pt12 Flashcards
(50 cards)
How is the severity of acute liver injury best assessed?
Prothrombin time and bilirubin levels (reflect synthetic dysfunction and excretory capacity).
Define chronic hepatitis.
Persistent hepatic inflammation > 6 months, due to viral, chemical (e.g., alcohol), or autoimmune causes.
How is hepatitis A virus transmitted and what is its typical outcome?
Fecal–oral spread; short incubation, self‐limiting, no chronic stage; rare fulminant hepatitis.
What prophylactic measures exist for hepatitis A?
Active immunization with inactivated vaccine; passive immunoglobulin for post‐exposure or short‐notice protection.
Describe the hepatitis B virus structure relevant to diagnostics and vaccination.
DNA virus with core antigen (HBcAg), e antigen (HBeAg) indicating infectivity, and surface antigen (HBsAg) used in vaccines.
What defines a chronic HBV carrier and their risks?
HBsAg persistence > 6 months; HBeAg or HBV DNA indicates high infectivity; risk of chronic hepatitis, cirrhosis, HCC.
Outline key features of hepatitis C infection.
RNA virus; blood‐borne/rare vertical transmission; short incubation; 60–90% become chronic carriers; high risk of cirrhosis and hepatocellular carcinoma; no vaccine.
How is acute HCV exposure in healthcare workers managed?
Immediate testing and early interferon‐based therapy post–needle‐stick to prevent chronic infection.
Which lab finding is true for haemolytic jaundice?
Increase in serum unconjugated bilirubin.
What is the principal transmission route for hepatitis A?
Faecal–oral route.
What are the three learning outcomes for this lecture?
Understand cirrhosis pathogenesis; describe liver tumour pathology; know alcoholic liver disease features.
How is cirrhosis defined histologically?
Diffuse, irreversible fibrosis and regenerative nodule formation following chronic hepatocyte necrosis.
What are the two main consequences of cirrhosis?
Impaired liver cell function and gross architectural distortion leading to portal hypertension and eventual liver failure.
List four major causes of cirrhosis.
Viral hepatitis (B, C, D), alcohol (Western world), autoimmune hepatitis, Wilson’s disease; plus drugs/NAFLD.
Describe the two histological patterns of nodules in cirrhosis.
Micronodular (small, uniform nodules) and macronodular (larger, variable nodules), often mixed.
What clinical signs arise from portal hypertension in cirrhosis?
Variceal haemorrhage (e.g., oesophageal varices), ascites, splenomegaly.
What features reflect decompensated cirrhosis?
Portal-systemic encephalopathy, hepatorenal syndrome, refractory ascites, coagulopathy.
Which primary malignancy arises almost exclusively on a background of cirrhosis?
Hepatocellular carcinoma (HCC).
Name three risk factors for HCC.
Chronic HBV/HCV infection, cirrhosis (especially viral), aflatoxin exposure; androgenic steroids & (weakly) OCPs.
Outline the stepwise progression to HCC.
Cirrhosis → dysplastic nodules → overt hepatocellular carcinoma.
How does well-differentiated HCC appear histologically?
Neoplastic hepatocyte cords, thicker than normal, with identifiable hepatocytic features.
What distinguishes poorly-differentiated HCC microscopically?
Pleomorphic cells, giant nuclei, loss of normal hepatic architecture.
What clinical presentation in a cirrhotic patient suggests HCC?
New weight loss, fever, anorexia, ascites or abdominal pain; or detection of a focal liver lesion.
Which tumour marker is elevated in ~⅔ of HCC patients?
Alpha-fetoprotein (AFP).