Report Pa Tho Genesis Diagnostics

REPORT: PATHOGENESIS, DIAGNOSTICS, TREATMENT AND PRINCIPLES OF PROFILAXIS OF THE ENTERAL VIRUS HEPATITIS (A and E) Sajid Mehmood

Adnan Akram

Aftab Ahmed

Accident & Emergency Department.

Department of Infectious Diseases.

Department of Infectious Diseases.

Royal Infirmary Liverpool.

University Hospital Riga.

Kaunas Medical University Hospital.

United Kingdom

Latvia

Kaunas. Lithuania

[email protected]

[email protected]

[email protected]

VHA- RNA picano virus, children and young adults feacal oral route, no carrier state, do not lead to chronic liver disease I.P- 15-14 days Clinical- Prodromal/preicteric phases lasts up to 2 wks, viramia leads to influenza like symptoms during the prodromal phase – mild fever, nausea, vomiting, diarrhea, malaise, upper abdominal discomfort. After 1-2 wks patient becomes icteric (non icteric can be). As the jaundice worsen urine becomes dark and feaces becomes pale because of cholistasis ( intra hepatic). 10 % of cases liver moderately enlarged and the spleen is palpable ( cytolytic syndrome) There after jaundice lessens and in majority illness is over withen 3-6 wks. Complications- Extrahepatic are rare but include – Arthritis, Vasculitis, Myocarditis, renal failure, rarely the disease may be very sever with fulfillment hepatitis- Liver coma- death. Investigations- 1. Liver biochemistry, a. in prodromal stage the serum bilirubin is normal, urine – positive bilirubin and urobilinogen. Increase Aminotransferases, serum ASAT, ALAT (ALAT>ASAT). b. Icteric stage- 1. serum bilirubin reflects the level of jaundice, 2. serum ASAT reaches max in 1-2 days after appearance of jaundice, 3. serum alkaline phosphatase mild elevation.( it is good for ASAT and ALAT to increase when bilirubin is increase or elseindicates development of fullminant hepatitis), (After jaundice has decreased ASAT may be increased for some wks even till 6 months.) 2. Blood analysis- leucopenia and relative lymphocytosis, virus in blood 2 wks before and 1 wk after jaundice, PT prolonged in severe cases, increase ESR. 3. Viral markers- Antibodies to HAV- IgG is common in the general population more than 50 yrs, Anti HAV IgM- Acute infection 4. Virus positive 2 wks before and 1wk after jaundice in stool. 5. Other methods- US- bile duct obstruction is suspected, liver biopsy- only if there is doubt of diagnosis this is indicated DD- other types of viral hepatitis drug induce hepatitis.

Treatment- Non specific 1, dietary measures- fluids (except in heart and kidney pathologies) 2. Rest Prophylaxis- 1. good hygien well cooked food. 2. vaccination ( active-formaldihide inactivated vaccine/ passive-normal Igs-0.04-0.06 ml/kg i.m gives protection for 2-3 months for risks persons). Prognosis is excellent. If HAV leads to end stages with complications- symptoms from CNS –Encephalopathy symptoms- somnolencia ( sleep during day), concentration problems hepper is small ( hepato cellular necrosis), from mouth bile order, dic syndrome brain edema aplastic anemia (thrombocyte, neutrophill, and RBC decrease). VHE Virus RNA (calcivirus), this can occur in any age the route o transmission by enteral route, infectivity is less than HAV, often water borne, no carrier state, I.P-5-6 wks Clinical- Prodromal period 1-2 wks, its influenza like, thus occuers symptoms similar to HAV (can be dyspeptic or mixed) all other clinics are same as HAV. HEV has 1-3% mortality from fulminant hepatic failure. Which ↑ in pregnant females up to 30%. Investigations 1. Anti HEV IgM 2. HEV RNA in serum or stools by PCR Treatment – non specific therapy Prevention -good hygiene, boiled water. Pathogenesis of viral hepatitis The mechanisms of liver cells injury are probably immunological. There are diffused hepatic involvement with more severe changers in the perivenular areas, Hepatocytes show degenerative changers ( swelling,cytoplasmic granularity,vaculations) Undergo necrosis. Associated with the necrosis there is a mono nuclear inflammatory cell infiltrate, prdominantly lymphocytes and there is a reactive hyperplacia of kupffer cells. Mild cholestasis is also seen. The extent of damage can be variable in individuals. For some who are affected single and small groups of hepatocytes die (spotty or focal necrosis) and for some multiple ascini are destroyed ( massive hepatic necrosis) resulting in fulminant hepatic failure. Between these 2 groups there are some with confluent necrosis of hepatocytes with collapse of reticuline frame work. Liver quickly recovers from injury before cljnical symptoms decrease.