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Viral Hepatitis 1

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VIRAL HEPATITIS

BY: DR PANKAJ
• Infection of hepatocytes Necrosis and inflammation of the liver

• Causes of viral hepatitis


Hepatitis caused by common Nonhepatotrophic viruses
(hepatotropic) viruses

Hepatitis A CMV
Hepatitis B EBV
Hepatitis C HSV
Hepatitis D Yellow fever virus
Hepatitis E Adenovirus
(All except HBV are RNA viruses)
Hepatitis A

• RNA virus
• MC type of viral hepatitis
• Occurs in epidemics
• Commonly affects children and young adults
• Overcrowding and poor sanitation facilitates the spread
• Source of infection: acutely infected persons
• Mode of spread: fecal-oral route
• Incubation period: 15-45 days ( 4 wk)
Hepatitis E

• RNA virus
• Occurs primarily in young to middle aged adults
• Source of infection : Zoonotic disease with animal reservoirs
• Mode of transmission: Enterically transmitted, water brone infection ( contamination of water supplies)
• IP: 5-6 wks
Outcome of infection:
• Clinically similar to hepatitis A ( self-limiting acute hepatitis)
• High mortality rate among Pregnant women ( fulminant hepatitis)
Prevention and control
Good sanitation and hygiene
vaccination
CLINICAL FEATURES OF VIRAL HEPATITIS

PREICTERIC ICTERIC CONVALESCENCE (RECOVERY)

 Lasts for 1-2 wks before the onset  Prodromal symptoms usually  Prodromal symptoms disappear
of jaundice. diminish and appetite improves
 Prodromal symptoms:  Clinical jaundice  Jaundice decrease
Anorexia/nausea/vomiting/ poor  Liver—enlarge and tender  Stool and urine become normal
appetite/ fatigue/ malaise/headache.  Pruritus----due to bile salt  Liver size decrease
 Low grade fever reteintion  Complete biochemical recovery:
 Upper vague abdominal pain  Dark urine and pale stool hep A/E (1-2 months) and Hep B/C
 Dark urine (conjugated (3-4 months)
hyperbilirubinemia)
 Clay colour stool
INVESTIGATIONS

Hematological: Leucopenia with relative lymphocytosis


• Increase in prothrombin time (PT)---In cases of extensive hepatocellular damage
LFT:
• Aminotranferases (AST, ALT): Raised and max level observed during prodromal phase (400-4000)
• Bilirubin: Both conjugated and unconjugated equally raised
• Alkaline phosphatase: may be raised but less than 2 times the normal
• Blood sugar: may be low
URINE: Increased urinary urobilinogen
SEROLOGICAL MARKERS

• IgM anti-HAV----acute infection


• IgG anti HAV---Recovery phage and immunity phase ( provides lifelong immunity)
• Raised AST and ALT
TREATMENT AND PREVENTION

• Supportive symptomatic management


• No specific treatment
• Active immunization: HAV vaccine
• Passive immunization: Immunoglobulins ( exposure to HAV is < 2 wk) and can protect
from HAV infection for 3 Months
HEPATITIS B
What Are The Hepatitis B Virus (HBV) Antigens And Antibodies?
1.Dane particle (Virion) has a double-shell structure containing several antigens (antigenic
material).
1. The outer envelope is called a surface antigen (HBsAg), the Australian antigen.
2. The inner core contains HBV-core antigen (HBcAg), and HBV-e antigen (HBeAg).
3. Within the core is double-stranded DNA (double-stranded viral deoxyribonucleic
acid).
4. There is an enzyme called DNA polymerase.
2.There are three antigens:
1. HBsAg
2. HBcAg
3. HBeAg
3.There are three Antibodies:
1. Anti-HBsAb
2. Anti-HBcAb
3. Anti-HBeAb
How will you discuss Chronic viral hepatitis due to HBV or (Chronic carrier)?
1.Chronic hepatitis is defined when >6 months surface antigen (HBsAg) is present with
normal liver function tests and normal microscopic findings on the liver biopsy.
2.2 to 10 % develop chronic disease.
3.Chronic hepatitis is divided into:
1. Chronic persistent hepatitis where abnormal liver function tests, relatively normal
microscopic findings on liver biopsy. This condition is seen in 6% of the patients.
2. Chronic active hepatitis where abnormal liver function tests and abnormal microscopic
findings on liver biopsy. This condition may be seen in 3% of the patients.
4.These patients may develop cirrhosis.
5.Cirrhotic patients have more chances of cancer, which almost increased 500 times.
6.Lab findings are:
1. HBsAg positive.
2. HbcAb-IgG (Total) is positive.
7.HBeAg positive indicates a highly infective stage and poor prognosis
How Will You Treat The Hepatitis B Virus (HBV)?
 In the case of fulminant hepatitis, liver transplantation is needed.
 Treatment of chronic HBV infection is indicated when HBV-DNA
>2000 IU/L and serum SGPT is raised.
 Antiviral medications are Lamivudine (Epivir), Adefovir (Hepsera),
Telbivudine (Tyzeka), and Entecavir (Baraclude).
 Interferon alpha-2 is used mainly for young patient
How will you diagnose the Hepatitis C Virus (HCV)?
1.Interpretation of HCV profile:
2.Acute infection = Anti-HCV antibody will be positive and quantitative HCV RNA
3.Clinical features of chronic HCV infection
•Usually asymptomatic. Positive HCV-Ab indicates present or past
infection
Laboratory workup
1.Anti-HCV is positive
2.PCR positive
3.HBs-antigen is negative Test Normal Early Acute Chronic Carrier Recovery
4.HAV-IgM is negative infection

Anti- Negativ Negative Positive Positive Positive Positive


HCV e

PCR Negativ Positive Positive Positive Positive Negative


e
What Are The Complications Of Hepatitis C Virus (HCV) Infection?
1.Fulminant hepatitis is seen in 1% to 2% of the patients.
2.Cirrhosis is seen in 5% of the cases.
3.Liver failure.
4.Liver cancer risk is 15%.
5.HCV infection is unlike HBV because this gives rise to more than 60% as a
chronic disease.
(some references say chronicity is from 50% to 80%)

How Will You Prevent The Spread Of The Hepatitis C Virus


(HCV)?
•There is no vaccination available for HCV.
•Proper testing of the blood donors for transfusion for HCV has
decreased the incidence.
HEPATITIS
• Dliver caused by the hepatitis D virus (HDV), which requires HBV
Hepatitis D is an inflammation of the
for its replication.
• Hepatitis D infection cannot occur in the absence of hepatitis B virus.
• HDV-HBV co-infection is considered the most severe form of chronic viral hepatitis due to more rapid
progression towards hepatocellular carcinoma and liver-related death.

•Hepatitis D infection can be prevented by hepatitis B immunization, but treatment success rates are low.

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