Chapter 38: Liver Diseases Flashcards
1
Q
Acute Viral Hepatitis
A
- Inflammation of the liver parenchyma
- caused by many viruses (cytomegalovirus, Epstein-Barr)
- “viral hepatitis” (Hepatitis A, B, C, D, & E)
2
Q
Hepatitis A (HAV)
A
- RNA virus spread by fecal-oral route
- Also called enteric hepatitis
- 2- to 7-week incubation period
- Prodromal period (Jaundice, RUQ pain. malaise, anorexia, nausea, low-grade fever, children may not experience jaundice)
- Followed by jaundice lasting approx 2 weeks
- Self-limited course
- Serologic Testing (Anti-HAV IgG (previous infection), IgM (acute infection))
- Treatment is supportive (rest, nutritious diet) and includes avoiding ETOH, acetaminophen, and hepatotoxins
- Prevention includes careful hand washing, segregation, cleaning of laundry and personal items, and immunization with y-globulin
3
Q
Hepatitis B (HBV)
A
- Partially double-stranded DNA virus
- Spread by parenteral contact with infected blood or blood products (Includes contaminated needles and sexual contact)
- Also called serum hepatitis
- 300 million (5%) of world population have chronic infection
- 1 to 1.25 million in United States
- Risk factors include Perinatal, health care settings (3%); transfusions and dialysis (1%); acupuncture, tattooing, extended overseas travel, residence in an institution
- Incubation period of 2 to 6 months
- Prodromal period that includes Asymptomatic or rashes, arthralgia, arthritis, angioedema, serum sickness, glomerulonephritis, jaundice (lasting 2 weeks on average)
4
Q
Serologic Testing of Hepatitis B (HBV)
A
- Surface antigen (HBsAg): early/active and chronic infection
- Surface antibody (HbsAb): resolution and immunity
- Core antigen (HBcAg): appears first in active infection
- Core antibody (HBcAb): seroconversion
- Hepatitis B e antigen (HBeAg): viral replication and infectivity
5
Q
Treatment of Hepatitis B (HBV)
A
- Persons with detectable virus and HBeAg positive readily transmit virus to their contacts, and should be counseled
- Supportive: Most nonfulminant infections resolve spontaneously. about 5% progress to chronic infection
- Liver transplant
- Interferon-alpha (24 to 48 weeks of therapy, Response rate of 33%)
- Lamivudine, Telbivudine
- Adefovir, Tenofovir
- Entecavir (TREATMENT OF CHOICE) (Response rate of 67%, Extremely expensive)
6
Q
Prevention of Hepatitis B (HBV)
A
- Immunizations (Doses given at 0, 1, and 6 months, 95% response rate, recommended as part of the childhood vaccination regimen and for high-risk individuals, and after exposure)
- Administration of HBIG postinoculation
- ^ Contains high levels of hepatitis B surface antibody
- ^ Given within 7 days of exposure
- ^ Indications include Neonates born to HBsAg-positive mothers, Prophylaxis after needlestick or sexual exposure in nonimmune persons, and After liver transplantation in patients who are HBsAg+ prior to transplantation
7
Q
Hepatitis C (HCV)
A
- Single-stranded RNA virus (Flavivirus)
- Spread through IV drug use or blood transfusions prior to 1990
- Also called non-A, non-B hepatitis
- 3% worldwide infected
- Have 6 types (Type 1: most common in the United States but has a lower response rate to treatment; Types 2 and 3: common in N. America; Types 4 to 6: common overseas)
8
Q
Acute and Chronic Hepatitis C (HCV)
A
- Acute HCV infection (Usually asymptomatic; Course is erratic with wide fluctuations on liver enzymes)
- Chronic HCV infection (Usually asymptomatic until advanced liver disease intervenes; Most common cause of end-stage liver disease with cirrhosis)
9
Q
Treatment for Acute Hepatitis C (HCV)
A
- Supportive and expectant
- Early treatment not recommended (20% to 40% of acute seropositive patients will convert to seronegativity and an undetectable viral load during 1st 6 months after infection; Immune globulin is not helpful in preventing infection
10
Q
Treatment for Chronic Hepatitis C (HCV)
A
- Assessed by a viral load and viral genotype
- Liver biopsy to stage disease activity
- Pegylated interferon-alpha with ribavirin and protease inhibitor (5% to 10% drop out of treatment because of side effects and cost (expensive); Type 1: 48 weeks; Other types: 24 weeks)
- Vaccinate against hepatitis A and B
- Counsel regarding blood-borne precautions
- Centers for Disease Control and Prevention does not currently recommend barrier methods for patients with long-term sexual partners because of the apparent low risk of infection
11
Q
Hepatitis D (Delta)
A
- Defective RNA virus that requires the helper function of
HBV to replicate - Infection appears to accelerate and worsen HBV infection symptoms
- Prevention of HBV infection also prevents HDV infection
- Transmitted parenterally and intimate contact
12
Q
Diagnosis and Prevention of Hepatitis D
A
- Diagnoisis: Anti-HDV IgM and IgG enzyme linked immunosorbent assay (ELISA)
- Prevention: Safe sexual practices, Avoidance of IV drug use, Vaccination of susceptible persons with HBV vaccine
- No specific treatment
13
Q
Hepatitis E (HEV)
A
- RNA virus spread via fecal-oral route (Contaminated H2O and
Parenteral transmission) - Most common in developing countries or recent travel to these areas
- Relatively high mortality rate in pregnant women
- Incubation period is 2 to 9 weeks
- Prodromal and icteric illness (Usually last only 2 weeks;
Similar to HAV infection) - Supportive treatment
- Prevention Includes Careful hand washing, Avoidance of undercooked foods, and Drinking safe H2O and beverages
14
Q
Chronic Hepatitis
A
- Group of diseases characterized by inflammation of the liver that lasts 6 months or longer
- Causes include Autoimmune disease, Viral hepatitis (B and C), Toxins, Metabolic diseases
- Pathogenesis includes Chronic low-grade liver inflammation of any cause (also called “triaditis” or “transaminitis”) and Inflammation confined to portal triads without destruction of normal liver structures
- Clinical Manifestations are Asymptomatic or mild, nonspecific symptoms
- Treatment: No drug treatment needed; excellent prognosis
15
Q
Chronic Active Hepatitis
A
- Progressive, destructive inflammatory disease of the liver lasting >6 months (Extends beyond the portal triad to hepatic lobule (piecemeal necrosis)
- May progress to cirrhosis
- clinical manifestations include Fatigue, malaise, nausea, anorexia, ascites, hepatomegaly, abdominal pain, and jaundice
- Laboratory diagnosis looks for abnormal liver enzymes and serologic studies
- Liver Biopsy confirms diagnosis, and grading and staging
- treatment depends on cause