hepatitis disease

1.  Hepatitis means inflammation of the liver
– Hepat (liver) + itis (inflammation)= Hepatitis
 Viral hepatitis means there is a specific virus that is causing
your liver to inflame (swell or become larger than normal)
 The liver is a vital organ that processes nutrients, filters the
blood, and fights infections. When the liver is inflamed or
damaged, its function can be affected.
 The condition can be self-limiting or can progress to
fibrosis (scarring), cirrhosis or liver cancer. Hepatitis
viruses are the most common cause of hepatitis in the
world but other infections, toxic substances (e.g. alcohol,
certain drugs), and autoimmune diseases can also cause
hepatitis.
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What Is Hepatitis?
1

2.  Hepatitis A virus (HAV), the etiologic agent of viral
hepatitis type A (infectious hepatitis);
 hepatitis B virus (HBV), which is associated with viral
hepatitis B (serum hepatitis)
 hepatitis C virus (HCV), the agent of hepatitis C (common
cause of post transfusion hepatitis)
 Hepatitis D virus. Etiologic agent of delta hepatitis; causes
infection only in presence of HBV.
 or hepatitis E virus (HEV), the agent of enterically
transmitted hepatitis.
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3. The characteristics of the five known hepatitis viruses
Virus Hepatitis A Hepatitis B Hepatitis
C
Hepatitis D Hepatitis E
Family Picornaviridae Hepadnaviridae Flaviviridae Unclassified Unclassified
Genus Hepatovirus Orthohepadnavir
us
Hepacivirus Deltavirus Hepevirus
Virion 27 nm,
icosahedral
42 nm, spherical 60 nm,
spherical
35 nm,
spherical
30–32 nm,
icosahedral
Envelope No Yes (HBsAg) Yes Yes (HBsAg) No
Genome ssRNA dsDNA ssRNA ssRNA ssRNA
Genome size 7.5 kb 3.2 kb 9.4 kb 1.7 kb 7.6 kb
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4. Characteristics CONT…
Virus Hepatitis A Hepatitis B Hepatitis C Hepatitis D Hepatitis E
Stability Heat- and
acid-stable
Acid-sensitive Ether-
sensitive,
acid-sensitive
Acid-sensitive Heat-stable
Transmission Fecal-oral Parenteral Parenteral Parenteral Fecal-oral
Prevalence High High Moderate Low, regional Regional
Fulminant
disease
Rare Rare Rare Frequent In pregnancy
Chronic
disease
Never Often Often Often Never
Incubation
period
30 days on
average (range
15-50 days)
60-90 days on
average (range
45-180 days)
6-7 weeks on
average (range 2-
6months)
HDV 2
to
8 weeks,
HEV 2
to
9 weeks
Vaccine
10 year
protection
3 injections,
lifetime none11/12/2019 4

5. Pathophysiology
Targets of the Hepatitis viruses are hepatocytes:
 Hepatocyte uptake involves a receptor on the plasma
membrane of the cell
 After entry into the cell, viral RNA is uncoated, and host
ribosomes bind to form polysomes. Viral proteins are
synthesized, and the viral genome is copied by a viral RNA
polymerase
 Minimal cellular morphologic changes result from hepatocyte
infection
 Lymphocytic infiltrate; varying degree of necrosis.
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6. How Hepatitis viruses replicate within the Hepatic cell
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7. Structure of Hepatitis A virus
Structure of Hepatitis B virus
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8. Structure of Hepatitis C virus
Structure of Hepatitis D virus
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9. Phases of infectious hepatitis
 Phase 1 - Viral replication; Patients are
asymptomatic during this phase.
 Phase 2 – Prodromal(early symptom or set of
symptoms that might indicate the start of a
disease before specific symptoms occur)
 Phase 3 - Icteric phase(jaundice, or yellowing of
the skin)
 Phase 4 - Convalescent phase; symptoms and
icterus resolve. Liver enzymes return to normal.
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10. Clinical Findings
In viral hepatitis-
 onset of jaundice is often preceded by gastrointestinal
symptoms such as nausea, vomiting, anorexia, and mild
fever.
 Jaundice may appear within a few days of the
prodromal period.
 Extra hepatic manifestations of viral hepatitis (primarily
type B) include a transient serum sickness-like
prodromal consisting of fever, skin rash, and
polyarthritis; necrotizing vasculitis (polyarteritis
nodosa); and glomerulonephritis.
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11.  Diseases associated with chronic HCV infections
include mixed cryoglobulinemia and
glomerulonephritis.
 The onset of disease tends to occur abruptly with HAV
(within 24 hours), in contrast to a more insidious onset
with HBV and HCV.
 Uncomplicated viral hepatitis rarely continues for more
than 10 weeks without improvement. Relapses occur in
5–20% of cases and are manifested by abnormalities in
liver function with or without the recurrence of clinical
symptoms.
Clinical Findings Cont…
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12. Clinical Findings Cont…
 Hepatitis C is usually clinically mild, with only minimal
to moderate elevation of liver enzymes. Hospitalization is
unusual, and jaundice occurs in less than 25% of patients.
 About 40% of chronic liver disease is HCV-related,
resulting in an estimated 8000–10,000 deaths annually in
the United States.
 Some are asymptomatic, or have mild symptoms; others
may only present with late complications (cirrhosis/HCC)
 End-stage liver disease associated with HCV is the most
frequent indication for adult liver transplants.
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13. Diagnosis
Liver biopsy usually in cases of:
o The diagnosis is uncertain.
o Other co-infections or disease may be present.
o The patient is immunocompromised.
o Asses severity of chronic hepatitis B or chronic hepatitis C.
* Urine analysis: presence of bilirubin.
* Serum bilirubin: Total bilirubin may be elevated in
infectious hepatitis. Bilirubin levels higher than 30 mg/dL
indicate more severe disease.
PCR: used to detect viral RNA  HCV
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14. * Alkaline phosphatase: if elevated significantly,
consider abscess or biliary obstruction.
* Prothrombin time (PT) if prolonged 
impaired synthetic function of the liver.
* BUN & serum creatinine  decreased renal
function suggests fulminant hepatic disease.
* Serum ammonia in patients with AMS or other
evidence of hepatic encephalopathy.
* CBC: lymphocytosis
Lab Studies con..
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15. Hepatitis B(HBV)--EPIDEMIOLOGY
 HBV is a DNA virus that belongs to the hepadnavirus family.
 2 billion people worldwide have past or present infections
 400 million people are chronic HBV carriers.
 Eight genotypes of HBV identified and re-labeled A through
H.
 HBV is the cause of 60% to 80% of worldwide Hepatocellular
Carcinoma(HCC).
 500,000 to 1 million deaths worldwide are attributed to it.
 5% to 10% of all liver transplants are attributed to HBV.
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16. AT Risk Groups
 IV drug users
 People receiving multiple blood transfusions
 Sexual promiscuity
 People in contact with HBV carriers
 Travelers to endemic areas of South
America, Southern Asia, and Africa
 Resident and employees of residential care
facilities
 Health Care Workers
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17. Transmission
Transmission 3 main ways:
Parentally/percutaneous route, Drug
Users, needle sticks, Hemodialysis
patients
Sexually
Vertical/ Perinatal route
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19. Hepatitis In Bangladesh
 Three thousand six hundred and ten patients with
acute hepatitis in two large hospitals in Dhaka city
were tested for HBsAg. Besides, 780 commercial
blood donors, 126 doctors and 576 apparently
healthy persons were also tested.
 Passive haemagglutination technique was applied
for this test. Patients with post-transfusion hepatitis
and doctors with acute hepatitis showed the highest
incidence, being 60% and 65.5% respectively.
 HBsAg was detected only in 15.4% of children and
27.2% of adult patients with acute hepatitis.
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20. Treatment
 Treatment of patients with hepatitis is supportive and directed at
allowing hepatocellular damage to resolve and repair itself.
 Only HBV and HCV have specific treatments, and those are only
partially effective.
 Recombinant interferon-alfa is currently the therapy of proved
benefit in the treatment of patients chronically infected with HBV
or HCV.
 Lamivudine, a reverse transcriptase inhibitor, reduces HBV DNA
levels, but viral replication resumes in the majority of patients
when treatment is stopped.
 Combination therapy of interferon-alfa and ribavirin against
chronic hepatitis C gives a sustained.
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21. Prevention & Control
Hepatitis A
 A vaccine is available that will prevent HAV infection for up to 10
years.
 The vaccines are safe, effective, and recommended for use in
persons over 1 year of age.
 Control measures are directed toward the prevention of fecal
contamination of food, water, or other sources by the individual.
Reasonable hygiene—such as hand washing, the use of disposable
plates and eating utensils, and the use of 0.5% sodium
hypochlorite.
 Immune (gamma) globulin (IG) is prepared from large pools of
normal adult plasma and confers passive protection in about 90%
of those exposed when given within 1–2 weeks after exposure to
hepatitis A.
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22. Prevention & Control Con…
Hepatitis B
 A vaccine for hepatitis B has been available since 1982. The initial
vaccine was prepared by purifying HBsAg associated with the 22-
nm particles from healthy HBsAg-positive carriers and treating the
particles with virus-inactivating agents (formalin, urea, heat).
 These vaccines consist of HBsAg produced by a recombinant
DNA in yeast cells or in continuous mammalian cell lines.
 The HBsAg expressed in yeast, with the morphologic
characteristics of free surface antigen in plasma though the
polypeptide antigen produced by recombinant yeast is not
glycosylated.
 Women who are HBV carriers or who acquire type B hepatitis
while pregnant can transmit the disease to their infants. The
effectiveness of hepatitis vaccine and HBIG in preventing hepatitis
B in infants born to HBV-positive mothers has been substantiated.
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23. Prevention & Control Con…
Hepatitis C
There is no vaccine for hepatitis C although several
candidate vaccines are undergoing tests. Control measures
focus on prevention activities that reduce risks for
contracting HCV. These include screening and testing
blood, plasma, organ, tissue.
Hepatitis D
Delta hepatitis can be prevented by vaccinating HBV-
susceptible persons with hepatitis B vaccine. However,
vaccination does not protect hepatitis B carriers from super
infection by HDV.
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25. Other Causes of Hepatitis
Alcoholic Hepatitis
Drug induced Hepatitis
Autoimmune Hepatitis
Ischemic Hepatitis
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27. Questions?
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