Hepatitis
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    Hepatitis Hepatitis Presentation Transcript

    • HEPAT There is growingI need to make people aware ofT the severity of the disease in theI region. People need to be extraS careful.
    • INTRODUCTION TO HEPATITIS SPEAKER: AMMARA FAROOQUI
    • HEPATITISInflammation of the liver • Acute hepatitis • Chronic hepatitis
    • CAUSES • Autoimmune hepatitis • Infections from viruses, bacteria, or parasites • Certain chemicals or poisonous organism • Liver damage from alcohol, poisonous mushrooms, or other poisons • Medications: Acetaminophen • Inherited disorders : cystic fibrosis , hemochromatosis, Wilsons disease
    • RISK FACTORS • Intravenous drug use • Overdosing on acetaminophen • Engaging in risky sexual behaviors • Eating contaminated foods • Traveling to an area where certain diseases are common • Living in a nursing home or rehabilitation center • Having a family member who recently had hepatitis A
    • Cont..• Using or abusing alcohol• Being an organ transplant recipient• Having HIV or AIDS• Having received a blood transfusion• Being a newborn of a mother with hepatitis B or C• Being a health care worker, because of bloodcontact• Receiving a tattoo• Receiving contaminated blood, sweat, tears,saliva, semen, vaginal secretions, menstrual bloodand breast milk.
    • PREVENTION1. To prevent from Viral Hepatitis • Vaccination • Immune Globulin for Traveling Abroad • Hand Washing • Avoid Used Needles • Protected Sex • Avoid Sharing Certain Personal Items • Wear Gloves When Handling Body Fluids • Avoid Contaminated Water and Food
    • 2. To prevent alcoholic hepatitis: • Limit the amount of alcohol consumption.3. To prevent toxic/drug-induced hepatitis: • Be aware of the lethal contents of all chemicals. • Face the spray away from the body. • Wear protective equipment if applicable
    • VIRAL HEPATITIS Hepatitis caused by viruses:Hepatitis A virus (HAV) Hepatitis B Virus (HBV) Hepatitis C Virus (HCV) Hepatiti Hepatiti s D Virus s E Virus (HDV) (HEV)
    • INTRODUCTION TO VIRAL HEPATITIS Hepatitis doesnt alwayspresent symptoms- Karen Gonzales SPEAKER: NOOR UL AINN
    •  Called HAV Infected Food water human waste , Anal –oral contact during sex .
    •  Called HBV STD. Injectedblood sharing of needles unprotected sex ,tatoo.
    •  Called HCV. Direct contact with blood. Unprotected sex.
    •  Cirrhosis [liver scaring ] Risk factor Older Male gender Heavy alcohol used.
    •  Called HDV. Already infected with HBV. Infected blood Unprotected sex. Infected needles.
    •  Drinking water. Anal or oral sex. Similar to HAV.
    •  Newly discovered. Relative of HCV. HXV is unknown.
    •  Mild flu Rash Diarrhea Mild fever Abdominal pain Vomiting Weightloss
    • Cont… Circulation problem Dark urine Dizziness Drowsiness Enlarged spleen Headache Hives Itchy skin Light closed feces Yellow skin .
    •  Difficulty gaining weight. Growing normally. Mental development.
    •  Blood sample Tissue sample Albumin level Liver function test Liver biopsy
    •  Tissuesample DNA test.HEV DIAGNOSED RT-PCR TEST Immune electron microscopy.
    • HEPATITIS A VIRUS SPEAKER: HIRA ARSHAD
    • Hepatitis a infection is causedby HAV (RNA single type ofserotype)The first successful vaccineInvented by maurice hillmenat merk.
    • hepatitis a vaccine is available as HAV(alone) HAV with the combination of HBV HAVRIX(hepatitis a vaccine) VAQTA (hepatitis a vaccine) TWINRIX (with hepatitis B vaccine)
    • Product HavrixManufacture by GLAXOSMITHKLINEYear licensed 1995Havrix is sterile suspensionInactivated virus for intramuscularadministration A vaccine is whole killed hepatitis a virus. It does not contain live virus so u cant get hepatitis from vaccines.
    • Manufactured by MERCKGeneric name: hepatitis a vaccineVaqta is inactivated whole virus vaccineDerived from hepatitis A.
    • The vaccine is usually given by injections intramuscularBy a health care professional , a series of 2 injectionsis usually given6 to 8 month period.
    • CHILDREN AND ADOLESCENTS.Primary immunization for children (12 months to 18years age)Consist of a single 0.5ml and 0.5 ml booster doseadministered between 6 to 12 months …ADULT DOSE.Primary immunization for adultsConsist of a single 1ml doseAnd 1ml booster dose administeredBetween 6 to 12 months
    • Manufactured by.GSKMain use .prevention of hepatitis A and BIT Contains inactivated hepatitis a virusand extract of hepatitis B virus.
    • TWINRIX adult is suitable foradult aged 16 years and over Twinrix children is suitable for adolescents 1 to 5 years
    • Shake well before use ,thoroughly agitation,TWINRIX is a slightly turbid white suspensionUse the sterile needles and sterile syringes . TWINRIX administer by intra muscular deltoid Region, only as a 1ml dose only. Do not administer by gluteal region, such injection may result in a suboptimal response
    • HEPATITIS B VIRUS SPEAKERS: RABIA BIBI SUNDUS MUKHTAR
    • HBV (hepatitis B virus)Genus : OrthohepadnavirusFamily : HepadnaviridaeArrangement: icosahedralDiameter: 42nmType: enveloped partially double strandedDNA virusHeat and pH resistantHBV virions are also known as Daneparticles.almost 1.2 million people worldwide dieeach year from HBV related diseases
    • Transmission of hepatitis B virus results fromexposure to infectious blood or body fluidscontaining blood. Possible forms of transmissioninclude sexual contact, blood transfusions andtransfusion with other human blood products, re-use of contaminated needles andsyringes, and vertical transmission from motherto child (MTCT) during childbirth.
    • The first vaccine became available in1981.The vaccine contains :HBsAgIt is produced by yeast cells, into whichthe genetic code for HBsAg has beeninserted.A course of three (3) vaccine injections isgiven. Afterward an immunesystem antibody to HBsAg is establishedin the bloodstream. The antibody isknown as anti-HBsAg. This antibody andimmune system memory then provideimmunity to hepatitis B infection.
    • Acute hepatitis B does not require medication. Chronic hepatitis B requires proper medication, currently, there are at least six drugs available:1. Interferon:• Usually a good choice for young people without serious liver disease.• Treatment duration is relatively short (24 to 48 weeks) compared to other hepatitis B therapies. Side effects:• Not available for people with failing livers.• Most expensive compared to the other drugs.• Pegylated interferon not approved for children.
    • 2. Lamivudine:• Least expensive.• One of the older hepatitis B drugs, so a lot is known about its safety.• Might be helpful in treating HIV co-infection in combination with tenofovir.• Approved for both children and adults. Side effects: • Often loses its effectiveness against the hepatitis B virus. • Requires long-term treatment.
    • 3. Adefovir dipivoxil• Can be used in patients with lamivudine-resistanthepatitis B virus.Side effects:•Can be toxic to your kidneys at high doses.•Requires long-term treatment.
    • 4. Entecavir:• Has an extremely low rate of resistance.• Might be helpful in patients with failing livers. Side effects:• A newer drug.•Requires long-term treatment.
    • 5. Telbivudine:• More powerful antiviral drug than lamivudine and adefovir.Side effects:• As likely as lamivudine to become resistant to hepatitis B virus.• Requires long-term treatment.• Not approved for children.
    • 6. Tenofovir: • Excellent at treating regular and drug-resistant types of hepatitis B virus. •Treats both HIV and the hepatitis B virus.Side effects:• Its a relatively new drug for treating hepatitis B.• Not approved for children.• Requires long-term treatment.• Regular monitoring of kidney function is necessary.
    • HEPATITIS C VIRUS SPEAKER: ANAM HASSAN
    • Hepatitis C virus (HCV or sometimes HVC) isa small (55–65 nm in size), enveloped,positive sense single-stranded RNA virus ofthe family Flaviviridae. Hepatitis C virus is the cause of hepatitisC in humans.
    • The Life Cycle ofHepatitis CThe hepatitis C virus must attach toand infect liver cells in order tocarry out its life cycle andreproduce - this is why it isassociated with liver disease. Whilelittle is known about the exactnatural processes of hepatitis C,like other viruses, it must completeeight key steps to carry out its lifecycle
    •  The hepatitis C virus is most commonly transmitted through exposure to infectious blood. receipt of contaminated blood transfusions, blood products and organ transplants; injections given with contaminated syringes and needle-stick injuries in health-care settings; being born to a hepatitis C- infected mother. Hepatitis C may be transmitted through sex with an infected person. Hepatitis C is not spread through breast milk, food or water or by casual contact such as hugging, kissing and sharing food or drinks with an infected person.
    •  There is no vaccine currently available for hepatitis C virus. Pegylated interferon and ribavirin for chronic HCV.
    •  Two new oral medications that are protease inhibitors, Boceprevir and Telaprevir, were approved FDA in May 2011 for patients with HCV genotype 1. They will be used in combination with pegylated interferon and ribavirin. Boceprevir and Telaprevir cannot be taken together and are not monotherapies.
    • SPEAKERBUSHRA KHAN
    • VIRION:HDV virion is enveloped ,spherical ,ssRNA(-) with a diameter of about 22 nm .Membrane proteins are originated from the HBV helper virus.
    •  bloodborne and sexual percutaneous (injecting drug use, haemophiliacs) permucosal (sexual) Risk factors include: Abusing intravenous (IV) or injection drugs Being infected while pregnant Carrying the hepatitis B virus Men having sexual intercourse with other men Receiving many blood transfusions.
    • Many of the medicines used to treat hepatitis B are not helpful for treating hepatitis D. Persons with long-term HDV infection may receive a medicine called alpha interferon for up to 12 months. A liver transplant for end-stage chronic hepatitis B may be effective.
    • No vaccines exist against HDV; however,vaccination against HBV of patients whoare not chronic HBV carriers, providesprotection against HDV infection.
    • HEPATITIS E VIRUS SPEAKER: MADIHA AHMED
    • Hepatitis E Virus(Hepeviridae family)VIRION:Non-enveloped, spherical, 32-34 nm in diameter. RNA genome is enclosed withina capsid composed of 60 capsid proteins, assembled into T=1 isometricicosahedral particle.
    • GENOME:Monopartite, linear, ssRNA(+) genome . The 5’ end is capped and the 3’terminus is polyadenylated.GENE EXPRESSION:ORF1 encodes nonstructural proteins; ORF2 encodes capsid protein; ORF3encodes small immunogenic protein.
    • By Oral,Fecal route. Zoonotic & Fomite.Host : Human, pig, monkey,some rodents,& chicken.
    • INFECTION : Secondary site : hepatocytes & possibly cells in biliary tract. Primary site : possibly the intestinal tract.
    • Treatment options for chronic hepatitis include: The first step in the treatment is reduction of immuno supression medication in 16 solid organ transplant recipients with chronic hepatitis E ,led to clearance of HEV in 4 cases (25%) . A second possible treatment option is administration of pegylated -interferon α with ribavirin. Treatment durations varied between 3 and 12 months. Ribavirin has also been used in a not -transplanted patient with severe acute hepatitis E who showed rapid improvement of symptoms and liver function tests during treatment .
    • No commercial HEV vaccine is currently available. Avaccine developed by GSK & the Walter Reed ArmyInstitute that was successfully tested in a Phase IIstudy(Shrestha 2007). However, this vaccine has not beenfurther developed.
    • A group from China reported data recently from a very large successful Phase III vaccine trial (Zhu 2010). This trial included almost 110,000 individuals who received either a recombinant HEV vaccine (“HEV 239”)or placebo. The vaccine efficacy after 3 doses was 100%. Moreover, the efficacy of this vaccine needs to beevaluated in special risks groups such as patients with end-stage liver disease or immuno suppressedindividuals. It is also unknown if HEV -239 also protects from HEV genotype 3 infection (Wedemeyer andPischke 2011)