Viral hepatitis

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this work is a search about viral hepatitis done by third year medical students

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Viral hepatitis

  1. 1. 3
  2. 2. Viral hepatitis 4 Viral hepatitis 25 October 2013
  3. 3. Normal liver What is hepatitis? What is viral hepatitis? Clinicopathology of viral hepatitis 5 Viral hepatitis 25 October 2013
  4. 4. Normal liver Normal anatomy -the largest parenchymal organ -The liver has a dual blood supply: the portal vein provides 60% to 70% the hepatic artery supplies 30% to 40%. 6 Viral hepatitis 25 October 2013
  5. 5. *FUNCTIONS OF THE LIVER: 1-Carbohydrate metabolism : Glycogenesis Glycogenolysis Gluconeogenesis 8 3-Protein metabolism :  anabolism  deamination  urea formation 4-Secretion of bile. 5-Detoxification 2-fat metabolism: 6-Metabolism of Ketogenesis. vitamins A,D,K,B Cholesterol synthesis. 7-Clotting factors 25 October 2013 Viral hepatitis
  6. 6. hepatic microarchitecture is based on 9 Viral hepatitis 25 October 2013
  7. 7. 12 Viral hepatitis 25 October 2013
  8. 8. -Hepatitis means inflammation in the liver -can be caused by variety of exposure to: 1-hepatitis virus 2-toxins 3-drugs 4- Bacteria 5- Parasites - Can be both acute and chronic 13 Viral hepatitis 25 October 2013
  9. 9. *Systemic viral infections can involve the liver as in : I. infectious mononucleosis (Epstein-Barr virus) which may cause a mild hepatitis during the acute phase. II. cytomegalovirus infection, particularly in the newborn or immunosuppressed patient. III. yellow fever (yellow fever virus), which has been a major and serious cause of hepatitis in tropical countries. 14 Viral hepatitis 25 October 2013
  10. 10. I. Infrequently, in children and immunosuppressed patients, the liver is affected in the course of rubella, adenovirus, herpes virus, or enterovirus infections. II. However, unless otherwise specified, the term viral hepatitis is applied for hepatic infections caused by a group of viruses known as hepatotropic virus (hepatitis viruses A, B, C, D, and E) that have a particular affinity for the liver . 15 Viral hepatitis 25 October 2013
  11. 11. 16 Viral hepatitis 25 October 2013
  12. 12. an acute infectious disease of the liver caused by the hepatitis A virus (HAV). Type of virus: ssRNA.  Frequency of chronic liver disease: Never  Frequency of acute liver disease: -Approximately 40% of all acute viral hepatitis is caused by HAV. incubation period: -is between two and six weeks and the average incubation period is 28 days. 17 Viral hepatitis 25 October 2013
  13. 13. transmission: -transmitted person-to-person by  ingestion of contaminated food or water or  through direct contact with an infectious person.  Hepatitis A can be transmitted by the parenteral route but very rarely by blood and blood products. 18 Viral hepatitis 25 October 2013
  14. 14. 19 Viral hepatitis 25 October 2013
  15. 15. Unlike other members of the Picornaviruses this virus requires an intact eukaryote initiating factor 4G (eIF4G) for the initiation of translation. The requirement for this factor results in an inability to shut down host protein synthesis unlike other picornaviruses. The virus must then inefficiently compete for the cellular translational machinery. There is no apparent virus-mediated cytotoxicity 20 Viral hepatitis 25 October 2013
  16. 16.  low-income regions (sub-Saharan Africa and parts of South Asia) have high endemicity levels 21 Viral hepatitis 25 October 2013
  17. 17. • specific diagnosis is made by the detection of HAVspecific IgM antibodies in the blood. 22 Viral hepatitis 25 October 2013
  18. 18. A. Hepatitis A can be prevented by vaccination good hygiene and sanitation. B. The vaccine protects against HAV in more than 95% of cases for longer than 20 years. 23 Viral hepatitis 25 October 2013
  19. 19. 24 Viral hepatitis 25 October 2013
  20. 20. 25 Viral hepatitis 25 October 2013
  21. 21.  Type of virus: Hepatitis B virus is an hepadna virus from hepatotrophic and DNA because it is a DNA virus The viruses replicate through an RNA intermediate form by reverse transcription. Frequency of chronic liver disease -10% The acute illness causes liver inflammation, vomiting, jaundice and rarely, death. 26 Viral hepatitis 25 October 2013
  22. 22.  Mean incubation period: 1–4 months.  Transmission:  Transmission of hepatitis B virus results from exposure to infectious blood or body fluids containing blood.  Possible forms of transmission include: sexual contact blood transfusion reuse of contaminated syringe vertical transmission between family members, possibly by contact of no intact skin or mucous membrane with secretions or saliva containing HBV. 27 Viral hepatitis 25 October 2013
  23. 23. 28 Viral hepatitis 25 October 2013
  24. 24. B 29 Viral hepatitis 25 October 2013
  25. 25. 30 Viral hepatitis 25 October 2013
  26. 26.  During HBV infection, the host immune response causes both hepatocellular damage and viral clearance.  the adaptive immune response, particularly virus-specific cytotoxic T lymphocytes (CTLs), contributes to most of the liver injury associated with HBV infection.  CTLs eliminate HBV infection by killing infected cells and producing antiviral cytokines, which are then used to purge HBV from viable hepatocytes. 31 Viral hepatitis 25 October 2013
  27. 27.  high prevalence areas such as china and South East Asia, Africa, transmission during childhood is a significant factor 32 Viral hepatitis 25 October 2013
  28. 28. 33 Viral hepatitis 25 October 2013
  29. 29.  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.  PCR tests have been developed to detect and measure the amount of HBV DNA. 34 Viral hepatitis 25 October 2013
  30. 30.  Several vaccines have been developed by Maurice Hillman for the prevention of hepatitis B virus infection.  the avoidance of 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 Viral hepatitis 25 October 2013
  31. 31. A. Hepatitis B virus DNA persists in the body after infection and in some people the disease recurs. Although rare, reactivation is seen most often in people with impaired immunity HBV goes through cycles of replication and non-replication. B. 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. 36 Viral hepatitis 25 October 2013
  32. 32. Acute hepatitis B infection does not usually require treatment because most adults clear the infection spontaneously. Early antiviral treatment may only be required in fewer than 1% of patients, whose infection takes a very aggressive course (fulminant hepatitis) or who are immunocomprimised . On the other hand, treatment of chronic infection may be necessary to reduce the risk of cirrhosis and liver cancer. Although none of the available drugs can clear the infection, they can stop the virus from replicating, Response to treatment differs between the genotypes. 37 Viral hepatitis 25 October 2013
  33. 33. 38 Viral hepatitis 25 October 2013
  34. 34. Type of virus: -ssRNA -HCV is a small-enveloped virus with one single-stranded positive-sense RNA molecule 39 Viral hepatitis 25 October 2013
  35. 35. Frequency of chronic liver disease: Hepatitis C virus (HCV) is a major cause of liver disease worldwide(∼80%).  Acute disease: Between 60% and 70% of people infected develop no symptoms Persistent infection: 85-100% 40 Viral hepatitis 25 October 2013
  36. 36. Clinical illness (jaundice): 30-40% (20-30%) Incubation period : Average 6-7 weeks 41 Viral hepatitis 25 October 2013
  37. 37. Mode of transmission: 1. Parental: inoculations and blood transfusion 2. Vertical transmission 3. Close personal contact – sexual contact. 4. intranasal cocaine use is a risk factor 42 Viral hepatitis 25 October 2013
  38. 38. 1) In primary HCV infection, liver cell damage correlates with the development of the host immune response -- not with infection and HCV viral replication. 2) Chronic HCV replication can occur without significant liver cell damage. 3) HCV infection of liver cells does not appear to kill the infected liver cells. 43 Viral hepatitis 25 October 2013
  39. 39. 5) Immunosuppression of people with HCV infection results in transient improvement in liver function tests, despite a surge in HCV RNA levels. 6) Liver cell damage is associated with an inflammatory infiltrate, and liver-infiltrating HCV immune cells associated with areas of liver damage suggest a causative role. 44 Viral hepatitis 25 October 2013
  40. 40.  Immune Responses to HCV Infection: • neutralizing antibodies are produced during HCV infection, but they do not appear to be protective against re-infection in humans or in chimpanzees • The more critical determinant seems to be the cell-mediated immune response, or the T-cell (Cd4) response. 45 Viral hepatitis 25 October 2013
  41. 41. o Prevalence is higher in some countries in Africa and Asia. o Egypt has the highest seroprevalence for HCV, up to 20% in some areas. 46 Viral hepatitis 25 October 2013
  42. 42. 47 Viral hepatitis 25 October 2013
  43. 43.  HCV antibody - generally used to diagnose hepatitis C infection. Not useful in the acute phase as it takes at least 4 weeks after infection before antibody appears.  HCV-RNA - various techniques are available e.g. PCR and branched DNA.  HCV-antigen - 48 Viral hepatitis 25 October 2013
  44. 44. Screening of blood, organ, tissue donors. High-risk behavior modification. Blood and body fluid precautions 49 Viral hepatitis 25 October 2013
  45. 45. 50 Viral hepatitis 25 October 2013
  46. 46. Interferon The response rate is around 50% but 50% of responders will relapse upon withdrawal of treatment. Ribavirin 51 Viral hepatitis 25 October 2013
  47. 47. 52 Viral hepatitis 25 October 2013
  48. 48. Virus type: unique RNA virus that is dependent for its life cycle on HBV. Frequency of chronic liver disease: % (coinfection); ≤70% for super infection. Mean incubation period: 1–4 months. Route of transmission: Parenteral. 53 Viral hepatitis 25 October 2013
  49. 49. Infection with HDV arises in the following settings: Acute coinfection : occurs following exposure to serum containing both HDV and HBV. The HBV must become established first to provide the HBsAg necessary for development of complete HDV virions. Super infection: occurs when a chronic carrier of HBV is exposed to a new inoculum of HDV. This results in disease 30–50 days later. Helper-independent latent infection : observed in the liver transplant setting. 54 Viral hepatitis 25 October 2013
  50. 50. HDV RNA detection. IgM anti-HDV is the most reliable indicator of recent HDV exposure. 55 Viral hepatitis 25 October 2013
  51. 51. 56 Viral hepatitis 25 October 2013
  52. 52.  limited to IFN-α.  Other antiviral agents for HBV have not shown effectiveness. 57 -HBV-HDV Coinfection: Pre or post exposure prophylaxis to prevent HBV infection. -HBV-HDV Super infection Education to reduce risk behaviors among persons with chronic HBV infection. Vaccination for HBV can also prevent HDV Viral hepatitis 25 October 2013 infection.
  53. 53. 58 Viral hepatitis 25 October 2013
  54. 54. Type of virus: I. Un enveloped, positive-stranded RNA virus in the Hepevirus genus .  frequency of chronic liver disease: Never In most cases the disease is self-limiting; HEV is not associated with chronic liver disease or persistent viremia.  Mean incubation period: 4–5 weeks  Route of transmission: Fecal-oral.  Illness severity: Increased with age  Diagnosis:  PCR for HEV RNA  detection of serum IgM and IgG antibodies 59 Viral hepatitis 25 October 2013
  55. 55. Hepatitis E is prevalent in most developing countries, and common in any country with a hot climate. 60 Viral hepatitis 25 October 2013
  56. 56.  Avoid drinking water (and beverages with ice) of unknown purity, uncooked shellfish, and uncooked fruit/vegetables not peeled or prepared by traveler.  IG prepared from donors in Western countries does not prevent infection.  Unknown efficacy of IG prepared from donors in endemic areas.  Vaccine 61 Viral hepatitis 25 October 2013
  57. 57. 62 Viral hepatitis 25 October 2013
  58. 58.  type of virus: A flavivirus bearing similarities to HCV  Transmission: HGV is transmitted by contaminated blood or blood products, and via sexual contact.  Liver diseases caused by the virus: However, HGV is inappropriately named: it is not hepatotropic and does not cause elevations in serum aminotransferases. Instead, the virus appears to replicate in the bone marrow and spleen. 63 Viral hepatitis 25 October 2013
  59. 59. 64 Viral hepatitis 25 October 2013
  60. 60. Each of the hepatotropic viruses can cause acute asymptomatic or symptomatic infection. A small number of HBV-infected adult patients develop chronic hepatitis. In contrast, HCV is notorious(infamous) for chronic infection. HAV and HEV do not cause chronic hepatitis. Although HBV and HCV are responsible for most cases of chronic hepatitis. 65 Viral hepatitis 25 October 2013
  61. 61. Yes, there are many other causes of chronic hepatitis including : i. chronic alcoholism. ii. drugs (e.g., isoniazid, α-methyldopa, methotrexate) iii. toxins
  62. 62.  acute asymptomatic infection with recovery .  Acute symptomatic hepatitis with recovery, anicteric(without jaundice) or icteric (jaundiced ).  Chronic hepatitis, without or with progression to cirrhosis.  Fulminant hepatitis with massive to submissive hepatic necrosis.
  63. 63.  identified only incidentally on the basis of minimally elevated serum transaminases or by the presence of antiviral antibodies  Worldwide, HAV and HBV infection are frequently subclinical events in childhood, verified only in adulthood by the presence of anti-HAV or anti-HBV antibodies.
  64. 64.  acute asymptomatic infection with recovery .  Acute symptomatic hepatitis with recovery, anicteric(without jaundice) or icteric (jaundiced ).  Chronic hepatitis, without or with progression to cirrhosis.  Fulminant hepatitis with massive to submissive hepatic necrosis.
  65. 65. o Acute hepatitis is liver inflammation that lasts less than six months and often is of sudden onset. o This type of hepatitis is most often caused by infection with the hepatitis A virus, but it also can occur as a result of infection with the hepatitis viruses B, C, D or E.
  66. 66. An incubation period. preicteric phase. icteric phase. Convalescence.
  67. 67. Anorexia Headache Malaise General Fatigue Influenza like symptoms Muscle and joint pains Discomfort in upper abdomen Diarrhea Distaste for cigarettes Fever, rash and arthralgia , in case of Hepatitis B sue to circulating immune complexes.
  68. 68. • It is usual in adult (but not children) with HAV but is absent in about half of the cases of HBV and the majority of cases of HCV. • caused by conjugated hyperbilirubinaemia due to intra hepatic cholestasis. • Symptoms: - Pain in Rt Hypochondrium -Pruritus due to retention of bile salts -High colored urine.
  69. 69.  The recovery phase begins with resolution of jaundice which occurs about six to eight weeks after exposure.  Symptoms typically diminish even though the liver still may be tender and enlarged. In most cases, liver function tests return to normal.
  70. 70.  Hepatitis and other causes of liver inflammation can damage the liver in two different ways: The first is direct damage caused by infection of liver cells The second mechanism is mediated by the immune system’s inflammatory response to the infection.
  71. 71. Macroscopically: The liver is enlarged and yellowish or greenish in color. Microscopically: take the form of  -diffuse swelling “ballooning degeneration”  An inconstant finding is cholestasis, with bile plugs in canaliculi and brown pigmentation of hepatocytes. 76 Viral hepatitis 25 October 2013
  72. 72. 77 Viral hepatitis 25 October 2013
  73. 73. Rupture of the cell membrane leads to cell death and focal loss of hepatocytes. The sinusoidal collagen reticulin framework collapses where the cells have disappeared, and scavenger macrophage aggregates mark sites of hepatocyte loss. Apoptosis, Apoptotic hepatocytes shrink, become intensely eosinophilic, and have fragmented nuclei; Apoptotic cells are rapidly phagocytosed by macrophages and hence might be difficult to find, despite a brisk rate of hepatocyte injury. Necrosis of Liver Cells : The necrosis is variable in extend and degrees.
  74. 74. Necrosis of Liver Cells : The necrosis is variable in extend and degrees.: 1. Necrosis of isolated liver cell or Piecemeal necrosis 2. Severe Necrosis 3. Bridging Necrosis: Extensive necrosis connecting portal to portal , central to central or portal to central parts of the adjacent lobule. 79 Viral hepatitis 25 October 2013
  75. 75.  Hypertrophy and hyperplasia of Kupffer cells: They often contain Lipofuscin derived from dead hepatocytes.  Infiltration of portal tract with inflammatory cells: Lymphocytes, plasma cells and macrophages.  Evidence of hepatocytic regeneration: during the recovery phase 81 Viral hepatitis 25 October 2013
  76. 76. Detail of lobular parenchyma in mild acute viral hepatitis C. Eosinophil condensation of hepatocellular cytoplasm (Mallory bodylike) and rounded eosinophil fragments of apoptotic hepatocyte, with a few adjacent mononuclear inflammatory cells. (H&E) 82 Viral hepatitis 25 October 2013
  77. 77. Acute viral hepatitis B. Centrilobular area of liver lobule, characterized by liver cell pleomorphism (including ballooning of hepatocytes), some canalicular bilirubin stasis, focal liver cell loss, and mononuclear (mainly lymphocytic) inflammatory infiltration. (H&E) 83 Viral hepatitis 25 October 2013
  78. 78. 1. Acute liver failure (Fulminant Hepatitis) 2. Progression to chronic hepatitis 3. Post necrotic liver cirrhosis 4. Hepatocellular carcinoma 5. Aplastic Anemia 84 Viral hepatitis 25 October 2013
  79. 79. 85 Viral hepatitis 25 October 2013
  80. 80.  Chronic hepatitis is defined as symptomatic, biochemical, or serologic evidence of continuing or relapsing hepatic disease for more than 6 months.  HCV infection causes chronic hepatitis at a high frequency while only a small number of patients with HBV infection develop chronic disease.  The clinical features of chronic hepatitis are extremely variable and are not predictive of outcome. .
  81. 81.  In some patients the only signs of chronic disease are persistent elevations of serum transaminases.  The most common symptom is fatigue; less common symptoms are malaise, loss of appetite, and occasional bouts of mild jaundice.
  82. 82.  Occasionally, in cases of HBV and HCV, immune complex disease may develop secondary to the presence of circulating antibody-antigen complexes, in the form of vasculitis and glomerulonephritis Cryoglobulinemia is found in about 35% of individuals with chronic hepatitis C.  Age at the time of infection is the best determinant of chronicity. The younger the age at the time of infection, the higher the probability of chronicity.
  83. 83.  HCV is by far the most common cause of chronic viral hepatitis.  HCV infection is potentially curable. Treatment is currently based on combination of pegylated IFN-α and ribavirin. The response to therapy depends on the viral genotype; patients with genotype 2 or 3 infection generally have the best responses. 89 Viral hepatitis 25 October 2013
  84. 84. microscopically  The histologic features of chronic hepatitis range from exceedingly mild to severe.  In the mildest forms, inflammation is limited to portal tracts and consists of lymphocytes, macrophages, occasional plasma cells, and rare neutrophils or eosinophils. Liver architecture is usually well preserved but hepatocyte apoptosis throughout the lobule may occur in all forms of chronic hepatitis.
  85. 85.  In chronic HCV infection, common findings (occurring in 55% of HCV infections) are lymphoid aggregates and bile duct reactive changes in the portal tracts, and focal mild to moderate macrovesicular steatosis., continued interface hepatitis and bridging necrosis between portal tracts and portal tracts-toterminal hepatic veins, are harbingers of progressive liver damage.  The hallmark of chronic liver damage is the deposition of fibrous tissue.
  86. 86. Liver biopsy specimen; chronic hepatitis with fibrosis and porto-portal bridge formation 92 Viral hepatitis 25 October 2013
  87. 87. Liver biopsy specimen showing ground-glass appearance of hepatocytes in a patient with hepatitis B. 93 Viral hepatitis 25 October 2013
  88. 88.  Continued loss of hepatocytes and fibrosis results in cirrhosis It is characterized by irregularly sized nodules separated by variable but mostly broad scars, (post-necrotic cirrhosis ) 94 Viral hepatitis 25 October 2013
  89. 89. 95 Viral hepatitis 25 October 2013
  90. 90. Grossly: I. macro nodular cirrhosis of the liver. II. Macro nodular lesions are greater than 3 mm and have thick septa as well as invasion of septa within the nodule. 96 Viral hepatitis 25 October 2013
  91. 91. Macronodular Cirrhosis: Larger nodules separated by wider scars and irregularly distributed throughout the nodular Cirrhosis: Small rather uniform 3mm nodules separated by thin fibrous septa usually due to a chemical agent as alcohol which diffuse uniformly throught the liver.
  92. 92. 98 Viral hepatitis 25 October 2013
  93. 93. Bridging confluent lytic necrosis in severe chronic viral hepatitis B. Inflamed portal tract ‘bridged’ through area of necrosis with centrilobular area (lower left). The upper right part corresponds to an area of extensive lytic necrosis in phase of postnecrotic collapse of the reticulin framework and early fibrosis. (H&E) 99 Viral hepatitis 25 October 2013
  94. 94. Jaundice the yellowing of some portions of your skin due to accumulation of toxins that are easily released through the epidermal layer.  fatigue and general weakness: your body does not function normally, not being able to sort out the poisons from the useful substances and it launches them all into the bloodstream, destroying itself from within
  95. 95.  weight loss and lack of muscle control: it is a natural consequence of the fatigue. Your system does not process whatever food you ingest if you do not eat, your muscle tone goes down and you start to lose control over your limbs. the presence of blood in your stool (turning the feces black and frazzled) and in your vomit: it is a sure sign that the linings of your stomach or the walls of the esophagus have been perforated;
  96. 96. high temperature: it is normal for a cirrhosis patient to be riddled with infectious agents and to often suffer from fever attacks. swelling in your abdominal cavity and your joints: this is due to the accumulation of liquid that cannot be eliminated because of the lack of proper function of the liver.
  97. 97.  acute asymptomatic infection with recovery .  Acute symptomatic hepatitis with recovery, anicteric(without jaundice) or icteric (jaundiced ).  Chronic hepatitis, without or with progression to cirrhosis.  Fulminant hepatitis with massive to submissive hepatic necrosis.
  98. 98.  Hepatic insufficiency that progresses from onset of symptoms to hepatic encephalopathy within 2 to 3 weeks in individuals who do not have chronic liver disease is termed fulminant hepatic failure.  Viral hepatitis is responsible for about 12% of cases of fulminant hepatic failure; of these 8% are caused by HBV infection and the rest by HAV.  The pathogenesis of fulminant hepatic failure varies depending on etiology. In the case of HBV-induced fulminant hepatitis, there is massive apoptosis
  99. 99. Grossly:  The distribution of liver destruction is extremely capricious, since the entire liver or only random areas may be involved.  With massive loss of mass, the liver may shrink to as little as 500 to 700 gm., and becomes a limp, red organ covered by a wrinkled, too-large capsule.  On transection ,necrotic areas have a muddy red, mushy appearance with hemorrhage. 105 Viral hepatitis 25 October 2013
  100. 100. 106 Viral hepatitis 25 October 2013
  101. 101. Microscopically:  complete destruction of hepatocytes -a collapsed reticulin framework and preserved portal tracts.  little inflammatory reaction.  Alternatively, with survival for several days, there is a massive influx of inflammatory cells to begin the phagocytic cleanup process.  Survival for more than a week may permit the replication of residual hepatocytes. 107 Viral hepatitis 25 October 2013
  102. 102. 108 Viral hepatitis 25 October 2013
  103. 103. 111 Viral hepatitis 25 October 2013
  104. 104. -Asmaa Ismael Mohamed -Asmaa Gamil Abdulkhaleh -Eslam mohamed darahem -Eslam Aziz -Eslam Magdy Asmaa gamil Abdeulkhalek 112 153 155 147 143 144 155 Viral hepatitis 25 October 2013
  105. 105. 113 Viral hepatitis 25 October 2013
  106. 106. 114 Viral hepatitis 25 October 2013
  107. 107. 115 Viral hepatitis 25 October 2013

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