Module 6.2 - Liver Disease Flashcards
What is hepatitis?
- An inflammation of the liver that can be caused by toxins, medications, and viruses
- Initially screened for by performing liver function tests , specifically ALTand AST in response to presenting symptoms
What causes Hepatitis A?
- Transmitted fecal-oral route, including contaminated food sources, water and shellfish
- Poor sanitation and crowding facilitates spread of virus
- Maximum infectivity occurs 2 weeks before symptoms of clinical illness
- Mortality rate is low and fulminant hepatitis A is uncommon
How is Hepatitis A diagnosed?
- IgM anti-HAV – excellent diagnostic test; occurs during the first week of clinical disease
- IgG anti-HAV – appears as IgM anti-HAV declines (within 3-6 months) and persists for years, conferring long-term immunity; an effective vaccine is available.
How is hepatitis A managed?
- Supportive care- bed rest until jaundice resolves, no heavy lifting/activity
- High-calorie diet- small, frequent meals with supplements, low protein, high carbohydrates, no fatty foods
- Avoid potentially hepatotoxic medications
- Alcohol restriction
- Hospitalization only if fulminant hepatic failure is suspected ( encephalopathy and severe coagulopathy)
- Anti-emetics for nausea and vomiting
What vaccinations are available for hepatitis A?
- Hepatitis A vaccine – consists of inactivated HAV
- Recommended for all children 1 year of age and older.
What causes Hepatitis B?
- Blood-borne virus; present in saliva, semen and vaginal secretions
- Over 2 billion people worldwide infection with 400million having chronic infections
Mode of transmission varies geographically-
- High-prevalence areas (Asia, Africa)- mainly during childbirth
- Intermediate-prevalence regions (Southern and Easter Europe) – mainly through trauma
- Low-prevalence regions (US and Western Europe)- mainly through IV drug abuse and unprotected intercourse
Who is at high risk for hepatitis B infection?
- Persons with HIV or HCV
- Injection drug users
- Men who have sex with men
- Individuals with multiple sexual partners or a history of sexually transmitted diseases
- Hemodialysis patients
- Inmates of correctional facilities
- From a region with high or intermediate prevalence rates
- Persons needing immunosuppressive therapy
- All pregnant women
- Individuals with chronically elevated ALT or AST
How is Hepatitis B diagnosed?
Diagnosis of HBV infection can be made through serologic detection of Hepatitis B surface antigen (HBsAg), hepatitis B core antigen (HBcAg), and Hepatitis B surface antibody (anti-HBs).
How do patients’s susceptible to Hepatitis B serologically present?
- Anti-HBc: Negative
- Anti-HBs: Negative
How do patients who are immune to Hepatitis B due to natural infection serologically present?
- HBsAg: Negative
- Anti-Hbc: Positive
- Anti-HBs: Positive
How do patients who are immune to Hepatitis B due to HBV Vaccination serologically present?
- HBsAg Negative
- Anti-HBc Negative
- HBsAg Negative
- Anti-HBs Positive
How do patients who are actively infected with Hepatitis B serologically present?
- HBsAg Positive
- Anti-HBc Positive
- IgM anti-HBc Positive
- Anti-HBs Negative
How do patients who are chronically infected with Hepatitis B serologically present?
- HBsAg Positive
- Anti-HBc Positive
- IgM anti-HBc Negative
- Anti-Hbs Negative
When is treatment for hepatitis B initiated?
- Treatment of chronic HBV is indicated if risk of liver-related morbidity or mortality in 5-10 years and the likelihood of achieving viral suppression are high
- Treatment is NOT indicated if the risk of liver-related morbidity or mortality in the next 20 years and the likelihood of achieving viral suppression are low.
- Considerations for safety, efficacy and cost should be taken when choosing anti-viral therapy
What are the treatment options for Hepatitis B?
1st line therapy:
- Peg interferon alpha: 180mcg SQ weekly x 48 weeks; many side effects; efficacy is limited
- Entecavir: 0.5-1 mg po daily; adjust dose for renal impairment
- Tenofovir: 300mg po daily
2nd line therapy:
- Adefovir: 10mg po daily; adjust does in renal impairment; less potent than other agents and linked to increasing rate of antiviral resistance; use as 2nd line drug following 1st year of therapy
- Lamivudine: 100mg po daily; not preferred due to resistance; adjust dose in renal impairment
- Telbivudine: 600mg po daily; renal impairment dosing; not preferred due to resistance
- Can be complicated by cirrhosis or hepatocellular carcinoma necessitating consideration for liver transplantation*
- Periodic testing of alpha-fetoprotein (AFP) levels and an ultrasound of the liver should be performed in patients with chronic HBV to monitor for hepatocellular carcinoma*
How does the hepatitis B vaccination work?
- Vaccine contains HBsAg, the primary antigenic protein in the viral envelope
- Promotes synthesis of specific antibodies directed against HBV
- Vaccines are made from a viral component rather than from a live virus; therefore, cannot cause disease.
- Vaccines administered in 3 doses (1st dose, 2nd dose one month later, 3rd dose 6 months later)
- Post exposure prophylaxis with immune globulin can be used to prevent HBV infection (perinatal transmission, needle sticks, etc.).
Who is at risk for Hepatitis C infection?
- HCV is a blood borne virus
- Primary risk groups are IV drug abusers; risk of sexual and perinatal transmission is small.
- Most people are asymptomatic, so they are unaware of infection
How is hepatitis C diagnosed?
- Anti-HCV (anti HCV antibody) – first line test for detection of HCV
- HCV PCR used to confirm HCV infection- gold standard for confirmation of infection; detects actual virus, not antibodies, differentiates between prior exposure from current viremia
What are the signs and symptoms associated with hepatitis?
Prodromal phase:
- Malaise, myalgia, arthralgia, fatigue
- Upper respiratory symptoms
- Anorexia, nausea/vomiting
- Diarrhea or constipation may occur
- Aversion to smoking (HBV)
- Skin rashes, arthritis, serum sickness in early HBV
- Fever (<103F, 39.5C)- more common in HAV
- Mild, constant RUQ abdominal pain/mid-epigastrium pain- aggravated by exertion
Icteric phase:
- Clinical jaundice occurs 5-10 days after prodromal phase- but can occur earlier
- Most patients never develop clinical icterus
- Prodromal symptoms usually worsen with the onset of jaundice
- Dark urine and clay-colored stools
Define chronic hepatitis
Chronic hepatitis is defined as symptomatic disease (fatigue, malaise, jaundice) with biochemical or serologic evidence of ongoing hepatic damage for more than 6 months.
What is fulminant hepatitis?
Defined by hepatic insufficiency with hepatic encephalopathy occurring within 2-3 weeks after symptoms onset; viral hepatitis accounts for 12% of fulminant liver failure; more than half the cases are due to drug or chemical toxicities; mortality rate is 80% without transplantation and 35% with transplantation.
What causes autoimmune hepatitis?
- A chronic, progressive hepatitis attributed to T-cell mediated autoimmunity (T-cell mediated immune attack of the liver)
- AIH can be triggered by viral infections or drugs, or it may be a component of other autoimmune disorders (rheumatoid arthritis, Sjogren syndrome, ulcerative colitis, etc.)
- Women (78% of cases) more frequently affected than men
What is Non-alcoholic Fatty Liver Disease (NALFD)?
Non-alcoholic fatty liver disease (NAFLD) is a group of disorders characterized by hepatic steatosis in the absence of heavy alcohol consumption, medication or hereditary disorders. There is presence of steatosis with NO evidence of hepatocellular injury in the form of ballooning of hepatocytes.
- Increased incidence in U.S. due to increasing prevalence of obesity
- 70% of overweight individuals have some form of NAFLD.
- Probably a consequence of hepatocyte fat accumulation and increased hepatic oxidative stress, leading to increased lipid peroxidation and ROS generation.
What is Non-alcoholic Steatohepatitis (NASH)?
- Type of NALFD- the most pathologic disorder of the group
- Presents WITH steatosis PLUS hepatocytes damage and inflammation.
- Progresses to cirrhosis in 10-20% of cases
- Strongly associated with the metabolic syndrome of dyslipidemia, hyperinsulinemia and insulin resistance.
- Patients frequently asymptomatic; some experience fatigue, RUQ discomfort, malaise.
How is Non-alcoholic Steatohepatitis (NASH) diagnosed?
- Elevated Serum aminotransferase levels present
- Imaging ( U/S, CT scan or MRI) can be used as initial screening tests, but are not reliable to determining steatohepatitis or fibrosis
- Liver biopsy – The gold standard test to determine if hepatic inflammation or fibrosis is present.
How is Non-alcoholic Steatohepatitis (NASH) managed?
- Lifestyle intervention - weight loss and exercise with the recommendation of losing at least 10% of body weight.
- Medications: Vitamin E 800 IU/day has been shown to improve liver histology in non-diabetic patients with biopsy-proven NASH.
- Treatment is targeted at correcting the associated obesity, hyperlipidemia and insulin resistance.
- May lead to cirrhosis and need for liver transplantation.
What is Hereditary Hemochromatosis?
- It is a homozygous recessive heritable disorder caused by excessive iron absorption; characterized by excessive iron accumulation in the parenchymal cells of various organs, particularly liver and pancreas- tissue damage is attributed to direct iron toxicity.
- Most common genetic disorder in Caucasians; more prevalent in northern European origin (especially Nordic or Celtic ancestry)
- Genetic predisposition increases the inappropriate absorption of dietary iron that can lead to cirrhosis, hepatocellular carcinoma, diabetes and heart disease.
What is and what causes Wilson Disease?
- A familial autosomal recessive disorder causing copper to be accumulated in the liver, which results in hepatic injury through ROS generation; lethal if not treated.
- Eventually copper is released into the bloodstream and deposited in brain, kidneys and corneas.
- Nearly all patients with neurological involvement will develop eye lesions, called Kayser-Fleischer rings- green-brown copper deposits in Descemet’s membrane of the corneal limbus.
