Viral Hepatitis,A,B,C,D,E,F,G and Liver problems Presented by: Dave Jay S. Manriquez RN.
Pathophysiology <ul><li>>pathophysiologic features are similar regardless of the cause </li></ul><ul><li>>hepatocytes unde...
 
Increased risk of hepatic cancer.  Increased risk of chronic hepatitis, cirrhosis and hepatic cancer.  Carrier state possi...
Hepatitis A <ul><li>HAV Hepatitis A virus; etiologic agent of Hep A (formerly infectious hepatitis) </li></ul><ul><li>Anti...
<ul><li>IgM anti-HAV IgM antibody to HAV; indicates recent infection with HAV; positive up to 6 mos after infection </li><...
<ul><li>HBV Hepatitis B virus; etiologic agent of Hep B (formerly serum hepatitis) </li></ul><ul><li>HBsAG </li></ul><ul><...
<ul><li>Anti-HBs </li></ul><ul><li>Antibody to hepatitis B surface antigen; indicates prior exposure and immunity to hepat...
Anti-HBe Antibody to hepatitis B e-antigen; suggests low titer of HBV HBcAg Hepatitis B core antigen; found in liver cells...
Anti-HBc Antibody to Hepatitis B core antigen;  most sensitive indicator of Hep B; appears late  in the acute phase of the...
Hepatitis C HCV Hepatitis C virus (formerly non-A, non-B virus); may be more than 1 virus
Hepatitis D HDV Hepatitis D virus (delta agent); etiologic agent to hepatitis D; HBV required for replication   HDAg Hepat...
Anti-HDV Antibody to HDV; indicates past or present infection with HDV
Hepatitis E  HEV Hepatitis E virus; etiologic agent of hep E
Hepatitis G HGV Hepatitis G virus; also known as GB virus C
  40-200 mg/24H (0.068-0.34mmol/24H) Fecal Urobilinogen   0.05-2.5mg024H (0.09-4.23 umol/24 H) Urine urobilinogen   0 Urin...
Albumin: Cirrhosis, Chronic Hepatitis, Edema, Ascites Globulin: Cirrhosis, Liver disease, Chronic obstructive jaundice vir...
Serum alkaline phosphatase is manufactured in bones, liver, kidneys and intestine andexcreted through biliary tract. In ab...
      150-250 mg/dL     Liver converts ammoniato urea. Ammonia level rises in liver failure. 20-120 ug/dL Serum ammonia   ...
  LDL <130ug/dL LDL (low-density lipoprotein)   Female: 35-85 mg/dL     Male: 35-70 mg/dL HDL (high-density lipoprotein) C...
To determine adequacy of portal blood flow Splenoportogram (splenic portal venography) For liver nad pancreas visualizatio...
  To detect hepatic neoplasms; diagnose cysts, abscesses and hematomas; and distinguish between ostructive nad nonobstruct...
Visualizes biliary structures via endoscopy. Endoscopic retrograde cholangiopancreatography (ERCP) To detect hepatic neopl...
<ul><li>Complications </li></ul><ul><li>Fulminant Hepatitis  (massive hepatic necrosis)  </li></ul><ul><ul><li>rare; seen ...
<ul><li>Chronic Hepatitis </li></ul><ul><ul><li>exists when liver inflammation continues beyond a period of 3-6 mos </li><...
Primary Hepatocellular Cancer Etiology: Hep B, Hep C, cirrhosis, chronic liver disease, hemochromatosis, ingestion of cert...
Hepatic Encephalopathy -Occurs with profound liver failure and may result from the accumulation of ammonia and other toxic...
<ul><li>Autoimmune Hepatitis </li></ul><ul><li>Characterized by hepatic inflammation with plasma cells & fibrosis </li></u...
Aplastic Anemia -rare; carries a high mortality rate when it occurs after acute viral hepatitis Mgt: supportive & palliative
<ul><li>Cirrhosis </li></ul><ul><ul><li>-  chronic, progressive disease characterized by widespread fibrosis (scarring) & ...
    Treat complications as needed Needle biopsy of liver establishes pathologic process, within 5 years, 75% die of compli...
  Prognosis: Depends on course of cardiac disease       Cause of chronic heart failure is treated if possible inc. conjuga...
Primarily supportive, Correction of vitamin & mineral deficiencies, treat complications as needed Liver biopsy: history of...
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Hepatitis A,B,C,D,E,F,G, its treatment and management including its pathophysiology

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Hepatitis A,B,C,D,E,F,G, its prevention, management, medical treatment and its pathophysiology.

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  • Why was HBV generalized as occurring mostly in homosexuals? It's a discriminatory comment!
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  • this slide is vry helpful and i can undertand it vry well..thank u..
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Hepatitis A,B,C,D,E,F,G, its treatment and management including its pathophysiology

  1. 1. Viral Hepatitis,A,B,C,D,E,F,G and Liver problems Presented by: Dave Jay S. Manriquez RN.
  2. 2. Pathophysiology <ul><li>>pathophysiologic features are similar regardless of the cause </li></ul><ul><li>>hepatocytes undergo pathologic changes induced by the body’s immune response to the virus </li></ul>
  3. 4. Increased risk of hepatic cancer. Increased risk of chronic hepatitis, cirrhosis and hepatic cancer. Carrier state possible. No carrier state or increased risk of chronic hepatitis, cirrhosis or heaptic cancer. - - Similar to HAV except very severe in pregnant women. Similar to HBV but greater likelihood of carrier state, chronic active hepatitis, and cirrhosis. Frequent occurrence of chronic carrier state and chronic liver disease. May be severe. Fatality rate: 1%-10%. Usually mild with recovery. Fatality rate:<1%. Outcome Icteric phase: dark urine, jaundice of sclera and skin, tender liver May develop arthralgias, rash Preicteric phase: headache, malaise, fatigue, anorexia, fever - - Similar to HAV. Very severe in pregnant women Similar to HBV Similar to HBV; less severe and anicteric May occur with or without symptoms May occur with or without symptoms; flulike illness Signs and Symptoms Hygiene - Hygiene, sanitation; no immunity Hygiene; hepatitis B vaccine (active) Hygiene anti-HCV interferon alfa-2b in combination with ribavirin (Rebetol) Hygiene, avoidance of risk factors; HBIG (passive), recombinant hepatitis B vaccine (active), hepatitis B vaccine (passive) Hygiene; immune globulin (passive), inactivated hepatitis A vaccine (active) Prophylaxis and active or passive immunity Anti-HGV - Anti-HEV HDAg-positive (anti-HDV), HDV RNA serum Anti-HCV or anti-HDV, HCV RNA HBsAg, HBV-DNA, anti-HBc-IgM, HbeAg, anti HBsAg Anti-HAV-IgM-positive in acute hepatitis; IgG-positive after infection Diagnostic Tests Does not appear to cause liver disease - Illness self-limiting; mortality rate in pregnant women 10%-20% Similar to hepatitis B; more severe if occurs with chronic hepatitis B; increased risk of hepatocellular carcinoma Can lead to chronic hepatitis More serious, may be fatal Mortality low; rarely causes fulminating hepatic failure Severity Percutaneous - Fecal-oral route; food-or water-borne; no carrier state Co-infects with hepatitis B; close personal contact; carrier state Contact with blood and body fluids; source of infection uncertain in many clients; carrier state Most cases in United States now result from heterosexual transmission; contact with blood and body fluids; carrier state Infected feces, fecal-oral route; may be airborne if copious secretions; shellfish from contaminated water; no carrier state Transmission Health care workers in hemodialysis, IV drug users, hemodialysis clients, chronic hepatitis B or C clients - Traveling or living in areas where incidence is high Same as for Hepatitis B Similar to that for hepatitis B; also, IV drug use, intranasal cocaine use, body peircing, multiple sex partners Health care workers in contact with body secretions, blood, and blood products; hemodialysis and post-transfusion clients; homosexually active males and drug abusers Close personal contact or by handling feces-contaminated wastes; poor sanitation; people who work with animals from HAV endemic areas or who eat raw or steamed shellfish Risk factors/ High-risk groups - - 14-60 days; mean 40 days New cases now infrequent; same as for hepatitis B 6-7 weeks 6 weeks to 6 months; mean 12-14 weeks About 30 days Incubation Period Associated with chronic viremia lasting 10 years; rarely causes frank hepatitis Is rare and difficult to diagnose because of lack of testing methods Parts of Asia, Africa, India, and Mexico where there is poor sanitation Hepatitis D virus causes hepatitis only in association with hepatitis B virus and only in presence of HBsAg Post-transfusion, those working around blood and blood products, IV drug users; occurs all year World-wide, especially in drug addicts, homosexuals, people exposed to blood and blood products; occurs all year Epidemic in areas of poor sanitation; common in fall and early winter Occurrence Hepatitis G (HGV) Hepatitis F Hepatitis E (HEV) Hepatitis D (Delta Hepatitis) Hepatitis C (HCV) Hepatitis B (HBV) Hepatitis A (HAV) Factor Comparison of Seven Types of Viral Hepatitis
  4. 5. Hepatitis A <ul><li>HAV Hepatitis A virus; etiologic agent of Hep A (formerly infectious hepatitis) </li></ul><ul><li>Anti-HAV Antibody to hepatitis A; appears in serum soon after onset of symptoms; disappears after 3-12 mos </li></ul>
  5. 6. <ul><li>IgM anti-HAV IgM antibody to HAV; indicates recent infection with HAV; positive up to 6 mos after infection </li></ul>
  6. 7. <ul><li>HBV Hepatitis B virus; etiologic agent of Hep B (formerly serum hepatitis) </li></ul><ul><li>HBsAG </li></ul><ul><li>Hepatitis B surface antigen (Australian antigen); indicates acute acute or chronic hepatitis B or carrier state; indicates infectious state </li></ul>Hepatitis B
  7. 8. <ul><li>Anti-HBs </li></ul><ul><li>Antibody to hepatitis B surface antigen; indicates prior exposure and immunity to hepatitis; </li></ul><ul><li>May indicate passive antibody to HBIG or immune response from hepatitis B vaccine </li></ul><ul><li>HBeAG </li></ul><ul><li>Hepatitis B e-antigen; present in serum early in course; indicates highly infectious stage of hep B; Persistence in serum indicates progression to chronic hepatitis </li></ul>
  8. 9. Anti-HBe Antibody to hepatitis B e-antigen; suggests low titer of HBV HBcAg Hepatitis B core antigen; found in liver cells; not easily detected in serum
  9. 10. Anti-HBc Antibody to Hepatitis B core antigen; most sensitive indicator of Hep B; appears late in the acute phase of the disease;Indicates infection of HBV at some time in the past IgM anti-HBc IgM antibody to HBcAg; present for up to 6 mos after HBV infection
  10. 11. Hepatitis C HCV Hepatitis C virus (formerly non-A, non-B virus); may be more than 1 virus
  11. 12. Hepatitis D HDV Hepatitis D virus (delta agent); etiologic agent to hepatitis D; HBV required for replication HDAg Hepatitis delta antigen; detectable in early acute HDV infection
  12. 13. Anti-HDV Antibody to HDV; indicates past or present infection with HDV
  13. 14. Hepatitis E HEV Hepatitis E virus; etiologic agent of hep E
  14. 15. Hepatitis G HGV Hepatitis G virus; also known as GB virus C
  15. 16.   40-200 mg/24H (0.068-0.34mmol/24H) Fecal Urobilinogen   0.05-2.5mg024H (0.09-4.23 umol/24 H) Urine urobilinogen   0 Urine bilirubin   0-0.9 mg/dL (1.7-20.5 umol/L) Serum bilirubin, total These studies measure the ability of the liver to conjugate and excrete bilirubin. Results are abnormal in liver and biliary tract disease and are associated with jaundice clinically. 0-0.3 mg/dL (0-5.1 umol/L Serum bilirubin, direct Clinical Functions Normal Test
  16. 17. Albumin: Cirrhosis, Chronic Hepatitis, Edema, Ascites Globulin: Cirrhosis, Liver disease, Chronic obstructive jaundice viral heaptitis 0.4-1.2 g/dL α2-Globulin 0.1-0.4 g/dL α1-Globulin   Albumin 3.2-5.6 g/dL Serum protein electrophoresis 1.5-3.0 g/dL Serum globulin 3.5-5.5 g/dL Serum albumin             Proteins are manufactured by the liver. Their levels may be affected in a variety of liver impairments. 7.0-7.5 g/dL (70-75g/L) Total serum protein Protein Studies
  17. 18. Serum alkaline phosphatase is manufactured in bones, liver, kidneys and intestine andexcreted through biliary tract. In absence of bone disease, it is a sensitive measure of biliary tract obstruction. 30-50 IU/L @ 34°C     Varies with method; 2-5 Bodansky units Serum alkaline phosphatase Prothrombin time may be prolonged in liver disease. It will not return to normal with Vitamin K in severe liver cell damage. 100% or 12-16 sec Prothrombin time A/G ratio is reversed in chronic liver disease (decreased albumin and increased globulin) A>G or 1.5:1-1-2.5:1 Albumin/globulin (A/G ratio) 0.5-1.6 g/dL γ-Globulin 0.5-1.1 g/dL β-Globulin
  18. 19.       150-250 mg/dL     Liver converts ammoniato urea. Ammonia level rises in liver failure. 20-120 ug/dL Serum ammonia   100-200 units (100-225 U/L) LDH Elevated in alcohol abuse. Marker for biliary cholestasis. 10-48 U/L GGT, GGTP         5-35 units (2.4-17 U/L) ALT, SGPT The studies are based on release on enzymes from damaged liver cells. These enzymes are elevated in liver cell damage. 10-40 units (4.8-19 U/L) AST, SGOT     Serum Aminotransferase or Transaminase Studies
  19. 20.   LDL <130ug/dL LDL (low-density lipoprotein)   Female: 35-85 mg/dL     Male: 35-70 mg/dL HDL (high-density lipoprotein) Cholesterol levels are elevated in biliary obstruction and decreased in parenchymal liver disease. 60% of total (fraction of total cholesterol:0.60) Ester   Cholesterol
  20. 21. To determine adequacy of portal blood flow Splenoportogram (splenic portal venography) For liver nad pancreas visualization Celiac axis arteriography For gallbladder and bile duct visualization Cholecystogram and cholangiogram To show size and shape of liver; to show replacement of liver tissue with scars, cyst or tumor Liver scan with radiotagged iodinated rose bengal, gold, technetium, or gallium To determine gross liver size Abdominal x-ray For varices, which indicates increased portal pressure Barium study of esophagus           Additional Studies
  21. 22.   To detect hepatic neoplasms; diagnose cysts, abscesses and hematomas; and distinguish between ostructive nad nonobstructive jaundice.Detects cerebral atrophy in hepatic encephalopathy. Computed Tomography (CT scan) To show size of abdominla organs and presence of masses Ultrasonography Abnormal in hepatic coma and impending hepatic coma Electroencephalogram Elevated in cirrhosis of the liver Measurement of portal pressure To determine anatomic changes in liver tissue Liver biopsy ( percutaneous or transjugular) Direct visualization of anterior surface of liver, gallbladder and mesentery through a trocar Laparoscopy
  22. 23. Visualizes biliary structures via endoscopy. Endoscopic retrograde cholangiopancreatography (ERCP) To detect hepatic neoplasms; diagnose cysts, abscesses, and hematomas. Detects cerebral atrophy in encephalopathy. Magnetic Resonance Imaging Visualizes hepatic circulation and detects presence andnature of hepatic masses Angiography
  23. 24. <ul><li>Complications </li></ul><ul><li>Fulminant Hepatitis (massive hepatic necrosis) </li></ul><ul><ul><li>rare; seen primarily in hepatitis B & D as well as in hepatitis A & E </li></ul></ul><ul><ul><li>causes severe illness & is fatal in 1%-2% of all cases & up to 20% of cases occurring in pregnant women </li></ul></ul><ul><ul><li>involves a progression of manifestations that include jaundice, hepatic encephalopathy and ascites </li></ul></ul><ul><ul><li>mortality rate varies with age: 90%-100% esp in people over 60 yo </li></ul></ul>
  24. 25. <ul><li>Chronic Hepatitis </li></ul><ul><ul><li>exists when liver inflammation continues beyond a period of 3-6 mos </li></ul></ul><ul><ul><li>causes: Viral Hep B(& with superimposed hep D), C, drugs & toxins(methyldopa, nitrofurantoin, amiodarone, isoniazid), autoimmune, genetic & metabolic disorders (Wilson’sdse, nonalcoholic steatohepatitis) </li></ul></ul>
  25. 26. Primary Hepatocellular Cancer Etiology: Hep B, Hep C, cirrhosis, chronic liver disease, hemochromatosis, ingestion of certain mycotoxins (aflatoxins), anabolic steroid use, & long-term androgen therapy -treatment: surgical resection of tumor ( if it’s confined to 1 lobe) -after dx, if intervention fails- client usually dies of hepatic failure within 3-6 mos
  26. 27. Hepatic Encephalopathy -Occurs with profound liver failure and may result from the accumulation of ammonia and other toxic metabolites in the blood Hepatic coma -most advanced stage of heaptic encephalopathy - cause: false neurotransmitter but the exact mechanism is not fully understood
  27. 28. <ul><li>Autoimmune Hepatitis </li></ul><ul><li>Characterized by hepatic inflammation with plasma cells & fibrosis </li></ul><ul><li>Generally a disease of young women but can occur in either gender at any age </li></ul><ul><li>25% od cases present as an acute attack of hepatitis or follow a viral illness i.e. Hep A, Epstein-Barr infection,or measles or exposure to a drug or toxin </li></ul><ul><li>CM: multiple spider nevi, acne, hirsutism, hepatomegaly </li></ul><ul><li>Extrahepatic manifestations: arthritis, thyroiditis, nephritis, ulcerative colitis, & Coombs’ positive Hemolytic anemia </li></ul>
  28. 29. Aplastic Anemia -rare; carries a high mortality rate when it occurs after acute viral hepatitis Mgt: supportive & palliative
  29. 30. <ul><li>Cirrhosis </li></ul><ul><ul><li>- chronic, progressive disease characterized by widespread fibrosis (scarring) & nodule formation </li></ul></ul><ul><ul><li>occurs when normal flow of blood, bile & hepatic metabolites is altered by fibrosis & changes in the hepatocytes, bile ductules, vascular channels & reticular cells </li></ul></ul>
  30. 31.     Treat complications as needed Needle biopsy of liver establishes pathologic process, within 5 years, 75% die of complications Increased aminotransferases increased gamma globulins As in alcoholic cirrhosis except less muscle wadting & more jaundice     Liver small & nodular     Post-acute viral (types B & C Hepatitis Postintoxication with industrial chemicals Some infections and metabolic disorders Most common worldwide Massive loss of liver cells, with irregular patterns of regenerating cells             Postnecrotic (Macronodular) Cirrhosis Intervention Diagnosis & Prognosis Assessment Data Pathology Etiology Definition
  31. 32.   Prognosis: Depends on course of cardiac disease       Cause of chronic heart failure is treated if possible inc. conjugate dbilirubin in serum, inc. sulfobromophthalein, dec. albumin in serum, inc. serum aminotransferases, inc. alkaline phosphatase, liver biopsy Slight jaundice, enlarged liver & ascites in person with severe cardiac impairment over 10-yr span, RUQ pain during acute congestion, cachexia, fluid retention, circulatory problems Early: Dark-colored liver enlarged by blood and edema fluid Late: Liver capsule thickens and nodular scarring occurs Atrioventricular valve disease, Prolonged constrictive pericarditis, Decompensated cor pulmonale Chronic liver disease asso. with severe right-sided long-term heart failre(fairly rare)           Cardiac Cirrhosis
  32. 33. Primarily supportive, Correction of vitamin & mineral deficiencies, treat complications as needed Liver biopsy: history of alcohol abuse, high AST, high bilirubin (slight), anemia, Prognosis: depends on presence of complications and continued abuse of alcohol May produce no symptoms for long periods, onset of symptoms may be insidious or abrupt Early: Weakness, fatigue, weight loss Later: Anorexia, nausea & vomiting Abdominal pain, ascites, menstrual irregularities, impotence, enlarged breasts in men, hematemesis, spider angiomas Scarring & collagen tissue deposits, regenerating nodules are very small, normal lobular structure is destroyed   Associated with alcohol abuse   Alcoholic Cirrhosis(Laennec's, micronodular) Small nodules form as a result of persistence of some offending agent           Alcoholic Cirrhosis

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