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Karaganda State Medical University

Department of Surgical disease No. 2 &


Pathological anatomy
Student Individual work with Teacher Report

Topic :- Hepatitis

Submitted to :- Dr. Mohammad Irfan


Submitted by :- Ravi Sankar Lovevanshi
Group No. - 3010
Karaganda,2016
Hepatitis A-
Hepatitis A (formerly known as infectious hepatitis) is
an acute infectious disease of the liver caused by
the hepatitis A virus(HAV).[1] Many cases have few or no
symptoms, especially in the young.[2] The time between
infection and symptoms, in those who develop them, is
between two and six weeks.[3] When symptoms occur, they
typically last eight weeks and may include nausea,
vomiting, diarrhea, jaundice, fever, and abdominal pain.
[2]
Around 1015% of people experience a recurrence of
symptoms during the six months after the initial infection.
[2]
Acute liver failure may rarely occur with this being more
common in the elderly.[2
Early symptoms of hepatitis A infection can be mistaken
for influenza, but some sufferers, especially children,
exhibit no symptoms at all. Symptoms typically appear 2 to
6 weeks (the incubation period) after the initial infection.
[10]
90% of children do not have symptoms. The time
between infection and symptoms, in those who develop
them, is between two and six weeks with an average of 28
days.[3]
The risk for symptomatic infection is directly related to
age, with more than 80% of adults having symptoms
compatible with acute viral hepatitis and the majority of
children having either asymptomatic or unrecognized
infections.[11]
Symptoms usually last less than 2 months, although some
people can be ill for as long as 6 months:[12]

SYMPTOMS-

Fatigue

Fever

Nausea

Appetite loss
Jaundice, a yellowing of the skin or whites of the eyes
due to hyperbilirubinemia

Bile is removed from blood stream and excreted in


urine, giving it a dark amber colour

Diarrhea

Light, or clay-coloured faeces (acholic faeces)


Hepatitis B is an infectious disease caused by
the hepatitis B virus (HBV) which affects the liver. It can
cause both acute and chronic infections. Many people
have no symptoms during the initial infection. Some
develop a rapid onset of sickness with vomiting,yellowish
skin, tiredness, dark urine and abdominal pain.[1] Often
these symptoms last a few weeks and rarely does the
initial infection result in death.[1][2] It may take 30 to 180
days for symptoms to begin.[1] In those who get infected
around the time of birth 90% develop chronic hepatitis
B while less than 10% of those infected after the age of
five do.[3] Most of those with chronic disease have no
symptoms; however, cirrhosis and liver cancer may
eventually develop.

Signs and symptoms-


loss of appetite, nausea, vomiting, body aches, mild fever,
and dark urine, and then progresses to development
of jaundice. It has been noted that itchy skin has been an
indication as a possible symptom of all hepatitis virus
types. chronic inflammation of the liver (chronic hepatitis),
leading to cirrhosis over a period of several years. This
type of infection dramatically increases the incidence
of hepatocellular carcinoma (liver cancer).
Pathology-
Hepatitis B virus primarily interferes with the

functions of the liver by replicating in hepatocytes. A


functional receptor is NTCP.[40] There is evidence that the
receptor in the closely related duck hepatitis B
virus is carboxypeptidase D.[47][48] The virions bind to the
host cell via the preS domain of the viral surface antigen
and are subsequently internalized by endocytosis. HBV-
preS-specific receptors are expressed primarily on
hepatocytes; however, viral DNA and proteins have also
been detected in extrahepatic sites, suggesting that
cellular receptors for HBV may also exist on extrahepatic
cells

Hepatitis c-Hepatitis C is an infectious


disease caused by the hepatitis C virus (HCV) that
primarily affects the liver.[1] During the initial infection
people often have mild or no symptoms. Occasionally a
fever, dark urine, abdominal pain, and yellow tinged
skin occurs. The virus persists in the liver in about 75% to
85% of those initially infected. Early on chronic infection
typically has no symptoms. Over many years however, it
often leads to liver disease and occasionally cirrhosis.[2] In
some cases, those with cirrhosis will develop
complications such as liver failure, liver cancer,
or esophageal and gastric varices.
Trasmission-
HCV is spread primarily by blood-to-blood
contact associated with intravenous drug use, poorly
sterilized medical equipment,needlestick injuries in
healthcare, and transfusions.[2][3] With blood screening the
risk from a transfusion is less than one per two million.[2] It
may also be spread from an infected mother to her baby
during birth.
Signs and symptoms

Acute infection

Hepatitis C infection causes acute symptoms in 15% of


cases.[13] Symptoms are generally mild and vague,
including a decreased appetite,
fatigue, nausea, muscle or joint pains, and weight
loss[14] and rarely does acute liver failure result.

Chronic- Chronic infection after several years may


cause cirrhosis or liver cancer.

Hepatitis D-
Hepatitis D (hepatitis delta) is a disease caused by
the hepatitis D virus (HDV), a small spherical
enveloped RNA virus. This is one of five
known hepatitis viruses: A, B, C, D, and E. HDV is
considered to be a subviral satellite because it can
propagate only in the presence of the hepatitis B
virus (HBV).[1] Transmission of HDV can occur either via
simultaneous infection with HBV (coinfection) or
superimposed on chronic hepatitis B or hepatitis B carrier
state.
Transmission

The routes of transmission of hepatitis D are similar to


those for hepatitis B. Infection is largely restricted to
persons at high risk of hepatitis B infection, particularly
injecting drug users and persons receiving clotting factor
concentrates. Worldwide more than 15 million people are
co-infected. HDV is rare in most developed countries, and
is mostly associated with intravenous drug use. However,
HDV is much more common in the immediate
Mediterranean region, sub-Saharan Africa, the Middle
East, and the northern part of South America.[23] In all,
about 20 million people may be infected with HDV.
PATHOGENESIS

HDV replicates only in the hepatocytes. The cellular damage


associated with HDV infection thus involves mainly the liver.
Immune-mediated liver damage is thought to be implicated in
HDV infection[28]. However, data from experimental
chimpanzees has also suggested a direct cytopathic effect of
HDV on hepatocytes, particularly in acute hepatitis setting[29-
32]. It is postulated that in acute HDV infection, infected
hepatocytes undergo degenerative changes characterized by
shrunken eosinophilic cytoplasm and pyknotic nuclei as well as
the presence of minimal inflammatory cells in the liver
parenchyma, consistent with cytopathic hepatocellular damage.
These findings are also evident from in vitro (cell culture
system)[33] and human studies[34,35]. Small delta antigen
expressed by infected hepatocytes is thought to be responsible
for this direct cytopathic effect of HDV[33], while large delta
antigen per se is non-cytotoxic, promotes persistence of HDV
(chronicity) and makes hepatocytes susceptible to immune-
mediated damage.

Hepatitis E-

Hepatitis E is a viral hepatitis (liver inflammation) caused


by infection with a virus called hepatitis E virus.[1] It is one
of five known human hepatitis viruses: A, B, C, D, and E.
HEV is a positive-sense single-stranded non-enveloped
RNA icosahedral virus, HEV has a fecal-oral transmission
route.[2][3] Infection with this virus was first documented in
1955 during an outbreak in New Delhi, India.
[4]
Apreventative vaccine (HEV 239) is approved for use in
China.

Signs and symptoms


Acute infection[edit]

The incubation period of hepatitis E varies from 3 to 8


weeks. After a short prodromal phase symptoms lasting
from days to weeks follow. They may include jaundice,
fatigue andnausea. The symptomatic phase coincides with
elevated hepatic aminotransferase levels.[9]
Viral RNA becomes detectable in stool and blood serum
during incubation period. Serum IgM and
IgG antibodies against HEV appear just before onset of
clinical symptoms. Recovery leads to virus clearance from
the blood, while the virus may persist in stool for much
longer. Recovery is also marked by disappearance of IgM
antibodies and increase of levels of IgG antibodies.[3][9]
Chronic infection[edit]

While usually an acute disease,


in immunocompromised subjectsparticularly in solid
organ transplanted patientshepatitis E may cause a
chronic infection.[10] Occasionally this may cause liver
fibrosis and cirrhosis.

TRANSMISSION-

It is spread mainly by the fecal-oral route due to fecal


contamination of water supplies or food; person-to-person
transmission is uncommon.
The incubation period following exposure to the
hepatitis E virus ranges from 3 to 8 weeks, with a
mean of 40 days. The period of communicability
is unknown.
The hepatitis E virus causes acute sporadic and
epidemic viral hepatitis. Symptomatic infection is
most common in young adults aged 1540 years.
Although infection is frequent in children, the
disease is mostly asymptomatic or causes a very
mild illness without jaundice (anicteric) that goes
undiagnosed.
Typical signs and symptoms of hepatitis include:
jaundice (yellow discolouration of the skin
and sclera of the eyes, dark urine and pale
stools);
anorexia (loss of appetite);
an enlarged, tender liver (hepatomegaly);
abdominal pain and tenderness;
nausea and vomiting;
fever.

Pathogenesis-Hepatitis E has been considered to be a


travel-associated, acute, self-limiting liver disease that
causes fulminant hepatic failure in specific high-risk
groups only. However, hepatitis E virus (HEV) infection
can also be acquired in industrialized countries-HEV
genotype 3 infection is a zoonosis, with pigs and rodents
serving as animal reservoirs. In recent years, cases of
chronic HEV infection that were associated with
progressive liver disease have been described in several
cohorts of immunocompromised individuals, including
recipients of organ transplants. The topic of hepatitis E is
therefore re-emerging and has raised the following
important questions: what is the risk for HEV infection in
Western countries (eg, from eating uncooked meat)? How
frequently does chronic hepatitis E develop among human
immunodeficiency virus-infected patients and recipients of
organ transplants? What are the treatment options? What
is the current status of vaccine development? What do we
know about the pathogenesis of HEV infection, and why
does it have a more severe course in pregnant women?
This review summarizes the current knowledge on the
pathogenesis and treatment of HEV infection.

Thanks For Attation

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