Hepatitis B is a disease caused by hepatitis B virus (HBV) which infe infect cts s the the live liverr of homi homino noid idae ae,, incl includ udin ing g huma humans ns,, and and caus causes es 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 billio bil lion n people people,, have have been been infect infected ed with with the hepati hepatitis tis B virus virus.. This This includ includes es 35 350 0 milli million on chroni chronic c carrie carriers rs of the virus. virus. Transm Transmiss ission ion of hepati hepatitis tis B virus virus result results s from from exposu exposure re to infect infectiou ious s blood blood or body 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 peri period od of 6 week weeks s to 4 mont months hs.. The The viru virus s inva invade des s the the live liverr and and multiplies within hepatic cell. (Introduction to Human Disease by Leonard Crowly) Hepatitis B, The virus that causes hepatitis hepatitis B can produce lifelong disease, resulting in scarring (cirrhosis) Liver tissue damage, or even death and is spread during sexual intercourse, needle sharing, and and pric pricke ked d by a hypo hypode derm rmic ic need needle le.. Symp Sympto toms ms are are jaun jaundi dice ce,, abdominal pain, nausea and vomiting, dark urine, and fever. (Prima Primary ry Care Care Medici Medicine: ne: Office Office Evalu Evaluati ation on and and Ma Manag nagem emen entt of the Adult Patient By Allan H. Goroll, Albert G. Mulley ) ANATOMY AND PHYSIOLOGY
The The live liverr is loca locate ted d in the the uppe upperr righ rightt-ha hand nd port portio ion n of the 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: •
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oxygenated bloo blood d flow flows s in from the hepatic artery nutrient-rich bloo blood d flow flows s in from the portal vein
The liver holds about one pint (13 percent) of the the body body’s ’s bloo blood d supply supply at any given given moment.
The liver consists 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. liver. All the blood leaving leaving the stomach and intestines 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.
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Production of certain proteins for blood plasma. Production of cholesterol and special proteins to help carry fats through the body. Conver Conversio sion n of excess excess glucos glucose e into into glycog glycogen en for storag storage. e. (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. Resi Resist stin ing g infe infect ctio ions ns by prod produc ucin ing g immu immune ne facto factors rs and and removing bacteria from the blood stream.
When When the liver has broken broken down down harmfu harmfull substa substance nces, s, its byproducts 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 many bil bile e ducts ducts that penetrat penetrate e the liver liver.. During During this this proces process, s, 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 comm common on hepa hepati tic c duct duct,, whic which h join joins s with with the the cyst cystic ic duct duct from from the 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 intestine and instead instead flows into the gallbladder, 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 elec electr trol olyt ytes es,, whil while e reta retain inin ing g all all the the orig origin inal al organ organic ic mole molecu cule les. s. Cholesterol is also released with the bile, dissolved in the acids and fats found in the concentrated solution. When food is released by the stoma stomach ch into into the the duod duoden enum um in the the form form of chym chyme, e, the the duod duoden enum um 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 called assays, assays, for detectio detection n of hepati hepatitis tis B virus virus infect infection ion involve serum or blood tests that detect either viral antigens (proteins produced by the virus) or antibodies prod produc uce ed by the the host 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 infe infect ctio ion n as it is bein being g clear cleared ed by the the host host.. The The infe infect ctio ious us viri virion on cont contai ains ns an inne innerr "cor "core e part partic icle le"" encl enclos osin ing g vira virall geno genome me.. The 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 the hepa hepati titi tis s B e anti antige gen n (HBeAg) will will appe appear ar.. Tradi Traditi tiona onall lly, y, the 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 immediately afterward afterwards. s. This conversio conversion n is usually usually associated 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. period. A person negative for HBsAg but positive for anti-HBs has either cleared an infection or has been vaccinated previously. Indivi Individual duals s who remai remain n HBsAg HBsAg positi positive ve for at least least six months months are [28] considered to be hepatitis B carriers. Carriers of the virus may have chro chroni nic c hepa hepati titi tis s B, whic which h woul would d be refl reflec ecte ted d by elev elevat ated ed seru serum m
alanine amino alanine aminotransf transferase erase leve levels ls and and infl inflam amma mati tion on of the the live liver, r, as reve reveal aled ed by biop biopsy sy.. Carr Carrie iers rs who who have have sero seroco conv nver erte ted d to HBeA HBeAg g negat negativ ive e statu status, s, parti particu cula larl rly y thos those e who who acqu acquir ired ed the the infe infect ctio ion n 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, 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, loads, characteristically have ground glass hepatocytes on biopsy. MEDICATION
For For peop people le with with short short-t -ter erm m (acu (acute te)) he hepa pati titi tis s B infect infection ion (HBV), (HBV), trea treatm tmen entt with with medi medici cine ne is not not us usua uall lly y reco recomm mmen ende ded. d. An Anti tivi vira rall medicine may be used for long-term (chronic) HBV infection if the virus is multiplying or liver damage exists or may develop. But But anti antivi vira rall ther therap apy y is not not reco recomm mmen ende ded d for for ever everyo yone ne who who has has chronic hepatitis B viral infection. It is an option for people who have or appea appearr likel likely y to deve develo lop p live liverr dama damage ge su such ch as cirrhosis cirrhosis.. Antivi Antiviral ral 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 longterm term (chr (chron onic ic)) hepa hepati titi tis s B base based d on the the pres presen ence ce of hepa hepati titi tis s B antigens in your blood, the level of hepatitis of hepatitis B virus DNA (HBV DNA) in your blood, and the levels of your liver enzymes enzymes..4
Medication Choices Interferons such as interferon alfa-2b and pegylated interferon alfa-2a Nucleo Nucleosid side e revers reverse e transc transcrip riptas tase e inhibi inhibitor tors s (NRTIs (NRTIs)) su such ch as adefovir,, entecavir adefovir entecavir,, lamivudine, and telbivudine
Examples Brand Name Intron A Pegasys
Chemical Name
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 sh shot ot once once a week week.. Pegi Pegint nter erfe fero ron n is us used ed more more ofte often n than 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. 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). cirrhosis). Interferons can cause or aggravate mental problems. Tell your doctor if you have a history of depression, depression, suicidal thoughts, anxiety, anxiety, drug or alcohol abuse, or mental illness.
How Well It Works It is important to weigh the benefits of treatment against the risks. Treat Treatmen mentt for HBV infect infection ion is consid considere ered d succes successfu sfull if blood blood tests 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 treatm treatment ent succe success ss is define defined. d. Relapse—w Relapse—whe hen n the the viru virus s star starts ts 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 Recent studies studies suggest suggest that peginterferon peginterferon works a little little 2, 3 better than interferon.
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. enzymes .1
How Well It Works Treat Treatmen mentt for HBV infect infection ion is consid considere ered d succes successfu sfull if blood blood tests 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 (the viru virus s star starts ts to mult multip iply ly agai again) n) is comm common on afte afterr 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 •
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After 1 year of treatment with lamivudine, up to one-third of hepati hepatitis tis B viruse viruses s may be resist resistant ant to the medicin medicine. e. After After 5 year years s of trea treatm tmen ent, t, up to 70 70% % of HBV HBV may may be resi resist stan antt to lamivudine. Resi Resist stan ance ce is less less of a prob proble lem m with with telb telbiv ivud udin ine e than than with 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 prot protei eins ns (hep (hepat atit itis is B su surf rfac ace e antig antigen en or HBsA HBsAg) g).. The The vacc vaccin ine e was was originally prepared from plasma obtained from patients who had longstanding hepatitis B virus infection. However, currently, these are more ofte often n made made us usin ing g recomb recombina inant nt DNA techno technolog logy, y, though though plasma 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 into infa infant nts s and adult adults, s, whic which h prov provid ides es prot protec ecti tion on for for 85 85–9 –90% 0% of [33] individuals. Prot Protec ecti tion on has has been been obse observ rved ed to last last 12 year years s in individuals who show adequate initial response to the primary course of vaccin vaccinati ations ons,, and that immun immunity ity is predic predicted ted to last last at least least 25 [34] years. Unlike hepatitis A, 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 Hyperthermia related 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 a cute (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 of contaminated food and drinks (hepatitis A and E) Sexual contact, intravenous infusions, perinatal transmission from mothers to infants (hepatitis B and C) SYMPTOMATOLOGY PREICTERIC PHASE Headache, malaise, fatigue, anorexia, fever
ICTERIC PHASE Light colored stools, dark urine, jaundice of skin and sclera Tender and enlarged liver, spleen, and lymph nodes
Hepatitis A and E are transmitted via oral-fecal route
Due to release of toxins by damaged liver or failure of the damaged liver cells to detoxify abnormal products Due to impaired bilirubin metabolism Due to overwhelming immune/inflammatory response
PATHOPHYSIOLOGY
Ingestion/ inoculation of hepatitis virus
Viral entry into the liver
Extensive replication of hepatitis virus within
Overwhelming immune/inflammation response to infected liver cells involving both B and T cells
Necrosis of infected hepatocytes/ Failure of surviving hepatocytes to Progressive destruction of remaining
LIVER FAILURE/ CIRRHOSIS