Looking At What Hepatitis Is Biology Essay

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HEPATITIS (plural HEPATITIDES) implies to injury to liver characterized by the presence of inflammatory cells in the tissue of organ. The name is from ancient Greek hepar ,the root being hepat- meaning 'liver', and -itis meaning, 'inflammation'. The condition can be self limiting, healing on its own, or can progress to It is inflammation of liver caused by viruses, bacterial infections, or continuous exposure to alcohol, drugs, or toxic chemicals, such as those found in aerosol sprays and paints thinners. Hepatitis can also result from an auto- immune disorder, in which the body mistakenly sends disease- fighting cells to attack its own healthy tissue, in this case the liver. no matter what is the cause ,hepatitis reduces the liver's ability to perform life-preserving functions, including filtering harmful infectious agents from the blood, storing blood sugar and converting it to useable energy forms ,and producing proteins necessary for life.

Description:

Hepatitis is usually characterized as viral hepatitis or non-viral hepatitis. Viral hepatitis can be considered 'acute' (a condition that comes on rapidly with severe symptoms and a short course) or 'chronic' (a condition that comes on slowly, may or may not have symptoms with a long course).Hepatitis is acute when it lasts less than six months and chronic when it persists longer. A group of viruses known as the Hepatitis viruses cause most cases of liver damage world- wide. Hepatitis can also be due to toxins (notably alcohol), other infections or from auto immune process. It may run a sub clinical course when the affected person may not feel ill. The patient becomes un-well and symptomatic when the disease impairs liver functions that include, among other things ,removal of harmful substances, regulation of blood composition ,and production of bile to help digestion.

Causes:

Acute:

Viral hepatitis: Hepatitis A through E,(more than 90% of viral cause),Herpes simplex, Cytomegalo virus, Yellow fever virus, adenoviruses.

Non-viral infection: toxoplasma, Leptospira, Q fever, rocky mountain spotted fever

Alcohol

Toxins: Amanita toxin in mushrooms, carbon tetra chloride

Drugs: Paracetamol, amoxicillin, anti TB medicines,and many others

Ischemic hepatitis(circulatory in-sufficiency)

Pregnancy

Auto immune conditions e.g systemic lupus erythematosus(SLE)

Metabolic diseases, e.g. Wilson's disease

Chronic:

Viral hepatitis: Hepatitis B with or without hepatitis D,C (neither hepatitis A nor E causes chronic hepatitis)

Auto immune: Auto immune hepatitis

Alcohol

Drugs: Mthyl dopa, nitrofurantoin, isoniazid, ketoconazole

Non alcoholic steato hepatitis

Heredity: Wilson's disease,α1-antitrypsin deficiency

Symptoms:

Primary biliary cirrhosis and primary sclerosing cholangitis occasionally mimic chronic hepatitis.

Acute:

Clinically, the course of acute hepatitis varies widely from mild symptoms requiring no treatment to hepatic failure needing liver transplantation. Acute viral hepatitis is more likely to be asymptomatic in younger people. Symptomatic individuals may present after convalescent stage of 7-10 days, with total illness lasting 2-6 weeks.

Initial features are of non specific flu like symptoms, common to almost all acute viral infections and may include: malaise, muscle and joint aches , fever, nausea or vomiting, diarrhea and head-ache. More specific symptoms, which can be present in acute hepatitis from any cause, are: profound loss of appetite, aversion to smoking among smokers, yellowing of eyes and skin (i.e jaundice) and abdominal discomfort. Physical findings are usually minimal, apart from jaundice (33%) and tender hepatomegaly (10%).There can be occasional lymphadenopathy (5%) or spleenomegaly(5%).

In acute hepatitis, symptoms often subside without treatment within a few weeks or months .About 5% of cases develop into an incurable form of the disease called chronic hepatitis, which may last for years.

Chronic:

Majority of patients will remain asymptomatic or mildly symptomatic, abnormal blood tests being the only manifestation .Features may be related to the extent of liver damage or the cause of hepatitis .Many experience return of symptoms related to acute hepatitis. jaundice can be a late feature and may indicate extensive damage .Other features include: Abdominal fullness from enlarged liver or spleen, low grade fever ,and fluid retention (ascites).Extensive damage and scarring of liver (i.e. cirrhosis) leads to weight loss, easy bruising and bleeding tendencies. Acne, abnormal menstruation, lung scarring, inflammation of thyroid gland and kidneys may be present in women with auto -immune hepatitis.

Types:Chronic hepatitis causes slowly progressive liver damage that may lead to cirrhosis, a condition in which healthy liver tissue is replaced with dead, non functional scar tissue. In some cases, cancer of the liver develops.

1. Alcoholic: Although, it has many different causes ,hepatitis most often results from infection by one of several hepatitis viruses. All hepatitis viruses are contagious, but each is passed from person to person differently.

It is distinct from cirrhosis caused by long term alcohol consumption. Alcoholic hepatitis can occur in patients with chronic alcoholic liver disease and alcoholic cirrhosis. Alcoholic hepatitis by itself does not lead to cirrhosis, but cirrhosis is more common in patients with long term alcohol consumption. Patients who drink alcohol to excess are also more often than others found to have hepatitis C. The combination of hepatitis C and alcohol consumption accelerates the development of cirrhosis.

Symptoms:

Loss of appetite

Nausea

Jaundice

Abdominal pain and tenderness

Fever

Ascites

Unintentional weight gain

Mental confusion

Fatigue

Symptoms vary with severity of the disease and are usually worse after a recent period of heavy drinking.

Treatment:

The objective of treatment is to discontinue alcohol ,and to provide a high carbohydrates, high calorie diet and to reduce protein break down in the body. Vitamins ,especially B1 and folic acid, are associated with improvement .An alcohol rehabilitation program or counseling may be necessary to break the alcohol addiction .Management of the complications of chronic liver disease may be needed .If cirrhosis develops ,liver transplant may be necessary.

Causes:

Alcoholic liver disease usually occurs after years of excessive drinking, the longer the use of alcohol, the greater the probability of liver disease. Acute alcoholic hepatitis can result from binge drinking, and may be life -threatening if severe.

Malnutrition develops as a result of empty calories from alcohol ,reduced appetite, and mal absorption .Malnutrition contributes to liver disease.

Toxicity of ethanol to liver ,individual susceptibility to alcohol-induced liver disease ,and genetic factors also contributes to development of disease.

Alcoholic liver disease does not effect at all heavy drinkers ,and women may be more susceptible than men .Drunkenness is not essential for disease development.

Changes start within the liver as inflammation and progress to fatty liver and cirrhosis. Cirrhosis is the final phase of alcoholic liver disease.

Test and Diagnosis:

A CBC may show anemia and other abnormalities.

Liver function tests such as ALP are abnormal.

Liver biopsy shows alcoholic liver disease.

Prognosis:

2. Drug Induced:Continued excessive drinking is associated with shorter life expectancy. The probable outcome is poor if drinking continues.

It is inflammation of liver that may occur when one takes certain medications.

Symptoms:

Dark urine

Diarrhea

Headache

Jaundice

Fatigue

Loss of appetite

Nausea and vomiting

Causes:

The liver helps the body to break down certain drugs, however, the way it does so differs from person to person. There-fore, many different drugs can cause drug-induced hepatitis.

Pain killers and fever reducers that contain acetaminophen are a common cause of liver inflammation. These medications can damage the liver when taken in doses that are not much greater than the recommended therapeutic dose.

NSAIDs may also cause drug-induced hepatitis .Drugs that causes hepatitis are:

Allopurinol

Amitriptyline

Amiodarone

Azathioprine

Hormonal contraceptives

Ibuprofen

Ketoconazole

Methotrexate

Isoniazid

Paracetamol

Methyl dopa

Phenytoin

Zidovudine

Nifedipine

Loratidine

Some herbs and nutritional supplements

Treatment:

There is no specific treatment for drug induced hepatitis other than stopping the drug that is causing the problem.

Those with acute hepatitis should avoid Physical exertion, alcohol, acetaminophen, and any other substances that are harmful to liver.

Causes:

The liver helps the body brek down certain drugs.However,the way it so differs from person to person.There fore, many different drugs can cause drug induced hepatitis.

Pain killers and fever reducersthat contains acetaminophen are a common cause of liver inflammatuion.These medications can damage the liver when taken in doses that are not much greater than the recommended therapeutic dose.

NSAIDs, such as Ibuprofen and Nproxen may also cause drug induced hepatitis.

Test and Diagnosis:

Blood tests will be done to check liver function. Liver enzymes may be increased.

A physical exam may reveal an enlarged liver and abdominal tenderness at upper part of belly area.

Prognosis:

Usually, drug related hepatitis goes away within days or weeks after the offending drug is stopped.

Prevention:

3. Other Toxins:

If you use over-the-counter medications containing acetaminophen (Tylenol),never use more than the recommended dose.

Other toxins can cause hepatitis:

Amatoxin-containing mushrooms, including the Death Cap (Amanita phalloides), the Destroying Angel(Amnita ocreata),and some species of Galerina. A portion of a single mushroom can be enough to be lethal (10 mg or less of α-amanitin).

White phosphorus ,an industrial toxin and war chemical

Carbon tetra chloride, chloroform, and trichloro-ethylene, all chlorinated hydrocarbons, cause steatohepatitis.

Cylindrospermopsin,a toxin from the cyan bacterium Cylindrospermopsis raciborskii and other cyan bacteria.

4. Metabolic Disorders:

Some metabolic disorders cause different forms of hepatitis. Hemochromatosis (due to iron accumulation) and Wilson's disease (copper accumulation) can cause liver inflammation and necrosis.

Non -alcoholic steatohepatitis (NASH) is effectively a consequence of metabolic syndrome.

5. Obstructive:

6. Auto Immune:Obstructive jaundice is the term used to describe jaundice due to obstruction of bile duct(by gall stones or external obstruction by cancer), if long standing it leads to destruction and inflammation of liver tissue.

Auto immune hepatitis is a disease in which the body's immune system attacks liver cells. This immune response causes inflammation of liver, also called hepatitis. Researchers think a genetic factor may make some people more susceptible to auto immune diseases. About 70% of those with auto immune hepatitis is female .Auto-immune hepatitis are classified as type І and II. Type I is more common in North America. It can occur at any age but most often starts in adolescence or young adult hood About half of those with type I have other auto immune disorders, such as:

Type I diabetes

Proliferative glomerulo nephritis, inflammation of blood vessels in kidneys , thyroiditis

Grave's disease

Ulcerative colitis

Auto immune hepatitis typically effecting girls aged 2-14, although adults can have it too.

Symptoms:

Fatigue

Jaundice

Skin rashes

Joint pain

Abdominal discomfort

Dark urine

Pale yellow or green colored stools

Diagnosis:

Blood tests

Liver biopsy

Tests:

Tests associated with auto immune hepatitis:

Positive ANA

Positive anti-liver kidney microsomal anti body

Positive anti-mitochondrial antibody

Higher than normal sedimentation rate

Higher than normal serum IgG

Treatment:

The primary treatment is medicine to suppress or slow down, an over active immune system. Drugs used are Corticosteroid called Prednisone; other medicine is Azthioprine (Imuran)

Prognosis:

The outcome varies; Corticosteroid therapy may slow disease progression. However, autoimmune hepatitis may progress to cirrhosis and require liver transplantation.

7. Ischemic Hepatitis:

:

4.Medical Aspects:

Symptoms:

Early symptoms of Hepatitis A infection can be mistaken for influenza,but some sufferers ,especially children ,exhibit no symptom at all. Symptoms typically appear 2 to 6 weeks ,after the initial infection,these are:

Jaundice

Fatigue

Loss of appetite

Nausea and vomiting

Low-grade fever

Pale or clay colored stools

Dark urine

Generalized itching

Diagnosis and Tests:http://upload.wikimedia.org/wikipedia/en/thumb/4/4b/HAV_Infection.png/220px-HAV_Infection.png

During the acute stage of infection ,the liver enzyme Alanine Transferase (ALT) is present in blood at levels much higher than is normal. Hepatitis A virus is present in blood , and feces of infected people up to two weeks before clinical illness develops.

Hepatitis serology tests may show:

IgM and IgG antibodies to Hepatitis A(IgM is usually positive before IgG)

Elevated liver enzymes (liver function tests)

Treatment:

There is no specific treatment for Hepatitis A. Sufferers are advised to rest , avoid fatty foods and alcohol because secretions from liver are needed to digest fats. Fatty foods are best avoided during the acute phase,eat balanced diet ,and stay hydrated.People with acute hepatitis should avoid alcohol and any substances that are toxic to liver,including acetaminophen(Tylenol) A.

Prognosis:

Over 85% of people with Hepatitis A recover within 3 months ,and over 99% of people recover by 6 months .The fatality rate is estimated at 0.1%,usually among the elderly and patients with chronic liver disease. Children have milder symptoms.HAV infection does not become a chronic.

Prevention:

Hepatitis A can be prevented by vaccination, good hygiene and sanitation .The vaccine protects against the virus in more than 95% of cases, it contains inactivated Hepatitis A virus providing active immunity against future infection.

The vaccine is given in two doses in the muscle of upper arm.The first dose provides protection 2-4 weeks after initial vaccination; the second booster dose,given 6 -12 months later ,provides protection for up to 20 years.

Hepatitis B:

It is disease caused by Hepatitis B virus which infects the liver of hominoidae,including humans,and causes an inflammation.Formerly known as "serum hepatitis" HBV is most serious form of hepatitis.Transmission of Hepatitis virus results from exposure to infectious blood or body fluids containing blood

1.Virology:

Hepatitis B virus is an hepadnavirus-hepa from hepatotrophic and dna because it is a DNA virus and it has a circular genome composed of partially double-stranded DNA.The viruses replicate through RNA intermediate form by reverse transcription,and in this respect they are similar to retro-virus.

a).Structure:

The virus particle, (virion) consists of an outer lipid envelope and an icosahedral nucleocapsid core composed of protein. The nucleocapsid encloses the viral DNA and a DNA polymerase that has reverse transcriptase activity. The outer envelope contains embedded proteins which are involved in viral entry into, susceptible cells. The virus is one of the smallest enveloped animal viruses with a virion diameter of 42 nm.http://upload.wikimedia.org/wikipedia/commons/thumb/2/2c/Hepatitis_B_virus_v2.png/220px-Hepatitis_B_virus_v2.png

b).Genome:

The genome of HBV is made of circular DNA, but it is unusual because the DNA is not fully double-stranded. One end of the full length strand is linked to the viral DNA polymerase. The genome is 3020-3320 nucleotides long and 1700-2800 nucleotides long .The viral DNA is found in the nucleus soon after infection of the cell. The partially double-stranded DNA is rendered fully double-stranded by completion of the (+) sense strand and removal of a protein molecule from the (-) sense strand and a short sequence of RNA from the (+) sense strand. There are four known genes encoded by the genome, called C, X, P, and S. The core protein is coded for by gene C (HBcAg), and its start codon in-frame AUG start codon from which the pre-core protein is produced. HBeAg is produced by proteolytic processing of the pre-core protein. The DNA polymerase is encoded by gene P. Gene S is the gene that codes for the surface antigen (HBsAg). The HBsAg gene is one long open reading frame but contains three in frame "start" (ATG) codons that divide the gene into three sections. Because of the multiple start codons, polypeptides of three. The function of the protein coded for by gene X is not fully understood.http://upload.wikimedia.org/wikipedia/commons/thumb/5/5b/HBV_genome.png/220px-HBV_genome.png

c).Replication:

http://upload.wikimedia.org/wikipedia/commons/thumb/8/8c/HBV_replication.png/220px-HBV_replication.png

Replication of Hepatitis B virus

The life cycle of hepatitis B virus is complex. Hepatitis B is one of a few known viruses which use reverse transcription as a part of its replication process. The virus gains entry into the cell by binding to an unknown receptor on the surface of the cell and enters it by endocytosis. Because the virus multiplies via RNA made by a host enzyme, the viral genomic DNA has to be transferred to the cell nucleus by host proteins. The partially double stranded viral DNA is then made fully double stranded and transformed into covalently closed circular DNA that serves as a moderate for transcription of four viral mRNAs. These four viral transcripts undergo additional processing and go on to form progeny virions which releases from the cell. The long mRNA is then transported back to the cytoplasm where the virion P protein synthesizes DNA via its reverse transcriptase activit

d). Serotypes and genotypes:

The virus is divided into four major serotypes based on antigenic epitopes presented on its envelope proteins, and into eight genotypes (A-H) according to overall nucleotide sequence variation of the genome. The genotypes have a distinct geographical distribution and are used in tracing the evolution and transmission of the virus. Differences between genotypes affect the disease severity, course and likelihood of complications, and response to treatment and possibly vaccination.

Genotypes differ by at least 8% of their sequence and were first reported in 1988 when six were initially described (A-F). Two further types have since been described (G and H).Within the genotypes, sub genotypes have been described and these differ by 4-8% of their sequence.

Genotype A is most commonly found in the Americas, Africa, India and Western Europe.

Genotype B is most commonly found in Asia and the United States.

Genotype C is most common in Asia and the United States. Sub genotype C1 is common in Japan, Korea and China. C2 is common in China, South-East Asia and Bangladesh, C3 in Africa.

Genotype D is most commonly found in Southern Europe, India and the United States and has been divided into 8 subtypes (D1-D8). In Turkey genotype D is also the most common type.

Genotype E is most commonly found in West and Southern Africa.

Genotype F is most commonly found in Central and South America and has been divided into two subgroups (F1 and F2).

Genotype G is most commonly found in Europe and the United States.

Genotype H is most commonly found in Central and South America and California in United States.Africa has five genotypes (A-E).

2. Pathogenesis:

Cirrhosis of liver and liver cancer may be caused .Hepatitis B virus primarily interferes with functions of liver by replicating in liver-cells, known as hepatocytes. The receptor is not yet known, though there is evidence that the receptor in the closely related to Hepatitis B virus is Carboxy peptidase D .During HBV infection, the host immune response causes both hepato cellular damage and viral clearance. Although the innate immune response does not play a significant role in these processes, the adaptive immune response, particularly virus-specific cytotoxic T lymphocytes, contributes to most of liver injury associated with HBV infection.

3. Epidemiology:

http://upload.wikimedia.org/wikipedia/commons/thumb/a/ac/Hepatitis_B_world_map_-_DALY_-_WHO2002.svg/220px-Hepatitis_B_world_map_-_DALY_-_WHO2002.svg.png

Molecule

Company

Target/mechanism

Clinical stage

Albuferon

Human Genome Sciences (Rockville, Maryland)

Interferon-albumin fusion protein

Phase 3

Telaprevir

Vertex Pharmaceuticals (Cambridge, Massachusetts)

NS3 protease inhibitor

Phase 2

Boceprevir

Schering-Plough (Kenilworth, New Jersey)

NS3 protease inhibitor

Phase 2

R1626

Roche (Basel, Switzerland)

NS5B polymerase inhibitor

Phase 2

IC41

Intercell (Vienna, Austria)

Therapeutic vaccine

Phase 2

VGX-410C

VGX Pharmaceuticals (Blue Bell, Pennsylvania)

Oral IRES inhibitor

Phase 2

Debio-025

Debiopharm, S.A. (Lausanne, Switzerland)

Cyclophilin inhibitor

Phase 2

Celgosivir

Migenix (Vancouver, Canada)

alpha-glucosidase 1 inhibitor

Phase 2

SCV-07

SciClone Pharmaceuticals (San Mateo, California)

Immune stimulant peptide

Phase 2

Nitazoxanide

Romark Laboratories (Tampa, FL)

Undisclosed

Phase 2

R7128

Pharmasset (Princeton, New Jersey), Roche

NS5B polymerase inhibitor

Phase 1/2

ITMN-191

InterMune (Brisbane, California)

NS3 protease inhibitor

Phase 1b

GI-5005

Globeimmune (Louisville, Kentucky)

Targeted molecular immunogen

Phase 1

GS-9190

Gilead Sciences (Foster City, California)

NS5B polymerase inhibitor

Phase 1

AZD-2836

Astra-Zeneca (London)

NS5A protein inhibitor

Phase 1

IMO-2125

Idera Pharmaceuticals (Cambridge, Massachusetts)

Toll-like receptor 9 agonist

Phase 1

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