Viral Hepatitis,A,B,C,D,E,F,G and Liver problems

Presented by: Dave Jay S. Manriquez RN.

Pathophysiology
>pathophysiologic features are similar regardless of the cause >hepatocytes undergo pathologic changes induced by the bodys immune response to the virus

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Factor
Occurrence

Hepatitis A (HAV)

Hepatitis B (HBV)

Hepatitis C (HCV) Hepatitis D (Delta Hepatitis)

Post-transfusion, Hepatitis D virus causes those working around hepatitis only in association blood and blood with hepatitis B virus and products, IV drug only in presence of HBsAg users; occurs all year

Hepatitis E (HEV)
Parts of Asia, Africa, India, and Mexico where there is poor sanitation

Hepatitis F

Hepatitis G (HGV)

Epidemic in areas of poor World-wide, especially sanitation; common in fall in drug addicts, and early winter homosexuals, people exposed to blood and blood products; occurs all year

Is rare and difficultAssociated with to diagnose chronic viremia because of lack of lasting 10 years; testing methods rarely causes frank hepatitis

Incubation Period

About 30 days

6 weeks to 6 months; mean 12-14 weeks

6-7 weeks

New cases now infrequent; 14-60 days; mean same as for hepatitis B 40 days Traveling or living in areas where incidence is high

Risk factors/ Close personal contact or Health care workers in High-risk groups by handling fecescontact with body contaminated wastes; secretions, blood, and poor sanitation; people blood products; who work with animals hemodialysis and postfrom HAV endemic areas transfusion clients; or who eat raw or homosexually active steamed shellfish males and drug abusers

Similar to that for Same as for Hepatitis B hepatitis B; also, IV drug use, intranasal cocaine use, body peircing, multiple sex partners

Health care workers in hemodialysis, IV drug users, hemodialysis clients, chronic hepatitis B or C clients

Transmission

Infected feces, fecal-oral route; may be airborne if copious secretions; shellfish from contaminated water; no carrier state

Most cases in United States now result from heterosexual transmission; contact with blood and body fluids; carrier state

Contact with blood and body fluids; source of infection uncertain in many clients; carrier state

Co-infects with hepatitis B; close personal contact; carrier state

Fecal-oral route; food-or waterborne; no carrier state

Percutaneous

Severity

Mortality low; rarely causes fulminating hepatic failure

More serious, may be Can lead to chronic fatal hepatitis

Similar to hepatitis B; more severe if occurs with chronic hepatitis B; increased risk of hepatocellular carcinoma

Illness self-limiting; mortality rate in pregnant women 10%-20%

Does not appear to cause liver disease

Diagnostic TestsAnti-HAV-IgM-positive in HBsAg, HBV-DNA, anti-Anti-HCV or antiacute hepatitis; IgGHBc-IgM, HbeAg, anti HDV, HCV RNA positive after infection HBsAg Prophylaxis and Hygiene; immune active or passiveglobulin (passive), immunity inactivated hepatitis A vaccine (active) Hygiene, avoidance of risk factors; HBIG (passive), recombinant hepatitis B vaccine (active), hepatitis B Hygiene anti-HCV interferon alfa-2b in combination with ribavirin (Rebetol)

HDAg-positive (anti-HDV), HDV RNA serum

Anti-HEV

Anti-HGV

Hygiene; hepatitis B vaccine Hygiene, (active) sanitation; no immunity

Hygiene

Hepatitis A
HAV Hepatitis A virus; etiologic agent of Hep A (formerly infectious hepatitis) Anti-HAV Antibody to hepatitis A; appears in serum soon after onset of symptoms; disappears after 3-12 mos

 IgM anti-HAV IgM antibody to HAV; indicates recent infection with HAV; positive up to 6 mos after infection

Hepatitis B
HBV Hepatitis B virus; etiologic agent of Hep B (formerly serum hepatitis) HBsAG Hepatitis B surface antigen (Australian antigen); indicates acute acute or chronic hepatitis B or carrier state; indicates infectious state

 Anti-HBs Antibody to hepatitis B surface antigen; indicates prior exposure and immunity to hepatitis; May indicate passive antibody to HBIG or immune response from hepatitis B vaccine HBeAG 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

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

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

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 Hepatitis delta antigen; detectable in early acute HDV infection

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

Test

Normal

Clinical Functions

Serum bilirubin, direct

0-0.3 mg/dL (0-5.1 umol/L

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.

Serum bilirubin, total Urine bilirubin Urine urobilinogen

0-0.9 mg/dL (1.7-20.5 umol/L) 0 0.05-2.5mg024H (0.09-4.23 umol/24 H) 40-200 mg/24H (0.068-0.34mmol/24H)

Fecal Urobilinogen

Protein Studies Total serum protein 7.0-7.5 g/dL (7075g/L) Serum albumin Serum globulin Serum protein electrophoresis Albumin 1-Globulin 3.5-5.5 g/dL 1.5-3.0 g/dL 3.2-5.6 g/dL 0.1-0.4 g/dL Proteins are manufactured by the liver. Their levels may be affected in a variety of liver impairments. Albumin: Cirrhosis, Chronic Hepatitis, Edema, Ascites Globulin: Cirrhosis, Liver disease, Chronic obstructive jaundice viral heaptitis

2-Globulin

0.4-1.2 g/dL

-Globulin -Globulin Albumin/globulin (A/G ratio)

0.5-1.1 g/dL 0.5-1.6 g/dL A>G or 1.5:1-1-2.5:1 A/G ratio is reversed in chronic liver disease (decreased albumin and increased globulin) Prothrombin time may be prolonged in liver disease. It will not return to normal with Vitamin K in severe liver cell damage. 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.

Prothrombin time

100% or 12-16 sec

Serum alkaline phosphatase

Varies with method; 2-5 Bodansky units 30-50 IU/L @ 34C

Serum Aminotransferase or Transaminase Studies AST, SGOT

10-40 units (4.8-19 U/L)

The studies are based on release on enzymes from damaged liver cells. These enzymes are elevated in liver cell damage. Elevated in alcohol abuse. Marker for biliary cholestasis. Liver converts ammoniato urea. Ammonia level rises in liver failure.

ALT, SGPT GGT, GGTP

5-35 units (2.4-17 U/L) 10-48 U/L

LDH Serum ammonia

100-200 units (100-225 U/L) 20-120 ug/dL

150-250 mg/dL

Cholesterol

Ester

60% of total (fraction Cholesterol levels are of total elevated in biliary cholesterol:0.60) obstruction and decreased in parenchymal liver disease. Male: 35-70 mg/dL

HDL (high-density lipoprotein) LDL (low-density lipoprotein)

Female: 35-85 mg/dL LDL <130ug/dL

Additional Studies

For varices, which indicates increased portal pressure To determine gross liver size To show size and shape of liver; to show replacement of liver tissue with scars, cyst or tumor

Barium study of esophagus Abdominal x-ray Liver scan with radiotagged iodinated rose bengal, gold, technetium, or gallium Cholecystogram and cholangiogram

For gallbladder and bile duct visualization

Celiac axis arteriographyFor liver nad pancreas visualization Splenoportogram (splenic portal venography) To determine adequacy of portal blood flow

Laparoscopy Liver biopsy ( percutaneous or transjugular) Measurement of portal pressure Electroencephalogram Ultrasonography

Direct visualization of anterior surface of liver, gallbladder and mesentery through a trocar To determine anatomic changes in liver tissue

Elevated in cirrhosis of the liver Abnormal in hepatic coma and impending hepatic coma To show size of abdominla organs and presence of masses

Computed Tomography To detect hepatic (CT scan) neoplasms; diagnose cysts, abscesses and hematomas; and distinguish between ostructive nad nonobstructive jaundice.Detects cerebral atrophy in hepatic encephalopathy.

Angiography

Visualizes hepatic circulation and detects presence andnature of hepatic masses

Magnetic Resonance Imaging

To detect hepatic neoplasms; diagnose cysts, abscesses, and hematomas. Detects cerebral atrophy in encephalopathy.

Endoscopic Visualizes biliary structures via endoscopy. retrograde cholangiopancreat ography (ERCP)

Complications

Fulminant Hepatitis (massive hepatic necrosis) rare; seen primarily in hepatitis B & D as well as in hepatitis A & E causes severe illness & is fatal in 1%-2% of all cases & up to 20% of cases occurring in pregnant women involves a progression of manifestations that include jaundice, hepatic encephalopathy and ascites mortality rate varies with age: 90%-100% esp in people over 60 yo

Chronic Hepatitis

exists when liver inflammation continues beyond a period of 3-6 mos causes: Viral Hep B(& with superimposed hep D), C, drugs & toxins(methyldopa, nitrofurantoin, amiodarone, isoniazid), autoimmune, genetic & metabolic disorders (Wilsonsdse, nonalcoholic steatohepatitis)

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 its confined to 1 lobe) -after dx, if intervention fails- client usually dies of hepatic failure within 3-6 mos

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

Autoimmune Hepatitis
-Characterized by hepatic inflammation with plasma cells & fibrosis -Generally a disease of young women but can occur in either gender at any age -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 -CM: multiple spider nevi, acne, hirsutism, hepatomegaly -Extrahepatic manifestations: arthritis, thyroiditis, nephritis, ulcerative colitis, & Coombs positive Hemolytic anemia

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

Cirrhosis
- chronic, progressive disease characterized by widespread fibrosis (scarring) & nodule formation occurs when normal flow of blood, bile & hepatic metabolites is altered by fibrosis & changes in the hepatocytes, bile ductules, vascular channels & reticular cells

Definition

Etiology

Pathology

Assessment Diagnosis & Intervention Data Prognosis

Postnecroti c (Macronod ular) Cirrhosis Most Post-acute common viral (types worldwide B&C Massive loss Hepatitis of liver cells, Postintoxica with irregular tion with patterns of industrial regenerating chemicals cells Some infections and metabolic disorders

Liver small & nodular

As in Needle biopsy Treat alcoholic of liver complications cirrhosis establishes as needed except less pathologic muscle process, wadting & within 5 more years, 75% jaundice die of complications Increased aminotransfer ases increased gamma globulins

Cardiac Cirrhosis

Cause of chronic heart failure is treated if possible

Chronic liver Atrioventric Early: DarkSlight inc. conjugate disease asso. ular valve colored liver jaundice, dbilirubin in with severe disease, enlarged by blood enlarged liver serum, inc. right-sided Prolonged and edema fluid & ascites in sulfobromopht long-term constrictive Late: Liver person with halein, dec. heart pericarditis, capsule thickens severe albumin in failre(fairly Decompens and nodular cardiac serum, inc. rare) ated cor scarring occurs impairment serum pulmonale over 10-yr aminotransfer span, RUQ ases, inc. pain during alkaline acute phosphatase, congestion, liver biopsy cachexia, fluid retention, circulatory problems Prognosis: Depends on course of cardiac disease

Alcoholic Cirrhosis

Liver biopsy: history of alcohol abuse, high AST, high bilirubin (slight), anemia, Prognosis: depends on presence of complications and continued abuse of alcohol

Primarily supportive, Correction of vitamin & mineral deficiencie s, treat complicati ons as needed

Alcoholic Associated Scarring & collagen May produce Cirrhosis(Laen with alcohol tissue deposits, no symptoms nec's, abuse regenerating for long micronodular) nodules are very periods, onset Small nodules small, normal of symptoms form as a lobular structure is may be result of destroyed insidious or persistence of abrupt some Early: offending Weakness, agent fatigue, weight loss Later: Anorexia, nausea & vomiting Abdominal pain, ascites, menstrual irregularities, impotence, enlarged breasts in men, hematemesis, spider angiomas