfusion and screening all donors for HBsAg and anti-hcv.

20 Post exposure prophylaxis using using HBIG and vaccine is recommended for household members with intimate contact including sex partners. Prophylaxis is given to unvaccinated persons after needle stick injuries with blood from an HBsAg +ve pt, Newborns of affected mother should receive HBV vaccine and HBIG within 12 hours of birth ( not more than 1 week of age), the combination of HBIG with vaccine is 98% effective in preventing vertical transmission.

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22 Prognosis: -most of acute viral hepatitis resolve without specific therapy -less than 0.1% of cases progress to fulminant liver necrosis -there is no carrier state for HAV and HEV -HEV infection during pregnancy is associated with development of acute liver failure and high mortality rate -HBV, HCV and HDV may persist as chronic infection, cirrhosis and hepatocellular carcinoma

23 -approximately 85% of person with HCV become chronically infected, about 20% of them develop cirrhosis, and 25% of them develop hepatocellular carcinoma

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25 Q: in hepatitis B virus infection, which one of the following antibodies is protective? a. anti-hbe b. anti-hbc c. anti-hbs d. anti-polymerase e. anti-hbv DNA

26 Q: the most common cause of fulminant hepatitis is? a. HAV b. HBV c. HCV d. HEV e. HGV

27 - In hepatitis A infection True or False 1.Virus is present in the stool before the onset of clinical illness? 2.Development of IgG antibodies have diagnostic value as anti-hav? 3.Virus specific IgM is detectable before the onset of clinical illness?

28 - In HBV 1.Persistance of HBs antigen more than 6 months indicate chronic stage? 2.Presence of HBe antibodies indicate continue active viral replication in the liver? 3.Interferon can be used in RX of patient with cirrhosis due to HBV?