ALIMENTARY SYSTEM II (PPA62205)

SELF-LEARNING PACKAGE

KULLIYYAH OF MEDICINE & HEALTH SCIENCES

(Student’s copy)

Course ALIMENTARY SYSTEM II (PPA62205)

Semester/Year
4/ 2
Topic
Viral hepatisis
Date
2nd June 2021
Time
11pm
Student’s Name/ ID
KALPPENA NAIDU RAJA GOPAL
Lecturer Name
AP Dr Hakimah binti Mahsin

Overview

This is the Self-Learning Package (SLP) for alimentary system II . The exercise will help
students to understand viral hepatitis

Topic Learning Outcomes (TLOs)

Students should be able to:

1. List clinical spectrum of viral hepatitis
2. Differentiate the general pathology and clinical manifestation of acute and chronic
hepatitis
3. Describe general characteristics of the causative agents
4. Describe general biochemical tests of liver functions in relation to viral hepatitis infection
5. Describe the infection profile, mode-of-spread, specific diagnosis methods, prevention
and control for Hepatitis A, B, C, D and E

References:

1. Robbins and Cotran , Pathologic Basis of Diseases 9th edition Elsevier Saunders
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A) Clinicopathologic syndrome of viral hepatitis
Exposure of hepatitis virus can develop 4 clinicopathologic syndromes. Briefly describe the
syndromes
Clinicopathologic syndrome
1. Acute asymptomatic
infection with recovery
2. Acute symptomatic
infection with
recovery
List the Key morphologic
feature of acute viral
hepatitis (your description
can be aided by
illustrations)
Description
Patients in this group are identified incidentally on the
basis of elevated serum transaminases or presence
of antiviral antibodies.
Worldwide, HAV and HBV infection are frequently
subclinical events in childhood, verified only in
adulthood by the presence of anti-HAV or anti-HBV
antibodies.
Regardless of the virus, the disease is more or less the
same and can be divided into four phases:
(1) an incubation period
(2) a symptomatic preicteric phase
(3) a symptomatic icteric phase
(4) convalescence.
The incubation period for the different viruses is not
same.Peak infectivity occurs during the last
asymptomatic days of the incubation period and the
early days of acute symptom.
Macroscopic: Livers involved  by mild acute 
hepatitis appear normal or slightly mottled. Also,
massive hepatic necrosis the liver  may shrink.
Microscopic: Evoke a  lymphoplasmacytic 
(mononuclear) infiltration. Like, hepatitis A may be
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especially rich in plasma cells.

Hepatocytes: hepatocyte injury  may result in 

necrosis or apoptosis. With  apoptosis,  hepatocytes 
shrink,  becoming intensely eosinophilic, and their 
nuclei become pyknotic and fragmented; effector 
T cells may be present in the  immediate 
vicinity. In severe acute hepatitis, confluent 
necrosis of hepatocytes  is seen around central 
vein.

Sinusiods: . In the former, the cytoplasm 
appears empty with only scattered wisps of 
cytoplasmic remnants. Eventually there is rupture 
of cell membranes leading to  “dropout” of 
hepatocytes, leaving collapsed sinusoidal collagen 
reticulin framework behind; scavenger macrophages 
mark sites  of  dropout 

Portal tracts: Portal inflammation  in acute hepatitis 

is minimal or absent.

3. Chronic hepatitis Chronic hepatitis is defined as symptomatic, biochemical, or

serologic evidence of continuing or relapsing hepatic disease
for more than 6 months.

In some patients the only signs of chronic disease are

persistent elevations of serum transaminases. Laboratory
studies may also reveal prolongation of the prothrombin time
and hyperglobulinemia, hyperbilirubinemia, and mild
elevations in alkaline phosphatase levels.

In symptomatic individuals, the most common finding is

fatigue; less common symptoms are malaise, loss of appetite,
and occasional bouts of mild jaundice.

In precirrhotic chronic hepatitis, physical findings are few, the

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most common being mild hepatomegaly, hepatic tenderness,

and mild splenomegaly. Occasionally, in cases of HBV and
HCV infection, immune complex disease may develop
secondary to the presence of circulating antibodyantigen
complexes, in the form of vasculitis and glomerulonephritis.
Cryoglobulinemia is found in about 35% of individuals with
chronic hepatitis C infection.

List the Key morphologic Macroscopic: Progressive chronic liver damage  is 

feature of chronic viral scarring
hepatitis (your description
can be aided by Microscopic: Histologic feature of chronic viral hepatitis is
illustrations) mononuclear portal infiltration

Hepatocytes:In chronic  hepatitis B, “ground-glass”
hepatocytes—cells with endoplasmic reticulum 
swollen by HBsAg—is a diagnostic hallmark.
Hepatitis C, particularly genotype 3, shows fatty 
change of scattered hepatocytes, although the 
infection may also cause systemic alterations 
leading to metabolic syndrome.

Sinusiods: Changes of hepatic sinusoids are crucial in the

pathogenesis of liver cirrhosis and portal hypertension

Portal tracts: Only portal tracts exhibit fibrosis, but 

in some  patients,  with  time,  fibrous 
septa(bands  of  dense  scar) extend between portal 
tract.
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4. Fulminant hepatitis Refer fulminant hepatic failure lecture

B. Features of specific viral aetiology (Table 16.2 Robbins basic pathology )

1. Hepatitis A virus

Viral Icosahedralcapsid, ssRNA virus

description

Transmission Oral- fecal

mode

Incubation 2-6 weeks

period

Clinical state

Acute present
hepatitis

Fulminant Present
hepatitis

Healthy none
carrier

Persistent none
infection

Chronic None
hepatitis

Cirrhosis None
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Hepatocellular None
carcinoma

Diagnosis Serum IgM

Prevention/
Control

2. Hepatitis B virus

Viral description partially dsDNA

(include description of
HBsAg

HBcAg

HBeAg

Transmission mode Parenteral, sexual  contact, perinatal

Incubation period 2 to 26 weeks (mean 8  weeks)

Clinical state

Acute hepatitis YES

Fulminant hepatitis YES

Healthy carrier PRESENT HAS THE VIRUS, BUT DON’T FEEL SICK

Persistent infection YES

Chronic hepatitis YES

Cirrhosis YES
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Hepatocellular YES

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carcinoma

Diagnosis

(illustrate the sequence Detection of HBsAg or  antibody to HBcAg;  PCR 

of serologic markers in for HBV DNA
acute infection and
chronic infection using
graphs )

Refer figure 16.10

Robbins basic
pathology

Prevention/Control Prevented by getting vaccine and HBIG (hepatitis B immune

globulin) soon after coming into contact with the virus.

Persons who have recently been exposed to HBV should get HBIG
and vaccine as soon as possible and preferably within 24 hours, but
not more than 2 weeks after the exposure.

Wash your hands thoroughly with soap and water after any
potential exposure to blood · Use condoms with sexual partners.
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3. Hepatitis C virus

Viral description ssRNA

Transmission mode Parenteral; intranasal cocaine  use is a risk factor

Incubation period 4 to 26 weeks (mean 9  weeks)

Clinical state

Acute hepatitis YES

Fulminant hepatitis YES

Healthy carrier PRESENT

Persistent infection YES

Chronic hepatitis YES

Cirrhosis YES

Hepatocellular YES –LEADING AETIOLOGY

carcinoma

Diagnosis 3rd-generation ELISA for  antibody detection; PCR 

for HCV RNA.
(illustrate the sequence
of serologic markers in
acute infection and
chronic infection using
graphs )

Refer figure 16.12

Robbins basic
pathology
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Prevention/control

The best way to prevent hepatitis C is by avoiding behaviors that

can spread the disease, especially injecting drugs. Getting tested for
hepatitis C is important, because treatments can cure most people
with hepatitis C in 8 to 12 weeks.

4. Hepatitis D virus

Viral description

( to explain the reason Circular defective ssRNA

require concurrent Hep
B infection)

Transmission mode Parenteral

Incubation period 2 to 26 weeks (mean 8  weeks)

Clinical state
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Define :

Coinfection:

Superinfection :

Acute hepatitis YES

Fulminant hepatitis PRESENT

Healthy carrier NIL(ONLY WITH HBV)

Persistent infection YES

Chronic hepatitis YES

Cirrhosis YES

Hepatocellular YES
carcinoma

Diagnosis Detection of IgM and IgG  antibodies; HDV RNA 

serum; HDAg in liver

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Prevention/control Prevention of hepatitis B with hepatitis B vaccine also protects

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against future hepatitis D infection.

5. Hepatitis E virus

Viral description ssRNA

Transmission Fecal-oral
mode

Incubation period 4 to 5 weeks

Clinical state

Acute hepatitis YES

Fulminant PRESENT
hepatitis

Healthy carrier NO

Persistent YES
infection

Chronic hepatitis NONE

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Cirrhosis YES

Hepatocellular YES
carcinoma

Diagnosis Serum IgM  and IgG antibodies;  PCR for HEV RNA

Prevention/ Prevention of hepatitis E relies primarily on good sanitation and the

availability of clean drinking water.
control
Travelers to developing countries can reduce their risk for infection by
not drinking unpurified water. Boiling and chlorination of water will
inactivate HEV.

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