1. This lecture was conducted during the Nephrology Unit Grand Ground by Medical Student rotated under Nephrology Division under the supervision and administration of Prof. Jamal Al Wakeel, Head of Nephrology Unit, Department of Medicine and Dr. Abdulkareem Al Suwaida, Chairman of the Department of Medicine. Nephrology Division is not responsible for the content of the presentation for it is intended for learning and/or education purpose only.

2. Acute Viral Hepatitis Presented By: Dr. Mahdi Al Namankani Medical Student May, 2008

3. Definition: Diffuse liver inflammation lasting less than 6 months

4. Causes: Hepatitis A HAV Infective hepatitis Hepatitis B HBV serum hepatitis HepatitisDHDV Hepatitis C HCV Post transfusion hepatitis Hepatitis E HEV Epidemic/ Entral virus 27 nm RNA 42 nm DNA Hepa virus 35 nm IncompleteRNA+HBsAg 30 – 60 nm RNA flavi firus 32 nm RNA transmissionFeco-oral Paraentral and post transfusion Sexual low risk 1-5 % Intrauterine low risk <5% Feco-oral Incubation p. 2 – 6 weeks 2 – 6 months 2 – 6 weeks Chronicity &liver cancer noYesYesYesNo Immunization-passive Non specific Ig Specific Ig IgM Non specific Ig -active HAV vaccine danger Heptavax HBV vaccine

5. Pathogenesis Initial viremia, with inflammation of GIT mucosa. Intrahepatic localization lead to A- diffuse centrilobular necrosis, with cellular infiltration around portal tracts B- intrahepatic cholestasis due to cellualar edema & inspissation of bile Other organ: splenomegaly – lymphoadenopathy Hypoplasia of BM

6. Clinical picture 1. Preicetric stage or prodromal stage: 3 – 9 days Sudden onset of influenza like picture: fever - headache – malaise – muscular pain Anorexia is marked with nausea – vomiting – distension Pain in Rt hypochondrium & epigastrium Dark urine – pale stool Transient itching Examination: fever with relative bradycardia + enlarged tender liver

7. Clinical picture Icteric stage: 2-4 w Jaundice with fever & improvement of general condition Anorexia nausea & vomiting diminish or disappear Urine is dark brown & frothy Stool are clay in color – bulky – offensive – greasy Examination: Soft tender enlarged liver Spleen is enlarged in 20 % L N 10% geralized lymphoadenopathy with LN of post. Triangle of neck

8. Clinical picture Convalescence stage: Signs & symptoms gradually disappear Jaundice may persist for some times due to affinity of bile pigment to elastic tissue Complete recovery of liver may take up to 6 months

9. Investigation: L F T : 1. serum bilirubin : total, direct and indirect 2. ALT – AST : from 500 – 2000 IU/L ALT > AST 3. Alkaline phosphatase – 5’nucleotidase – GGT: Blood : Leucopenia with relative lymphocytosis, ESR

10. Urine : Early bilirubin appearance Bile salt : granular casts – frothy urine - +ve hay sulfur test Stool: Pale – clay with staetorrhea Diminished stercobilinogen Serology others Chronic stage Acute stage Fecal HAV Anti HAV IgG Anti HAV IgM Hepatitis A Anti HDV IgG Anti HDV IgM Hepatitis D Anti HEV IgG Anti HEV IgM Hepatitis E

11. Hepatitis B marker: significance Corresponding Ab Significanceantigen Appear after 3 m Reflecting recovery & immunity Anti HBs Appear after 6 week Acute infection, remain for 3 ms Chronic infection if >6 ms HBsAg(surface) Appear after 2 m Reflecting sever acute & chronic form Anti HBc Detected on Liver Biopsy only (not serum) HBcAg(core) Appear after 2.5 m Non replicating virus Anti HBe Reflect ongoing viral replication (chronicity) HBeAg(envolop) Most sensitive indication for viral replication & chronicity (Dan particle) It is detected by PCR HBV DNA

13. Serological gap:Serological gap: It is a window last several weeks between disappearing of HBs Ag & appearance of Anti Hbs. Anti HBc Ab may represent serological evidence of recent HBV infection Blood free from Hbs Ag & Anti Hbs (but containing anti – HBC) is the major cause of trasfusion HBV infection

14. Hepatitis C markers: significancetimetechniqueMarker Exposure to infection not immunity After 3 – 6 ms of infection 2 nd & 3 rd generation ELISA or RIBA test HCV Ab Indicate active virus After 1 – 2 weeks PCR – quantitative PCR is more accurate & assess interferon ttt HCV RNA

15. Course & Complication: Complete recovary: Occur in most cases of virus A – E Less common in virus B – D & in small case of virus C Relapse: Characteristic of virus C – less common in B – D Present by reappearance of CL.p. or biochemical Abnormalities ( biliruben & enzymes )

16. Fulminant hepatitis: ( Acute liver failure ) Acute hepatic necrosis – acute yellow atrophy After typical onset deep jaundice, vomiting, encephalopathy & coma Patient usually dies in 10 days Prolonged cholestasis Prolonged cholestasis Cholestatic jaundice Watson’s syndrom Cholestatic jaundice Watson’s syndrom After 3 W of jaundice, condition improves but jaundice deepens & patients starts to itch After 3 W of jaundice, condition improves but jaundice deepens & patients starts to itch This is due to intra hepatic Biliary obstruction by inflammation This is due to intra hepatic Biliary obstruction by inflammation Jaundice persist to 6 m then recovery Jaundice persist to 6 m then recovery

17. post hepatitis syndrome: post hepatitis syndrome: Common intelligent Features : anxiety, fatigue, anorexia, Rt upper abdominal discomfort Palpable liver raised copula of diaphragm in X Ray LFT & biopsy are normal Chronic sequelae: In C, B, D not in A & E Chronic active hepatits Chronic persistent hepatitis Post hepatic cirrhosis Hepatocellular carcinoma

18. Extrahepatic manifestation of hepatitis comments Associated virus Clinical condition 60 % have HBV HBV Polyarteitis nodosea Mainly mesengioproliferative –result in CRF HCV & HBV Glomeronephritis Blistering lesion on back of hands HCV Porphyria cutnea tarda Type 2 (mixed – essential) HCVCryoglobulinemia Virus isolated from salivary tissue HCV Sjogren syndrom 60 % have HCV HCV Lichen planus Studies involve small number of patients Impotance need evaluation Others associated with HCV Erythema nodusm – erythema multiforme Polymyosistis – hachimoto’s thyroiditis Diabetes mellitus – bahcet’s syndrome Down syndrome – Aplastic anemia

19. Treatment: Rest: Bed rest till LFT normal Diet: Protein: gives freely except with Liver failure CHO: gives freely Fats: better avoided Alcohol & hepatotoxic: contraindicated

20. Drugs: Vitamins especially K parental Cholestyramine: for itching Corticosteroids are indicated in : fulminant cases – cholestatic jaundice Interferon: reduce risk of chronic hepatitis in acute hepatitis C Prophylaxis: Screening: of blood for hepatitis Ag, disposable syringes, avoid sharing razors or tooth brush passive prophylaxis: passive prophylaxis: Hepatitis A : gamma globulin in contact or preicteric phase patient Hepatitis B: (HBIG) rich with anti HBs

21. Active prophylaxis: Hepatitis A: Inactivated HAV 0.5 – 1 ml IM to be repeated after 6 -12m Hepatitis B: Recombinant HBV vaccine (Heptavax) IM in 3doses at 0 - 1 - 6 m High risk people: Medical doctors & nurses Hemophiliacs & hemolytic anemia Prenatal drug abusers Babies porn to HBsAg +ve mother Now for all infant & children N.P: HBV is prophylactic against hepatitis D viral infection