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

1. Viral Hepatitis,A,B,C,D,E,F,G and Liver problems Presented by: Dave Jay S. Manriquez RN.

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

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

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

11. Hepatitis C HCV Hepatitis C virus (formerly non-A, non-B virus); may be more than 1 virus

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

13. Anti-HDV Antibody to HDV; indicates past or present infection with HDV

14. Hepatitis E HEV Hepatitis E virus; etiologic agent of hep E

15. Hepatitis G HGV Hepatitis G virus; also known as GB virus C

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

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

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

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

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

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

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

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

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

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

29. Aplastic Anemia -rare; carries a high mortality rate when it occurs after acute viral hepatitis Mgt: supportive & palliative

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

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

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