referat

HEPATITIS IN CHILDREN
Mahdi Arif Prasetya (712019042)

Departemen Ilmu kesehatan Anak

RS Muhammadiyah Palembang
Fakultas Kedokteran Universitas
Muhammadiyah Palembang
2020
 STATUS
CHAPTER I
BED SITE TEACHING
PRELIMINARY

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Background

Hepatitis is a process of inflammation and necrosis of liver tissue

that can be caused by infections, drugs, toxins, metabolic disorders,
or autoimmune disorders. Viral, bacterial or parasitic infections are
the most common cause of acute hepatitis. Viral hepatitis is the
most common cause of infection. In this paper only described about
viral hepatitis. Viral hepatitis is still a major health problem, both in
developing and developed countries

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 PURPOSE

1. Know the definition, risk factors, clinical symptoms,

and management of hepatitis in children.
2. Improve the ability in scientific writing in the
medical field.
3. Meet one of the requirements of the Clinical
Registrar's graduation at the Children's Health Sciences
Section of the Palembang Muhammadiyah Hospital,
Faculty of Medicine, Muhammadiyah University,
Palembang.

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Benefits

The benefits of writing this referral are:

Add insight and understanding of Hepatitis in Children

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 STATUS
CHAPTER II
BED SITE TEACHING
LITERATURE REVIEW

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Definition of Hepatitis

Hepatitis is a process of inflammation

and necrosis of liver tissue that can be
caused by infection, drugs, toxins,
metabolic disorders, or autoimmune
disorders. Viral, bacterial or parasitic
infections are the most common cause
of acute hepatitis.

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Etiology of hepatitis
1. Infection
Hepatitis A,B,C,D,E,G
2. Non infection
chemicals from drugs (ex; paracetamol)
Autoimmune hepatitis
Alcohol
Metabolic disorders (ex; dm )

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clinical symptoms

clinical manifestations that can be

divided into 4 stages,
1. incubation period
2. Prodromal period
3. jaundice phase
4. healing phase

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Bilirubin metabolism

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 Pemeriksaan Fisik
Hepatitis Classification

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HEPATITIS A

Virology
HAV is a 27-nm non-developing RNA virus, including the genus
Hepatovirus, the Picornavirus family. The genome consists of 5'NTR-
P1-P2-P3-3'NTR. VHA is thermostable, acid resistant, and resistant to
bile so it is efficient in oral faecal transmission. There are 4 genotypes
but only 1 serotype. Liver damage that occurs due to the immune
mechanism mediated by T-cells. HAV infection does not cause
chronic or persistent hepatitis. HAV infection induces long-term
protection against re-infection.

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Hepatitis A
Epidemiology of Hepatitis A
In developing countries where HAV is still endemic such as Africa,
South America, Central Asia and Southeast Asia, exposure to HAV is
almost 100% in children aged 10 years. In Indonesia the prevalence in
Jakarta, Bandung and Makassar ranges from 35% -45% at the age of 5
years, and reaches more than 90% at the age of 30 years. In Papua at the
age of 5 years the prevalence of anti-HAV reaches almost 100%. A
seroprevalence study in Yogyakarta in 1997 showed 30-65% from 4
years to 37 years (Juffrie et al). In 2008 an outbreak occurred around the
Gadjah Mada University campus that attacked more than 500 sufferers,
who were thought to have come from street vendors around the campus
(Harisus). In developed countries the prevalence of anti-HAV in the
general population is below 20% and the age of infection is older than in
developing countries
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Hepatitis A
Pathogenesis of Hepatitis A
HAV enters the liver from the digestive tract through the bloodstream,
into the hepatocytes, and replicates in the hepatocytes that involve
RNA-dependent polymerase. HAV is bound by specific
immunoglobulin A (IgA) in the mucosa of the digestive tract which
acts as a mediator between HAV and hepatocytes through
asialoglycoprotein receptors on hepatocytes. Besides IgA, fibronectin
and alpha-2-macroglobulin can also bind to HAV. From the liver, HAV
is eliminated through sinusoids, canaliculi, into the intestine before the
onset of clinical or laboratory symptoms.

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Hepatitis A
Clinical Symptoms of Hepatitis A
1. The incubation period, lasts for 18-50 days (average 28 days).
2. Prodromal period, occurs for 4 days to 1 week or more.
Symptoms are fatigue, malaise, decreased appetite, nausea,
vomiting, discomfort in the upper right area, fever (usually <39o
C), feeling cold, headache, flu-like symptoms. The sign found is
usually mild hepatomegaly with tenderness.
3. The jaundice phase, starting with dark yellow urine, like tea,
is followed by putty-colored stools, then the color of the sclera
and skin slowly turns yellow. Symptoms of anorexia, lethargy,
nausea and vomiting get worse.
4. The healing phase, jaundice disappears and the stool color
returns to normal within 4 weeks after onset.

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Hepatitis A
Diagnosis of Hepatitis A
The diagnosis of hepatitis A was made based on the
results of the anti-HAV IgM examination. These
antibodies are found 1-2 weeks after being infected
with HAV and last for 3-6 months. anti-HAV IgG can
be detected 5-6 weeks after infection, lasting for
decades, providing protection against HAV for life

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Hepatitis A Treatment
Treatment involves resting and preventing
hepatotoxic substances, such as
acetaminophen. In patients with cholestatic
type corticosteroids can be given in the
short term.

Prevention
General prevention includes advice to patients, namely:
improvement of food-beverage hygiene, improvement
of environmental and personal sanitation and isolation
of the patient (up to 2 weeks after symptoms occur).
Special prevention by immunization. There are 2 forms
of immunization, namely passive immunization with
immunoglobulin (IG), and active immunization with
inactivated vaccines (Havrix, Vaqta and Avaxim).
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 Hepatitis B
Virology
Human hepatitis B virus (HBV) is a type 1 hepadnavirus and is the
first hepadna virus to be discovered. This hepatotropic virus
contains DNA with a circular double ring consisting of 3200
nucleotides with a diameter of 42 nm and consisting of 4 genes.
HBV can be found in 3 components, namely complete particles with
a diameter of 42 nm, round particles with a diameter of 22 nm, and
stem particles with a width of 22 nm with lengths varying to 200
nm.

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Hepatitis B
Epidemiology
;In developed countries like the United Kingdom, the United
States, and Scandinavian countries the prevalence of HBsAg
varies between 0.1% -0.2% while in Africa and East 10% -15%.
In isolated communities such as Eskimos in Alaska the
prevalence can reach 45% and Aboriginal in Australia reaches
85%.

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Hepatitis B
patogenesis
the hepatitis B virus is a nonsitopathic virus and causes tissue
damage through immunological reactions. The severity of liver
tissue damage reflects the degree of immunological response.
In hepatocytes infected by HBV through cellular immunity
mechanisms there is exposure to viral antigens, namely HBcAg
and HbeAg, on the cell surface that joins class I major
histocompatibility complex (MHC I) and becomes the target of
T cells cytotoxic (CTL) for the lysis process.
Kirim masukan

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Hepatitis B
Clinical symptom:
1. Hepatitis B akut
Treatment:
2.Hepatitis B kronis
supportive and
monitoring of
disease
Diagnosis : symptoms
diagnosis of hepatitis B is a clinical and
serological diagnosis

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Hepatitis B

Prevention
passive HBIG vaccination and
active vaccination

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Hepatitis C
Virology
HCV is an RNA virus with a positive genome, including
the family Flaviviridae and Pestivirus because of the
genetic organization that resembles one another. HCVs
with a diameter of 30-60 nm, with a length of 9.4 kb or
9413 nucleotides, having an open reading frame (ORF)
can encode a protein composed of 3010 amino acids.

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Hepatitis C
Epidemiology
Epidemiological surveys estimate that there are 170 million
people with chronic HCV worldwide. The prevalence of
chronic infection in adults varies between 0.5% -25%. In the
United States seroprevalence of HCV infection is 1.8% of the
entire population. In Indonesia the prevalence of HCV varies
greatly, around 0.5% to 3.37%. From donor blood tests in
cities, namely Jakarta by 2.5%, Surabaya 2.3%, Medan 1.5%,
Bandung 2.7%, Yogyakarta 1%, Bali 1.3%, Mataram 0.5% ,
Manado 3.0%, Makassar 1.0%, and Banjarmasin 1.0% .18

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Hepatitis C
Acute hepatitis C
the incubation period is around 7 weeks which is between 2-30
weeks. the symptoms are not specific namely feeling tired, weak,
anorexia, and weight loss.

Chronic hepatitis C
Most sufferers are not aware of the disease, other than minimal and
non-specific symptoms such as fatigue, nausea, myalgia, discomfort
in the right upper abdomen, itching and weight loss

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Hepatitis C
Diagnostic
1.Uji saring
2. Uji konfirmasi

Hepatitis C treatment
The goal of treatment is to eliminate the
virus and prevent the progression of the
disease to cirrhosis and hepatocellular
carcinoma. Currently the FDA's
recommendation is treatment with a
combination of interferon and ribafirin
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HEPATITIS C
PREVENTION
1. Filter effective for blood, tissue, and
organ donors.
2. Screening tests on individuals in
areas with high HCV prevalence to
prevent further spread.
3. Health education for workers who
work closely with blood and body
fluids.

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HEPATITIS D
Virology
HDV is a 36 mm RNA virus. The outer layer
is HBsAg which encloses the RNA genome
and delta antigen.

epidemiology
It is estimated that there are at least 15 million people infected with
HDV worldwide with the assumption that 5% of people with HBV are
infected by HDV. HDV infections occur throughout the world with a
high prevalence in South America, West Africa, the Middle East, the
Mediterranean, and several islands in the Pacific Islands. The
incubation period for superinfection is 2-8 weeks while the co-infection
is the same as HBV infection.
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Hepatitis D
pathogenesis
HDV is a cytopathic virus causing direct damage to
liver cells. No specific features were found on the
histopathological examination of the liver except the
degree of damage was more severe. The mechanism
by which HDV infection causes liver damage is still
unclear.

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Hepatitis D
clinical symptoms
In superinfection, clinical symptoms of acute
hepatitis are rare but chronic hepatitis is common
and in superinfection events the risk of fulminant
hepatitis is higher

Diagnosis
The diagnosis is made based on the presence of
anti-HDV IgM which occurs around 2-4 weeks
after infection with co-infection and 10 weeks on
superinfection, using the RIA or Elisa method.

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Hepatitis D
Hepatitis D treatment
The use of interferon-alpha in patients with chronic
HDV for at least one year. If there is no result where
ALT levels remain high and HDV RNA is still present,
then treatment is stopped. If a positive response is
indicated by the loss of HDV RNA and ALT becomes
normal, then interferon administration is continued until
HBsAg disappears from the serum.

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Hepatitis D
Prevention of Hepatitis D
No vaccine has been found against HDV, but
because HDV replication cannot occur
without HBV infection, immunization against
HBV also prevents HDV infection.

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Hepatitis E
Virology of Hepatitis E
The hepatitis E virus has a diameter of 32-34 nm,
spherical in shape and is a particle that has no
cover. An RNA virus consisting of 7500 pairs of
single-chain nucleotides

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Hepatitis E
epidemiology
In addition to India, an epidemic also occurred in the
Kyrgyz Republic, the Soviet Union in 1955-1956 which
attacked 10800 sufferers, especially young people to middle
age. It also occurred in Burma and Nepal in 1976 with
20,000 and 10,000 cases. Epidemics also occurred in Africa
in 1980-1981. In Indonesia there was an outbreak of
hepatitis E in Central Kalimantan in 1987-1988 with the
number of sufferers of 2000 people.

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Hepatitis E
clinical symptoms
The incubation period is 2-9 weeks. Its
subclinical form cannot be recognized because
it gives flu-like symptoms. The manifested
clinical form with jaundice will heal itself such
as hepatitis A. Improvement of
hyperbilirubinemia and ALT is achieved after 3
weeks of the onset of illness

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Hepatitis E
Diagnosis of Hepatitis E
The diagnosis of acute hepatitis E is determined by:
1. Immune electron microscope (IEM); check the virus in the
patient's stool.
2. Detection of specific antibodies to the virus using a fluorescent
antibody-blocking assay.
3. Western blot and EIA IgM and IgG anti HEV; Anti HEV IgM
was found one week for the onset of clinical symptoms.
4. PCR to look for HEV RNA from serum and stool.

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Hepatitis E
prevention
Because there is no vaccine to prevent hepatitis
E, the main effort for prevention is the provision
of clean water.

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Hepatitis G
Virology of Hepatitis G
The hepatitis G virus (HGV), the GB-C virus is
a single chain RNA virus consisting of 9400
pairs of nucleotides and belongs to the
flaviridae group, transmitted parenterally.

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HEPATITIS G
The prevalence of HGV / GB-C virus in
blood donors and the general population in
developed countries is between 1-2%. In
tropical and subtropical countries the
prevalence is between 5% -10%. The high
prevalence of HGV / VGB-C in the tropics
and subtropics may be due to the presence
of insects and other vectors.

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HEPATITIS G
Pathogenesis of Hepatitis G
Most patients infected with HGV / GB-
C virus experience viremia but no
significant change in histopathological
features and ALT levels are within
normal limits.

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 HEPATITIS G
Clinical Overview of Hepatitis G
HGV / GB-C virus infection does not
cause symptoms of inflammation in the
liver. Coinfection with other viruses
does not make the course of HBV or
HCV worse.
Diagnosis of Hepatitis G
Diagnosis of HGV / GB-C virus
based on the discovery of RNA
Prevention of Hepatitis G viruses by means of RT-PCR.
There is no method of preventing
HGV / GB-C virus infections

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 conclution

1. Hepatitis A is a disease caused by the Hepatitis A virus (HAV).

HAV is transmitted from person to person through the faecal-oral
mechanism. Someone cancontracting from eating food contaminated
with HAV.
2. Hepatitis B is a disease caused by the Hepatitis B virus (HBV).
In general a person can contract HBV through sexual contact, use
syringe that alternates at IDU, using contaminated tools90% of blood
from sufferers (razors, tattoos, piercings) comes from infected mothers
HBV, blood transfusion, and through doctor's equipment.

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conclution
5. Hepatitis C is a disease caused by the Hepatitis C virus
(HCV). Specific transmission through the blood, for example in blood
donors, or injecting drug use. Most disease events are asymptomatic,
but there are also those who show symptoms including anorexia, nausea
and vomiting, fever and fatigue, continues to become jaundice. The
diagnosis is dengn virological test and serology test.
4. Hepatitis D is a disease caused by the Hepatitis D virus
(HDV). Transmission usually occurs through close contact in families in
areas with a high prevalence, especially in developing countries by means
of parenteral inapparent. Whereas in areas with low prevalence,
transmission through lesions on the skin is more common, especially in
the use of drugs by injection, transfusion in patients with blood diseases,
and nosocomial infections.
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conclution
5. Hepatitis E is a disease caused by the hepatitis virus (HEV).
Clinical features of hepatitis E vary from mild or subclinical to fatal
cases that cause death. The incubation period is 2-9 weeks. Its
subclinical form cannot be recognized because it gives flu-like
symptoms. The manifested clinical form with jaundice will heal
itself such as hepatitis A.
6. Hepatitis G is a disease caused by the hepatitis virus (HGV). HGV
/ GB-C virus is a blood-borne virus, often found in people with blood
diseases who experience repeated transfusions. Most patients
infected with HGV / GB-C virus experience viremia but no
significant change in histopathological features and ALT levels are
within normal limits.

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