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  • Hepatitis B
  • Sadaf Baig ppt

    1. 1. Today We WillDefine hepatitis, viral hepatitis & the liverLearn about the 5 different types of viral hepatitis
    2. 2. What Is Hepatitis?Hepatitis means inflammation of the liver ◦ Hepat (liver) + itis (inflammation)= HepatitisViral hepatitis means there is a specific virus that is causing your liver to inflame (swell or become larger than normal)
    3. 3. The LiverIs located in the upper right quadrant of the abdomen •Cleans the blood •Regulates hormones •Helps with blood clotting •Produces bile •Produces important proteins •Maintains blood sugar levels •And much, much, more• The liver is essential for life !
    4. 4. Inflammation Walls of scar tissue begin to Healthy liver cells form become trapped by a wall of scar tissue
    5. 5. Viral Hepatitis 5 types: A: fecal-oral transmission B: sexual fluids & blood to blood C: blood to blood D: travels with B Vaccine E: fecal–oral transmission PreventableAdapted from Corneil, 2003
    6. 6. Hepatitis ACa used by hepatitis A virusCaHumans as their reservoirSOC: Infected feces, HAV-contaminated foodPOC: 1–2 weeks before the onset of symptoms until about 7 daysafter the patient becomes jaundiced.Fecal oral contaminationOral anal sexual activity contamination,shellfish from contaminated waterIncubation 18 – 45 daysImmune globulin within two weeks of exposure
    7. 7. EtiologyHepatitis A virus (HAV) HAV is one kind of picornavirus and used to be classified as enterovirus type72, but recently, it is considered to be classified as heparnavirus Hepatitis A virion is a naked spherical particle, diameter 27nm Consists of a genome of linear, single-stranded RNA, 7.5kb. The genome may be divided into 3 coding region: P1 region (encoding structural protein), P2 and P3 regions (encoding non-structure protein) During acute stage of infection, HAV can be found in blood and feces of infected human and primates Marmoset and chimpanzee are susceptible animals
    8. 8. Etiology Hepatitis A virus (HAV)  HAV can not cause cytopathy, replicate within cytoplasma of hepatocytes and via bill are discharged with feces  7 genetypes, 1, 2, 3, 7 types from humanbody  Only one antigen-antibody system. Anti-HAV IgM is diagnostic evidence of recent infection, IgG is protective antibody.  Resistance of HAV: 56°C, 30 min, usually temperature 1 week, dry feces at 25°C 30 days, fresh water, sea water ,shellfish or soil for several months. 70% alcohol at 25°C , 3 min, 100°C, 5 min and ultraviolet, 1 min
    9. 9. HAV
    10. 10. HEV
    11. 11. Pathogenesis:Hepatitis A, EInoculation of the pathogen (entrance gate – small intestine).Viremia.Viral fixation on hepatocytes, intracellular localization.Primary replication of the virus.Excretion with a goal to intestine.Part of the viruses caused viremia (prodromal period of the disease).Activation of immune system, that causes cytolysis, mesenchimal inflammation and cholestasis.Immune response, elimination of the virus.
    12. 12. Hepatitis ASIGNS AND SYMPTOMS •Most are anicteric and asymptomatic •Flu-like URTI with low-grade fever •Anorexia •Indigestion •nausea •Aversion to cigarette smoke and other strong odors •May or may not be jaundiced
    13. 13. Hepatitis EHepatitis E Virus (HEV)Reservoir: Infected Humans and Animals: wild and domestic esp. swineIncubation: 14-60 daysPeriod of Communicability:-Not known.- Hepa-E virus has been detected in stools 14 days after theonset of jaundice and approximately 4 weeks after ingestion ofcontaminated food orwater and persists for about 2 weeks.Source of infection: - Contaminated water in areas of poor sanitation -household member,sex partners, shared injection equipment S/S: JAUNDICE is almost always present
    14. 14. EpidemiologySource of infectionHepatitis A and E: patients with acute hepatitis and person with sublinical infectionRoute of transmissionHepatitis A and E: fecal-oral route predominantly
    15. 15. pathogenesisHepatitis A: HAV invade into human body by mouth and cause viremia.After one week,the HAV reach liver cells replicate within.Then enter intestien with bill and appear in feces.someone believe that damage of liver cells maybe caused by immune response.Due to: ◦ HAV does not cause cytopathy
    16. 16. ◦ After HAV replicating and discharging,liver cells damage begin◦ Animal experiment proved that immune complex may attend the pathogenesis of HA◦ Complement level reduce the pathogenesis maybe following:activated T cell secrete γ- INF that promote the representation of HLA- Ⅰantigen on the liver cells,CTL may kill the target cell infected with HAV
    17. 17. Pathology ◦ Degeneration ◦ Necrosis ◦ Regeneration ◦ Infiltration of inflammatory cells ◦ Hyperplasia of interstitial cells
    18. 18. Clinical picture1. Preicetric stage or prodromal stage:3 – 9 days Sudden onset of influenza like picture: fever - headache – malaise – muscular pain Anorexia is marked with nausea – vomiting – distension Pain in Rt hypochondrium & epigastrium Dark urine – pale stool Transient itching Examination: fever with relative bradycardia + enlarged tender liver
    19. 19. Clinical picture Icteric stage: 2-4 w Jaundice with fever & improvement of general condition Anorexia nausea & vomiting diminish or disappear Urine is dark brown & frothy Stool are clay in color – bulky – offensive – greasy Examination: Soft tender enlarged liver Spleen is enlarged in 20 % L N 10% generalized lymph adenopathy with LN of post. Triangle of neck
    20. 20. Clinical pictureConvalescence stage: Signs & symptoms gradually disappear Jaundice may persist for some times due to affinity of bile pigment to elastic tissue Complete recovery of liver may take up to 6 months
    21. 21. Investigation:L FT:1. serum bilirubin : total, direct and indirect2. ALT – AST : from 500 – 2000 IU/L ALT > AST3. Alkaline phosphatase – 5’nucleotidase – GGT:Blood : Leucopenia with relative lymphocytosis, ESR
    22. 22. Urine : Early bilirubin appearance Bile salt : granular casts – frothy urine - +ve hay sulfur testStool: Pale – clay with stetorrheaSerology Acute stage Chronic stage others Hepatitis A Anti HAV IgM Anti HAV IgG Fecal HAV Hepatitis D Anti HDV IgM Anti HDV IgG Hepatitis E Anti HEV IgM Anti HEV IgG
    23. 23. Susceptibility and immunity of population Hepatitis A Most adult has anti-HAV due to covert infection. Infant under 6 month acquired antibody from mother. Young children is susceptible Hepatitis E Common susceptible. Children appear covert infection, adult show overt infection
    24. 24. Etiology Hepatitis B virus (HBV)HBV is a kind of hepadnovirusThree particles in serum: spherical particles and tubular particles with a diameter of 20 nm, composed of HBsAg large particles with a diameter of 42 nm, named Dane particle. It consists of an outer protein shell (envelope, contain HBsAg) and an inner body ( core, contain HBcAg, HBeAg, HBV- DNA and DNAP )
    25. 25. Etiology Hepatitis B virus (HBV)Hepatitis B viron genome is a small circular, partially double stranded DNA with 3200 nucleotides long. HBV DNA is asymmetry in length of two strands: minus strand (long strand, L) has full length. Four open reading frames (ORF) coded on the minus strand: C, S, X, and P region
    26. 26. 大球形 颗粒 管 形 颗 小球形 粒 颗粒HBV
    27. 27. Etiology  Hepatitis B virus (HBV)  Four open reading frames (ORF) S region: include pre-s1, pre-s2 and S gene, encoded pre-s1 protein, pre-s2 protein and HBsAg. Pre-s1 protein + pre-s2 protein + HBsAg—large protein Pre-s2 protein + HBsAg—middle protein HBsAg—major protein C region included pre-c and C gene, encode HBeAg and HBcAg X region encoded HBxAg P region encoded DNA polymerase
    28. 28. EtiologyHBcAg—anti-HBc system HBcAg can be found in the nuclei of liver cells, no free HBcAg in serum HBcAg is the marker of replication of HBV The stage called window phase Anti-HBc IgM is a marker of acute infection and acute attack of chronic infection of HBV. Anti-HBc IgG is the marker of past infection, high titer means low level replication of HBV
    29. 29. EtiologyHBSAg Related to chronocity, activity of hepatitis B or liver cancerResistance Resistant to heating and common disinfections. Chimpanzee is susceptible to HBV
    30. 30. Hepatitis BHepatitis B Virus (HBV)Reservoir: HumansSource of infection: -infected individuals - receipt of blood transfusion orother blood products - use of shared needles - history of tattooing, ear or bodypiercing, or acupunctureIncubation: 30-180 daysPeriod of communicability:-1-2 months before and after the onset ofsymptomsMode of transmission: Heterosexualtransmission, contact with blood and bodyfluids
    31. 31. Hepatitis BSIGNS AND SYMPTOMS •Loss of appetite, •dyspepsia, •abdominal pain •Gen. aching malaise and weakness •Jaundice •Ligh-colored stools and dark urine •Hepatomegaly and splenomegaly •Enlarged posterior cervical lymph nodes
    32. 32. Pathogenesis:Hepatitis BInoculation of the pathogen.Viremia.Viral integration and replication in hepatocytes, also may be in blood cells, bone marrow, lymph nodes, spleen.Activation of immune system, that causes cytolysis, mesenchimal inflammation and cholestasis.Immune response, elimination or persistence of the virus.
    33. 33. Hepatitis B marker: antigen Significance Corresponding significance Ab HBsAg Appear after 6 week Anti HBs Appear after 3 m (surface) Acute infection, remain Reflecting recovery for 3 ms & immunity Chronic infection if >6 ms HBcAg Detected on Liver Anti HBc Appear after 2 m (core) Biopsy only (not serum) Reflecting sever acute & chronic form HBeAg Reflect ongoing viral Anti HBe Appear after 2.5 m (envolop) replication (chronicity) Non replicating virus HBV DNA Most sensitive indication for viral replication & chronicity (Dan particle) It is detected by PCR
    34. 34. •Serological gap:It is a window last several weeks between disappearing of HBs Ag & appearance of Anti Hbs. Anti HBc Ab may represent serological evidence of recent HBV infectionBlood free from Hbs Ag & Anti Hbs (but containing anti – HBC) is the major cause of trasfusion HBV infection
    35. 35. Etiology Hepatitis C virus (HCV) HCV is a member of flavivirus family. HCV genome is a single stranded positive-sense RNA and contains 9.4kb The genome contains 5’-non coding region, C region, E region and NS region HCV genome may be divided into many types and subtypes. Resistance Antigen-antibody system The concentration of HCV in blood is low, HCV Ag has not be detected, anti-HCV is the indicator of infection and the marker of infectivity HCV-RNA HCV-RNA may be detected from blood or liver tissue, it’s the direct evidence of infectivity
    36. 36. HCV
    37. 37. • Hepatitis C – Is similar to that of HB. CTL and some cytokines play an important action – The chronicity is related to the variability of gene – HCV infection is related to HCC closely but HCV does not integrate to liver cells, so from HCV infection to HCC may be related to chronic inflammation and cirrhosis
    38. 38. Natural History of Hep C 20% Only 20% will Clear the show symptoms Virus Initially ! Healthy Acute Chronic Liver Infection Infection 80% Virus Continues to Damage LiverAdapted from Lauer and Walker, NEJM 2001
    39. 39. Natural History Con’t Chronic Cirrhosis Liver Hepatitis 20-30% Cancer 1-4%/yearMost symptoms begin to show only when liver is more severely damaged
    40. 40. Epidemiology Route of transmission Hepatitis B, C, and D:humoral transmission (parenteral transmission)Mather to infent transmission(vertical transmission)Sexual contact transmissionInsect transmission
    41. 41. Hepatitis CHepatitis C Virus (HCV)Source of infection: -Parenteral drug, needlestick injuries, Blood transfusion -High-risk sexual contact (multiple partners, history of other STDs, anal sex, etc.)Incubation: 15-160 daysContact with blood and body fluids: transfusion of blood and bloodproductsPeriod of communicability: -one or more weeks before onset of symptoms and persists in most persons
    42. 42. Hepatitis CSIGNS AND SYMPTOMS •Asymptomatic or experience mild symptoms •Fatigue •Abdominal pain and poor appetite •Jaundice •Headaches •joint aches •muscle aches •nausea
    43. 43. Hepatitis DHepatitis D Virus (HDV)Reservoir: humans Animals: chimpanzee and pigsSource of infection: same as Hepa-BIncubation: 30-180 daysPeriod of communicability: not been yet determined,but virus excretion in stool has been demonstrated up to 14days after onset of illnessCo-infects with hepatitis B, close personal contact
    44. 44. Pathogenesis:Hepatitis DNeed virus hepatitis B for its replication, develops only in infected HBV patients
    45. 45. Hepatitis DSIGNS AND SYMPTOMS •Similar to those with hepatitis B •May progress to chronic active hepatitis and cirrhosis •always associated with a coexistent hepatitis B virus infection, either simultaneous new infections (co- infection) or a chronic hepatitis B infection (superinfection)
    46. 46. Pathogenesis Initial viremia, with inflammation of GIT mucosa. Intrahepatic localization lead to A- diffuse centrilobular necrosis, with cellular infiltration around portal tracts B- intrahepatic cholestasis due to cellualar edema & inspissation of bile Other organ: splenomegaly – lymphoadenopathy Hypoplasia of BM