Hepatitis B is a disease caused by hepatitis B virus (HBV) which

infects the liver of hominoidae, including humans, and causes an

inflammation called hepatitis. Originally known as "serum hepatitis",
the disease has caused epidemics in parts of Asia and Africa, and it is
endemic in China. About a third of the world's population, more than 2
billion people, have been infected with the hepatitis B virus. This
includes 350 million chronic carriers of the virus. Transmission of
hepatitis B virus results from exposure to infectious blood or body
fluids containing blood.
(by http://en.wikipedia.org/wiki/Hepatitis_B)

Hepatitis B virus (HBV) is a DNA-containing virus, it is larger

than the Hepa A virus, it composed of an inner coat (protein shell coat
called hepa B core antigen HbcAg) and the outer coat (composed of
lipid and protein called hepa B surface antigen), with an incubation
period of 6 weeks to 4 months. The virus invades the liver and
multiplies within hepatic cell.
(Introduction to Human Disease by Leonard Crowly)

Hepatitis B, The virus that causes hepatitis B can produce life-

long disease, resulting in scarring (cirrhosis) Liver tissue damage, or
even death and is spread during sexual intercourse, needle sharing,
and pricked by a hypodermic needle. Symptoms are jaundice,
abdominal pain, nausea and vomiting, dark urine, and fever.
(Primary Care Medicine: Office Evaluation and Management of the
Adult Patient By Allan H. Goroll, Albert G. Mulley)

ANATOMY AND PHYSIOLOGY

The liver is located in the upper right-hand portion of the

abdominal cavity, beneath the diaphragm and on top of the stomach,
right kidney and intestines. The liver, a dark reddish-brown organ that
weighs about 3 pounds, has multiple functions.
There are two distinct sources that supply blood to the liver:

• oxygenated
blood flows in
from the
hepatic artery
• nutrient-rich
blood flows in
from the portal
vein

The liver holds about

one pint (13 percent)
of the body’s blood
supply at any given
moment.

The liver consists

of two main lobes, both of which are made up of thousands of lobules.
These lobules are connected to small ducts that connect with larger
ducts to ultimately form the hepatic duct. The hepatic duct transports
the bile produced by the liver cells to the gallbladder and duodenum
(the first part of the small intestine).

The liver regulates most chemical levels in the blood and excretes a
product called “bile,” which helps carry away waste products from the
liver. All the blood leaving the stomach and intestines passes through
the liver. The liver processes this blood and breaks down the nutrients
and drugs into forms that are easier to use for the rest of the body.
More than 500 vital functions have been identified with the liver.

Some of the more well-known functions include the following:

• Production of bile, which helps carry away waste and break

down fats in the small intestine during digestion.
 • Production of certain proteins for blood plasma.
• Production of cholesterol and special proteins to help carry
fats through the body.
• Conversion of excess glucose into glycogen for storage.
(This glycogen can later be converted back to glucose for
energy.)
• Regulation of blood levels of amino acids, which form the
building blocks of proteins.
• Processing of hemoglobin for use of its iron content. (The
liver stores iron.)
• Conversion of poisonous ammonia to urea. (Urea is one of
the end products of protein metabolism that is excreted in
the urine.)
• Clearing the blood of drugs and other poisonous
substances.
• Regulating blood clotting.
• Resisting infections by producing immune factors and
removing bacteria from the blood stream.

When the liver has broken down harmful substances, its by-
products are excreted into the bile or blood. Bile by-products enter the
intestine and ultimately leave the body in the feces. Blood by-products
are filtered out by the kidneys, and leave the body in the form of urine.

Bile is produced by hepatocytes in the liver, draining through the

many bile ducts that penetrate the liver. During this process, the
epithelial cells add a watery solution that is rich in bicarbonates that
dilutes and increases alkalinity of the solution. Bile then flows into the
common hepatic duct, which joins with the cystic duct from the
gallbladder to form the common bile duct. The common bile duct in
turn joins with the pancreatic duct to empty into the duodenum. If the
sphincter of Oddi is closed, bile is prevented from draining into the
intestine and instead flows into the gallbladder, where it is stored and
concentrated to up to five times its original potency between meals.
This concentration occurs through the absorption of water and small
electrolytes, while retaining all the original organic molecules.
Cholesterol is also released with the bile, dissolved in the acids and
fats found in the concentrated solution. When food is released by the
stomach into the duodenum in the form of chyme, the duodenum
releases cholecystokinin, which causes the gallbladder to release the
concentrated bile to complete digestion.

The human liver can produce close to one liter of bile per day
(depending on body size). About 95% of the salts secreted in bile are
reabsorbed in the terminal ileum and re-used. Blood from the ileum
flows directly to the hepatic portal vein and returns to the liver where
the hepatocytes reabsorb the salts and return them to the bile ducts to
be re-used, sometimes two to three times with each meal.

DIAGNOSIS

The tests, called assays, for detection of hepatitis B virus infection

involve serum or blood tests that detect either viral antigens (proteins
produced by the virus) or antibodies produced by the host.
Interpretation of these assays is complex.[9]

The hepatitis B surface antigen (HBsAg) is most frequently used to

screen for the presence of this infection. It is the first detectable viral
antigen to appear during infection. However, early in an infection, this
antigen may not be present and it may be undetectable later in the
infection as it is being cleared by the host. The infectious virion
contains an inner "core particle" enclosing viral genome. The
icosahedral core particle is made of 180 or 240 copies of core protein,
alternatively known as hepatitis B core antigen, or HBcAg. During this
'window' in which the host remains infected but is successfully clearing
the virus, IgM antibodies to the hepatitis B core antigen (anti-HBc IgM)
may be the only serological evidence of disease.

Shortly after the appearance of the HBsAg, another antigen named as

the hepatitis B e antigen (HBeAg) will appear. Traditionally, the
presence of HBeAg in a host's serum is associated with much higher
rates of viral replication and enhanced infectivity; however, variants of
the hepatitis B virus do not produce the 'e' antigen, so this rule does
not always hold true. During the natural course of an infection, the
HBeAg may be cleared, and antibodies to the 'e' antigen (anti-HBe) will
arise immediately afterwards. This conversion is usually associated
with a dramatic decline in viral replication.

If the host is able to clear the infection, eventually the HBsAg will
become undetectable and will be followed by IgG antibodies to the
hepatitis B surface antigen and core antigen, (anti-HBs and anti HBc
IgG).[7] The time between the removal of the HBsAg and the
appearance of anti-HBs is called the window period. A person negative
for HBsAg but positive for anti-HBs has either cleared an infection or
has been vaccinated previously.

Individuals who remain HBsAg positive for at least six months are
considered to be hepatitis B carriers.[28] Carriers of the virus may have
chronic hepatitis B, which would be reflected by elevated serum
alanine aminotransferase levels and inflammation of the liver, as
revealed by biopsy. Carriers who have seroconverted to HBeAg
negative status, particularly those who acquired the infection as
adults, have very little viral multiplication and hence may be at little
risk of long-term complications or of transmitting infection to others.[29]

PCR tests have been developed to detect and measure the amount of
HBV DNA, called the viral load, in clinical specimens. These tests are
used to assess a person's infection status and to monitor treatment.[30]
Individuals with high viral loads, characteristically have ground glass
hepatocytes on biopsy.
MEDICATION

For people with short-term (acute) hepatitis B infection (HBV),

treatment with medicine is not usually recommended. Antiviral
medicine may be used for long-term (chronic) HBV infection if the virus
is multiplying or liver damage exists or may develop.

But antiviral therapy is not recommended for everyone who has

chronic hepatitis B viral infection. It is an option for people who have or
appear likely to develop liver damage such as cirrhosis. Antiviral
therapy may not help if you already have severe liver damage.

The American Association for the Study of Liver Disease has made
recommendations on who should receive antiviral treatment for long-
term (chronic) hepatitis B based on the presence of hepatitis B
antigens in your blood, the level of hepatitis B virus DNA (HBV DNA) in
your blood, and the levels of your liver enzymes.4

Medication Choices

Interferons such as interferon alfa-2b and pegylated interferon

alfa-2a
Nucleoside reverse transcriptase inhibitors (NRTIs) such as
adefovir, entecavir, lamivudine, and telbivudine

Examples
Brand Name Chemical Name

Intron A

Pegasys
How It Works

Interferon is a man-made copy of a protein that your body makes in

response to infection. It helps the immune system fight disease and
may slow or stop the growth of the hepatitis B virus in your body.

Interferon is given as a shot 3 times a week. A slow release form of

interferon, pegylated interferon (also known as peginterferon), is given
as a shot once a week. Peginterferon is used more often than
interferon to treat hepatitis B. Treatment with interferons can last 4
months to 1 year.

Why It Is Used

Interferons are used to treat long-term (chronic) HBV infection in adults

and children who are at risk for liver disease. The American Association
for the Study of Liver Disease has made recommendations on who
should receive treatment for hepatitis B based on the presence of
hepatitis B antigen in your blood, the level of hepatitis B virus DNA
(HBV DNA) in your blood, and the levels of your liver enzymes.1

Treatment with interferons is not recommended if you are using illegal

drugs or drinking too much alcohol. It is also not recommended if you
have had an organ transplant or if you have advanced liver scarring
(cirrhosis).

Interferons can cause or aggravate mental problems. Tell your doctor if

you have a history of depression, suicidal thoughts, anxiety, drug or
alcohol abuse, or mental illness.

How Well It Works

It is important to weigh the benefits of treatment against the risks.

Treatment for HBV infection is considered successful if blood tests
show that the virus is no longer multiplying in the body, if liver enzyme
levels return to normal, and if liver damage (such as inflammation and
scarring) improves.

The success of interferon treatment for hepatitis B depends on how

treatment success is defined. Relapse—when the virus starts to
multiply again—is common after treatment is stopped. Interferons stop
the growth of the virus over the long term in about 35% of people who
use them.1 Recent studies suggest that peginterferon works a little
better than interferon.2, 3
Interferons work best for people who have high levels of liver enzymes
and in whom the virus is multiplying. They are also more likely to work
in people who have a strong immune system, who have had hepatitis
for a short amount of time, and who became infected after childhood.4

Examples
Brand Name Chemical Name

Hepsera

Baraclude

Epivir-HBV

Tyzeka

How It Works

Nucleoside reverse transcriptase inhibitors (NRTIs) are medicines that

slow the ability of the hepatitis B virus (HBV) to multiply in the body.
They are taken as pills once a day for at least a year, and usually much
longer. Entecavir is also available as a liquid that you swallow.

Adefovir, entecavir, and telbivudine are approved by the U.S. Food and
Drug Administration (FDA) for use in adults. Lamivudine is approved for
use by adults and by children ages 2 to 17.

Why It Is Used

NRTIs are used to treat long-term (chronic) HBV infection in adults and
children who are at risk for liver disease. The American Association for
the Study of Liver Disease has made recommendations on who should
receive treatment for chronic hepatitis B based on the presence of
hepatitis B antigens in your blood, the level of hepatitis B virus DNA
(HBV DNA) in your blood, and the levels of your liver enzymes.1

How Well It Works

Treatment for HBV infection is considered successful if blood tests

show that the virus is no longer multiplying in the body, if liver enzyme
levels return to normal, and if liver damage (such as inflammation and
scarring) improves. NRTIs work in most of the people who take them,
but relapse (the virus starts to multiply again) is common after a
medicine is stopped, so you may have to take the medicine for a long
time.1, 2
The hepatitis B virus may develop resistance to some of the NRTIs:1

• After 1 year of treatment with lamivudine, up to one-third of

hepatitis B viruses may be resistant to the medicine. After 5
years of treatment, up to 70% of HBV may be resistant to
lamivudine.
• Resistance is less of a problem with telbivudine than with
lamivudine. But resistance to telbivudine goes up greatly after
one year of treatment.
• Resistance is less of a problem with adefovir. After 5 years of
adefovir treatment, less than one-third of HBV may be resistant
to the medicine.
• Resistance is rare with entecavir, especially when it is used as
the first medicine to treat hepatitis B. It is slightly more common
when entecavir is used after lamivudine treatment.

PREVENTION

Several vaccines have been developed for the prevention of hepatitis B

virus infection. These rely on the use of one of the viral envelope
proteins (hepatitis B surface antigen or HBsAg). The vaccine was
originally prepared from plasma obtained from patients who had long-
standing hepatitis B virus infection. However, currently, these are more
often made using recombinant DNA technology, though plasma-
derived vaccines continue to be used; the two types of vaccines are
equally effective and safe.[31]

Following vaccination, hepatitis B surface antigen may be detected in

serum for several days; this is known as vaccine antigenaemia. [32] The
vaccine is administered in either two-, three-, or four-dose schedules
into infants and adults, which provides protection for 85–90% of
individuals.[33] Protection has been observed to last 12 years in
individuals who show adequate initial response to the primary course
of vaccinations, and that immunity is predicted to last at least 25
years.[34]

Unlike hepatitis A, hepatitis B does not generally spread through water

and food. Instead, it is transmitted through body fluids; prevention is
thus the avoidance of such transmission: unprotected sexual contact,
blood transfusions, re-use of contaminated needles and syringes, and
vertical transmission during child birth. Infants may be vaccinated at
birth.[35]

Nursing Diagnosis

1. Acute pain r/t enlargement of the liver

2. Fatigue related to disrupted metabolism???
3. Deficient knowledge relatd to lack of resources
4. Risk for defient fluid voume related to vomiting r/t presence of
ammonia secondary to hapatitis B
5. Hyperthermia related to inflammatory process
6. risk for bleeding related to decrease throbopietin and blood clotting
factor production

Nursing interventions

1. Encourage adequate nutrition

2. Explain the posibble ways the hepatitis B is transmitted
*perinatal (from mother to baby at birth)
* early childhood infections (inapparent infection through close
interpersonal contact with infected household contacts)
* unsafe injections practices
* blood transfusions
* sexual contact
3. Promote comfort
4. replacement of fluids that are lost from vomiting and diarrhoea.
5. Administer drugs, including interferon and anti-viral agents to treat
the underlying problem
6. Advise to increase oral fluid intake
7. perfrom tepid sponge bath
8. monitor intake and output
9. Explain ways to preventing hepatitis through immnization and safety
precautions
10. Advised not to be involved in strenuous and physical activities that
may cause injury
11. Explain significance of compliance to medication adn treatment
regimen

Prognosis

Hepatitis B virus infection may either be acute (self-limiting) or chronic

(long-standing). Persons with self-limiting infection clear the infection
spontaneously within weeks to months.

Children are less likely than adults to clear the infection. More than
95% of people who become infected as adults or older children will
stage a full recovery and develop protective immunity to the virus.
However, this drops to 30% for younger children, and only 5% of
newborns that acquire the infection from their mother at birth will clear
the infection[42]. This population has a 40% lifetime risk of death from
cirrhosis or hepatocellular carcinoma.[38] Of those infected between
the age of one to six, 70% will clear the infection.[43]

Hepatitis D (HDV) can only occur with a concomitant hepatitis B

infection, because HDV uses the HBV surface antigen to form a capsid.
[44] Co-infection with hepatitis D increases the risk of liver cirrhosis
and liver cancer.[45] Polyarteritis nodosa is more common in people
with hepatitis B infection.
Reactivation

Hepatitis B virus DNA persists in the body after infection and in some
people the disease recurs.[46] Although rare, reactivation is seen most
often in people with impaired immunity.[47] HBV goes through cycles
of replication and non-replication. Approximately 50% of patients
experience acute reactivation. Male patients with baseline ALT of 200
UL/L are three times more likely to develop a reactivation than patients
with lower levels. Patients who undergo chemotherapy are at risk for
HBV reactivation. The current view is that immunosuppressive drugs
favor increased HBV replication while inhibiting cytotoxic T cell
function in the liver.

*Each year an estimated 150,000 persons in the United States get

hepatitis B. More than 10,000 will require hospital care, and as many
as 5,000 will die from complications of the infection. About 90% of all
those infected will have acute disease only. A very large majority of
these patients will recover within three months. It is the remaining
10%, with chronic infection, who account for most serious
complications and deaths from HBV infection. In the United States,
perhaps only 2% of all those who are infected will become chronically
ill. The course of chronic HBV infection in any particular patient is
unpredictable. Some patients who do well at first may later develop
serious complications. Even when no symptoms of liver disease
develop, chronic carriers remain a threat to others by serving as a
source of infection.

ETIOLOGY
PREDISPOSING FACTOR
Age Degenerative functioning
of body organs, including
 liver, associated with
aging, places individuals
at risk to a variety of
disorders including
hepatitis
PRECIPITATING FACTORS
Poor sanitation, ingestion Hepatitis A and E are
of contaminated food and transmitted via oral-fecal
drinks (hepatitis A and E) route
Sexual contact,
intravenous infusions,
perinatal transmission
from mothers to infants
(hepatitis B and C)
SYMPTOMATOLOGY
PREICTERIC PHASE
Headache, malaise, Due to release of toxins
fatigue, anorexia, fever by damaged liver or
failure of the damaged
liver cells to detoxify
abnormal products
ICTERIC PHASE
Light colored stools, dark Due to impaired bilirubin
urine, jaundice of skin metabolism
and sclera
Tender and enlarged Due to overwhelming
liver, spleen, and lymph immune/inflammatory
nodes response
 PATHOPHYSIOLOGY

Ingestion/
inoculation of
hepatitis virus

Viral entry into

the liver

Extensive
replication of
hepatitis virus
within
hepatocytes

Overwhelming
immune/inflammation
response to infected liver
cells involving both B and T
cells

Necrosis of
infected
hepatocytes/
cytolytic

Failure of
surviving
hepatocytes to
regenerate
Progressive destruction
of remaining
hepatocytes

LIVER FAILURE/
CIRRHOSIS