Chapter 31_2 flashcards
(19 cards)
Hepatitis A Virus (HAV): Transmission & Course
Transmission: Fecal-oral route (contaminated food/water). Course: Acute, self-limiting illness. Does not become chronic. A vaccine is available.
Hepatitis B Virus (HBV): Transmission & Course
Transmission: Blood, body fluids, sexual contact. Course: Can be acute or progress to chronic infection (90% of infants, 5% of adults). Chronic infection increases risk for cirrhosis and hepatocellular cancer. A vaccine is available.
HBV Diagnosis: Key Serology Markers
HBsAg (Hepatitis B surface antigen): Indicates active infection. Anti-HBs (Antibody to HBsAg): Indicates immunity from vaccination or prior infection. Anti-HBc (Antibody to core antigen): IgM indicates acute infection; IgG indicates chronic/past infection.
Hepatitis C Virus (HCV): Transmission & Course
Transmission: Primarily via blood (e.g., IV drug use). Course: Acute infection is often mild or asymptomatic. High rate of progression to chronic infection (~70%), which is a major cause of cirrhosis and liver cancer. Virus mutates rapidly; no vaccine available.
HCV Diagnosis & Treatment
Diagnosis: HCV RNA assay detects the virus; anti-HCV antibodies indicate exposure. Genotyping is done to guide treatment. Treatment: Highly effective direct-acting antiviral medications can now cure HCV infection.
Hepatitis D Virus (HDV)
A “defective” virus that requires the presence of Hepatitis B virus (HBV) to replicate. It accelerates the progression of liver disease in those already infected with HBV.
Hepatitis E Virus (HEV)
Transmitted via the fecal-oral route, similar to HAV. It is the most common cause of hepatitis in parts of Asia and Africa.
Non-alcoholic Fatty Liver Disease (NAFLD): Pathophysiology
The accumulation of fat (steatosis) in the liver not caused by alcohol. Strongly associated with metabolic syndrome, obesity, and insulin resistance.
Non-alcoholic Steatohepatitis (NASH)
The most severe and progressive form of NAFLD where fatty liver is accompanied by inflammation and scarring (fibrosis). NASH can lead to cirrhosis and liver cancer.
NAFLD/NASH: Diagnosis & Treatment
Diagnosis: Often found due to elevated liver enzymes. Liver biopsy is the gold standard for diagnosing NASH. Non-invasive tests like transient elastography (FibroScan) are increasingly used. Treatment: Weight loss, exercise, management of metabolic syndrome components (diabetes, hyperlipidemia).
Alcohol-Related Liver Disease: Pathophysiology
Chronic, excessive alcohol use is directly toxic to hepatocytes. It begins with steatosis (fatty liver), progresses to alcoholic hepatitis (inflammation), and can lead to cirrhosis (irreversible scarring).
Alcohol-Related Liver Disease: Signs & Diagnosis
Signs: In addition to general liver failure signs, may see withdrawal symptoms (delirium tremens, seizures) with abstinence. Diagnosis: History of alcohol use is key. Elevated AST and ALT, with the AST level typically higher than the ALT.
Cirrhosis: Definition
The final, irreversible stage of chronic liver disease, where the liver tissue is replaced by fibrosis and scar tissue, disrupting its structure and function.
Primary Biliary Cholangitis (PBC): Pathophysiology & Diagnosis
An autoimmune disease causing inflammation and fibrous destruction of the intrahepatic bile ducts. Hallmark diagnostic finding is the presence of anti-mitochondrial antibodies (AMAs) in the blood.
Primary Biliary Cholangitis (PBC): Treatment
The primary medication is Ursodeoxycholic acid (UDCA), which can delay disease progression. Obeticholic acid (OCA) or fibrates may be added if the response to UDCA is inadequate.
Crigler-Najjar Syndrome: Pathophysiology & Consequence
A rare genetic disorder causing a deficiency of the enzyme glucuronyl transferase, which is needed to conjugate bilirubin. This leads to high levels of unconjugated bilirubin, which can cause kernicterus (brain damage). Liver transplant is needed for the most severe form (Type I).
Gilbert’s Syndrome: Pathophysiology & Presentation
A common, mild genetic condition causing decreased activity of the enzyme glucuronyl transferase. Leads to elevated unconjugated bilirubin and mild jaundice during periods of stress, illness, or fasting. No treatment is necessary.
Hemochromatosis: Pathophysiology & Treatment
A genetic disorder causing excessive absorption and accumulation of iron in the liver, leading to damage and potential cirrhosis. Treatment involves regular phlebotomy (blood removal) to reduce iron stores.
Wilson Disease: Pathophysiology & Key Sign
A rare inherited disorder of excessive copper deposition in the liver, brain, and eyes. A key diagnostic sign is the presence of Kayser-Fleischer rings (copper rings) in the cornea.
