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Pathophysiology of Viral Hepatitis
Under the guidance Presented By
Dr. Asis Bala Mr. Shivpal
Dept. of Pharmacology & Toxicology Dept. of Pharmacology
&Toxicology
NIPER Hajipur NIPER Hajipur
1
Content
2
 Introduction
 Epidemiology
 Hepatitis Virus
 Symptoms
 Structure of Virus
 Pathophysiology
 Diagnosis
 Treatment
 New drugs under the clinical trail
 Risk Factors
 Prevention
• Reference
Introduction
3
 ‘Hepatitis’ derived from two words:-
Hepar – Liver
Titis – Inflammation
 Means- Inflammation in liver.
 The term viral hepatitis is used to describe infection of the liver caused by
hepatotropic viruses.
 Currently there are 5 main varieties of viruses causing viral hepatitis:
Hepatitis A virus (HAV),
Hepatitis B virus (HBV),
Hepatitis C virus (HCV),
Hepatitis delta virus (HDV) ,
Hepatitis E virus (HEV).
 Some other viruses:-
• cytomegalovirus(CMV)
• Herpes simplex virus (HSV) etc.
Figure 1
Epidemiology
4
 The World Health Organization (WHO) estimated that 1 in 3
people in the world have been infected by either HBV or HCV.
 1.3 million people have died in 2015.
 2 billion people have been infected with HBV.
 Approximately 185 million people are infected with HCV and
20 million people are infected with HEV.
 In high endemic regions more than 90% children get infected
by HAV by the age of 10.
 Viral hepatitis results in around 1.4 million deaths each year,
HBV and HCV are responsible for about 90% .
 “2030 Agenda for Sustainable Development Goals” of WHO
has identified specific actions to prevent viral hepatitis.
Hepatitis Viruses
5
Hepatitis
A
Hepatitis
B
Hepatitis
C
Hepatitis
D
Hepatitis
E
Type ssRNA dsDNA ssRNA ssRNA ssRNA
Incubation
Period
30 days 90 days 50 days 50days 40days
Route Feaco-oral Parentral Parentral Parentral Feaco-oral
Severity Mild Sever Mild Sever Mild
Symptoms
6
 Fever, a flu-like illness
 Fatigue
 Dark urine
 Loss of appetite
 Nausea, Vomiting
 Joint pain
 Jaundice (yellowing of the skin and eyes)
 Pain in the upper right abdomen (due to the inflamed liver)
 People with chronic Hepatitis B develop serious liver conditions, such as
cirrhosis (scarring of the liver) or liver cancer.
Structure of Virus
7
Figure 2
Pathophysiology
8
Figure 3
9
Figure 4
Diagnosis
10
 Liver function Test.
 Total Bilirubin
 Serum glutamic pyruvic transaminase (SGPT)
 Serum glutamic oxaloacetic transaminase (SGOT)
 Cholesterol
 Albumin
 Total protein
 Ultrasound of liver.
 Serologic and viral markers:-
 1. HBsAg :-HBsAg appears early in the blood after about 6 weeks of infection and its
detection is an indicator of active HBV infection.
 2. Anti-HBs:- Specific antibody to HBsAg in serum called anti-HBs appears late, about 3
months after the onset. Anti- HBs response may be both IgM and IgG type.
 3. HBeAg:-derived from core protein is present transiently (3-6 weeks) during an acute
attack.
 4. Anti-HBe :-Antibody to HBeAg called anti-HBe appears after disappearance of HBeA.
 5. Antibody to HBcAg called anti-HBc can be detected in the serum of acute hepatitis B
patients.
 6. HBcAg:- derived from core protein cannot be detected in the blood.
 7. Anti-HBcV-DNA :-Detection of HBV-DNA by molecular hybridisation using the Southern
blot techniques.
Risk Factors
11
 Have unprotected sex with multiple sex partners or with someone who's
infected with HBV.
 Share needles during IV drug use.
 Live with someone who has a chronic HBV infection.
 Are an infant born to an infected mother.
 Age.
 Any liver injury.
Treatment of Hepatitis B
12
 Interferon alpha (α-IFN) is the first-line treatment.
 Anti viral drugs:-
lamivudine
Telbuvidine
Emtricitabine
Adefovir
 Liver transplantation.
 Hepatitis B vaccine(preventive).
New Drugs Under The Clinical
Trail
13
 Total 263 drugs are ongoing clinical trail for HBV.
 ABI-H0731:- target viral core protein.
 Inarigivir:- to block replication of viral DNA.
 JNJ-3989:-Under the study.
 Bulevirtide:- under the study.
Prevention
14
 WHO recommends that all infants receive the hepatitis B vaccine as soon as
possible after birth, preferably within 24 hours.
 Simple environmental procedures can limit the risk of infection to health care
workers, laboratory personnel, and others.
Examples
 Gloves should be used when handling all potentially infectious materials;
 protective garments should be worn and removed before leaving the work
area;
 masks and eye protection or droplets from infectious material.
 only disposable needles should be used;
 needles should be discarded directly into special containers.
 work surfaces should be decontaminated using a bleach solution; and
laboratory personnel should refrain from eating, drinking, and smoking in the
work area.
Reference
15
 Mohan Harsh,’’A textbooh of Pathology’’,6th edition, Jaypee Brothers
Medical Publisher pvt. Ltd.
 Doo Hyun Kim, Hong Seok Kang, and Kyun-Hwan Kim ,Roles of
hepatocyte nuclear factors in hepatitis B virus infection, World Journal of
s.
 Intracellular interleukin-32γ mediates antiviral activity of cytokines
against hepatitis B virus, Nature communications.
16

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Viral hepatitis :- Pathophsiology of Hepatitis B

  • 1. Pathophysiology of Viral Hepatitis Under the guidance Presented By Dr. Asis Bala Mr. Shivpal Dept. of Pharmacology & Toxicology Dept. of Pharmacology &Toxicology NIPER Hajipur NIPER Hajipur 1
  • 2. Content 2  Introduction  Epidemiology  Hepatitis Virus  Symptoms  Structure of Virus  Pathophysiology  Diagnosis  Treatment  New drugs under the clinical trail  Risk Factors  Prevention • Reference
  • 3. Introduction 3  ‘Hepatitis’ derived from two words:- Hepar – Liver Titis – Inflammation  Means- Inflammation in liver.  The term viral hepatitis is used to describe infection of the liver caused by hepatotropic viruses.  Currently there are 5 main varieties of viruses causing viral hepatitis: Hepatitis A virus (HAV), Hepatitis B virus (HBV), Hepatitis C virus (HCV), Hepatitis delta virus (HDV) , Hepatitis E virus (HEV).  Some other viruses:- • cytomegalovirus(CMV) • Herpes simplex virus (HSV) etc. Figure 1
  • 4. Epidemiology 4  The World Health Organization (WHO) estimated that 1 in 3 people in the world have been infected by either HBV or HCV.  1.3 million people have died in 2015.  2 billion people have been infected with HBV.  Approximately 185 million people are infected with HCV and 20 million people are infected with HEV.  In high endemic regions more than 90% children get infected by HAV by the age of 10.  Viral hepatitis results in around 1.4 million deaths each year, HBV and HCV are responsible for about 90% .  “2030 Agenda for Sustainable Development Goals” of WHO has identified specific actions to prevent viral hepatitis.
  • 5. Hepatitis Viruses 5 Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E Type ssRNA dsDNA ssRNA ssRNA ssRNA Incubation Period 30 days 90 days 50 days 50days 40days Route Feaco-oral Parentral Parentral Parentral Feaco-oral Severity Mild Sever Mild Sever Mild
  • 6. Symptoms 6  Fever, a flu-like illness  Fatigue  Dark urine  Loss of appetite  Nausea, Vomiting  Joint pain  Jaundice (yellowing of the skin and eyes)  Pain in the upper right abdomen (due to the inflamed liver)  People with chronic Hepatitis B develop serious liver conditions, such as cirrhosis (scarring of the liver) or liver cancer.
  • 10. Diagnosis 10  Liver function Test.  Total Bilirubin  Serum glutamic pyruvic transaminase (SGPT)  Serum glutamic oxaloacetic transaminase (SGOT)  Cholesterol  Albumin  Total protein  Ultrasound of liver.  Serologic and viral markers:-  1. HBsAg :-HBsAg appears early in the blood after about 6 weeks of infection and its detection is an indicator of active HBV infection.  2. Anti-HBs:- Specific antibody to HBsAg in serum called anti-HBs appears late, about 3 months after the onset. Anti- HBs response may be both IgM and IgG type.  3. HBeAg:-derived from core protein is present transiently (3-6 weeks) during an acute attack.  4. Anti-HBe :-Antibody to HBeAg called anti-HBe appears after disappearance of HBeA.  5. Antibody to HBcAg called anti-HBc can be detected in the serum of acute hepatitis B patients.  6. HBcAg:- derived from core protein cannot be detected in the blood.  7. Anti-HBcV-DNA :-Detection of HBV-DNA by molecular hybridisation using the Southern blot techniques.
  • 11. Risk Factors 11  Have unprotected sex with multiple sex partners or with someone who's infected with HBV.  Share needles during IV drug use.  Live with someone who has a chronic HBV infection.  Are an infant born to an infected mother.  Age.  Any liver injury.
  • 12. Treatment of Hepatitis B 12  Interferon alpha (α-IFN) is the first-line treatment.  Anti viral drugs:- lamivudine Telbuvidine Emtricitabine Adefovir  Liver transplantation.  Hepatitis B vaccine(preventive).
  • 13. New Drugs Under The Clinical Trail 13  Total 263 drugs are ongoing clinical trail for HBV.  ABI-H0731:- target viral core protein.  Inarigivir:- to block replication of viral DNA.  JNJ-3989:-Under the study.  Bulevirtide:- under the study.
  • 14. Prevention 14  WHO recommends that all infants receive the hepatitis B vaccine as soon as possible after birth, preferably within 24 hours.  Simple environmental procedures can limit the risk of infection to health care workers, laboratory personnel, and others. Examples  Gloves should be used when handling all potentially infectious materials;  protective garments should be worn and removed before leaving the work area;  masks and eye protection or droplets from infectious material.  only disposable needles should be used;  needles should be discarded directly into special containers.  work surfaces should be decontaminated using a bleach solution; and laboratory personnel should refrain from eating, drinking, and smoking in the work area.
  • 15. Reference 15  Mohan Harsh,’’A textbooh of Pathology’’,6th edition, Jaypee Brothers Medical Publisher pvt. Ltd.  Doo Hyun Kim, Hong Seok Kang, and Kyun-Hwan Kim ,Roles of hepatocyte nuclear factors in hepatitis B virus infection, World Journal of s.  Intracellular interleukin-32γ mediates antiviral activity of cytokines against hepatitis B virus, Nature communications.
  • 16. 16