Hepatitis B Virus infection, management.pptx

HumbleCkIvan 83 views 16 slides Jun 21, 2024
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About This Presentation

Key facts
Hepatitis B is a viral infection that attacks the liver and can cause both acute and chronic disease.
The virus is most commonly transmitted from mother to child during birth and delivery, in early childhood, as well as through contact with blood or other body fluids during sex with an inf...


Slide Content

Viral Hepatitis Chelangat k. Ivan MCO MSFH Feb. 2024

INTRODUCTION Hepatitis is the inflammation of the liver, Hepatitis can be caused by viruses, bacteria and non infectious agents such as toxins dugs and alcohol. Viral hepatitis is the inflammation of the liver caused by viruses The commonest causes of viral hepatitis include one of the five hetero types; A, B, C, D, and E. Other viruses include CMV,HSV, EBV, Adenovirus, yellow fever viruses among others. Hepatitis A and E viruses usually cause acute infections which are self limiting HBV and HCV infections may progress to chronic infections with long term complications such as liver cirrhosis, liver failure and HCC HDV only exists in the presence of HBV

Hepatitis B Hepatitis B infection is caused by hepatitis B virus (HBV), an enveloped DNA virus that infects the liver, causing hepatocellular necrosis and inflammation. HBV infection can be either acute or chronic Associated illness ranges in severity from asymptomatic to symptomatic, progressive disease Chronic hepatitis B (CHB) – Defined as persistence of HBsAg for 6months ore more - is a major public health concern

HBsAg Nucleocapsid is 27 nm surrounded by am outer envelope of the surface protein ( HBsAg ) embedded in membranous lipid derived from host cell It indicates current Hepatitis B Infection POSITIVE HBsAg tests can be due to recent vaccination but this positivity is unlikely to persist beyond 14 days post-vaccination. It is present in sera of patients with viral hepatitis B (with or without clinical symptoms).

HBcAg HBcAg (core antigen) is an an Hepatitis B viral protein. Its an indicator of active viral replication . This means the person infected with hepatitis B can likely transmit the virus on to another person. HBcAg IS NOT SECRETED ( does not circulate in blood). It is readily detected in hepatocytes after biopsy The presence of both HBcAg and HBeAg proteins together acts as a marker of viral replication, and antibodies to these antigens are markers of declining replication(anti- HBcAg & anti- HBeAg ).

HBeAg Can be found between icosahedral nucleocapsid core and lipid envelope Its an indicator of active viral replication ; this means that the person infected with hepatitis B can likely transmit the virus on to another person HBeAg is secreted and accumulates in serum T he presence of HBeAg in the serum of patients can serve as marker of active replication in chronic hepatitis.

Prevalence of HBV infection About 2 billion people in the world are exposed to HBV infection and majority of which live in sub-Saharan Africa and southeast Asia. Globally 257 million people are living with chronic HBV infection. I n Uganda it is estimated that 4.1% of the population aged 15-64 years has chronic HBV infection ( UPHIA, 2016 ); The prevalence vary in regions being highest in north and lowest in south west.

Hepatitis B Transmission Endemic Countries Vertical transmission (in utero, birth, breast feeding) Early childhood, close interpersonal contact (infected blood) Unsterilized medical equipment Unprotected penetrative sex Blood transfusion Injection drug a buse Instruments used for tattooing's/piercings/razor Needle stick Rarely – toothbrush NOT contaminated food/water, sharing Clothes, food/water/utensils or greeting, Kissing

Natural History And Consequences Of Hepatitis B Infection Depending on the age of exposure, HBV can be eliminated by natural immunity. Infection that is acquired in the neonatal period leads to chronicity in more than 90% of the exposed. This rate drops to 30%-50% for infections acquired before 6 years of age. Infection acquired above 5 years of age will spontaneously be eliminated in over 90% of the infected individuals within 6 months. Those that fail to eliminate the infection enter the chronic phase of disease that has different outcomes: the majority will remain asymptomatic; a few will progress to liver cirrhosis that remains stable (compensated) and a small percentage may decompensate and suffer complications such as ascites, hepatic encephalopathy, haematemesis ( variceal bleeding), infections, malnutrition, kidney failure and liver cancer that increase the risk of death.

Clinical Presentation Acute symptomatic disease (2-3month, lasts 2-4month) Loss of appetite , Nausea, Vomiting , Low Grade Fever Myalgia, arthralgia , Fatigability Jaundice, dark urine, and light colored stool RUQ And Epigastric Pain Fulminant Hepatitis and CHB Hepatic Encephalopathy Somnolence Disturbance In Sleep Pattern Mental Confusion Coma Ascites GI Bleeding Coagulopathy Ascites

Physical exam Patients with acute hepatitis are asymptomatic but physical examination may reveal; Low grade fever Jaundice Hepatomegaly (mildly enlarged soft liver) Splenomegaly (5-15 %) Chronic hepatitis Hepato -splenomegaly Muscle wasting, palmer erythema, spider angioma Cirrhosis; Ascites, Jaundice, Peripheral Edema, Gynecomastia , Testicular Atrophy. Collateral Veins.

Diagnosis HBsAg POSITIVE Household contact/ spouses should be screened; Discus the benefits of I nitiating treatment if eligible Monitoring if not eligible Baseline tests to asses the eligibility for treatment CBC, LFTs(ALT and AST),HIV, HBV viral load, Abd . U/S Baseline Before initiation of treatment; RFTs, or Urinalysis -dipstick (proteinuria and glycosuria if RFTs not available) HBeAg ; if + ve at T-0, = significant active replication. I t can be used to monitor the response to Rx. if turns – ve and is replaced by antibody, consider stopping Rx. after 12month of Rx. If – ve at T-0,= no significant active replication OR mutant virus which cannot secrete this antigen. HBV DNA AFP .

Treatment WHO TO TREAT Category 1; All Patients who have clinical evidence of cirrhosis OR adults with APRI Score > 2 These should be treated regardless of HBV vial load Category 2; Co-infection with HBV and HIV Regardless of WHO stage, CD4 cell count, viral load(HBV or HIV) Category 3; All patients who do not have clinical evidence of cirrhosis and have APRI score <2 but have; Persistent elevation of ALT after excluding other causes of liver enzyme elevation; Viral load of more than 20,000IU/mL

Goals of treatment Suppression of HBV replication to undetectable levels Decrease necroinflamation and fibrosis Prevent progression to cirrhosis, liver failure and HCC Treatment options TDF 300mg od TDF+3TC 600mg od

Control measures Immunization Use of condoms Avoid sharing sharps Screening of blood products Standard precautions Use of gloves Protective garments, mask and gaggles Proper disposal of needles Bleach solutions to decontaminate work surfaces Autoclaving for metal objects
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