VIVA: Pathology - Liver, biliary tract and pancreas Flashcards
A 55-year-old man presents to the ED with haematemesis. Hepatitis B serology results from a previous admission are available:
- HBsAg positive
- Anti-HBc total positive, IgM anti-HBc negative
- Anti-HBs negative
What is the most likely diagnosis, and why?
- HBsAg positive: indicates current infection*
- Anti-HBc total positive: indicates exposure to HBV
- IgM anti-HBc negative: exposure not acute/recent
- Anti-HBs negative: no current immunity to HBV*
- Diagnosis: chronic hepatitis B*
*needed to pass
How may hepatitis B lead to upper gastrointestinal bleeding?
Cirrhosis and portal hypertension* with development of oesophageal varices*
Coagulopathy* due to loss of synthetic function (unable to produce coagulation proteins)
- 2/3 to pass
What are the other complications of hepatitis-B-induced cirrhosis?
3 to pass:
- Jaundice
- Hepatorenal and hepatopulmonary syndrome
- Hepatic encephalopathy
- Ascites, pleural effusions
- Splenomegaly
- Hypogonadism (testicular trophy, amenorrhoea etc)
- Hepatocellular carcinoma
In general how may a patient acquire hepatitis B?
2 to pass:
- Congenital (i.e. vertical; most common worldwide)
- Contaminated blood products (e.g. IVDU, transfusions, needlestick injury)
- Bodily fluids (e.g. sexual)
What are the other possible outcomes of hepatitis B exposure?
2 to pass:
- Asymptomatic
- Acute hepatitis
- Non-progressive chronic hepatitis
- Carrier state
Describe the pathological features of the liver in alcoholic liver disease
- Hepatic steatosis*:
- Fatty change
- Perivenular fibrosis - Hepatitis*:
- Liver cell necrosis
- Inflammation
- Mallory bodies
- Fatty change
- Fibrosis - Cirrhosis*:
- Extensive fibrosis
- Hyperplastic nodules - Hepatocellular carcinoma*
- needed to pass
Which of the pathological features of alcoholic liver disease are reversible?
- Steatosis and hepatitis are reversible
- Cirrhosis irreversible
What are the possible sequelae of cirrhosis?
- Portal hypertension*
- GIT bleeding
- Hepatic failure
- Coagulopathy
- Hepatocellular carcinoma
- Hepatorenal syndrome
- Hepatopulmonary syndrome
- Encephalopathy
- Infection
*needed to pass + 3 others
Describe the pathogenesis of acute calculous cholecystitis
Chemical irritation of obstructed gallbladder*:
- Mucosal phospholipases hydrolyse luminal lecithins to toxic lysolecithins
- Protective glycoprotein mucus layer is disrupted
- Allows bile salts to have detergent action on exposed mucosal epithelium
- Prostaglandins contribute to inflammation
- Gallbladder dysmotility develops
- Distension and increased intraluminal pressure decreases mucosal blood flow
*needed to pass + 2 others
What are the complications of cholecystitis?
- Bacterial infection (cholangitis, sepsis)*
- Perforation and localised abscess
- Rupture and peritonitis
- Biliary fistula
- Porcelain gallbladder (calcification)
*needed to pass + 2 others
What is the causative agent of hepatitis A?
Hepatitis A virus*:
- Small unenveloped ssRNA picornavirus
- Icosahedral capsid
*needed to pass
How is hepatitis A transmitted?
Faecal oral spread
How do the clinical outcomes of hepatitis A differ from hepatitis B?
3/6 to pass:
- Self-limiting illness
- No carrier state
- No chronic state
- No association with hepatocellular carcinoma
- Rarely leads to fulminant disease
- Low fatality rate of 0.1%
How is hepatitis A diagnosed serologically?
- Acutely IgM anti-HAV*
- Followed by appearance/persistence of IgG anti-HAV
*needed to pass
What type of virus causes hepatitis C?
Flaviviridae* family RNA* virus
*1/2 needed to pass
What are the risk factors for acquiring hepatitis C?
- IVDU* (54%)
- Multiple sex partners (36%)
- Recent surgery (16%)
- Needlestick (10%)
- Multiple contacts with HCV-infected person (10%)
- Healthcare workers (1.5%)
- Unknown (32%)
- Children (perinatal; 6%)
*needed to pass + 2 others
What is the natural course of hepatitis C?
- Incubation 2-26 weeks (mean 6-12 weeks)
- Asymptomatic in 85%*
- HCV RNA detectable in 1-3 weeks
- Anti-HCV Ab 50-70% while symptomatic
- Usually a mild disease
- Persistent infection and chronic hepatitis in 80-85%*
- Cirrhosis in 20-30%
- Fulminant hepatitis rare
*needed to pass
What are the causes of jaundice?
Predominantly unconjugated*:
- Increased bilirubin production (e.g. haemolysis, resorption of haemorrhage, thalassaemia)
- Decreased hepatic intake (e.g. drug interference with membrane carrier systems, Gilbert syndrome)
- Impaired conjugation (e.g. physiological jaundice of newborn, breastmilk jaundice, Crigler-Najjar syndrome, Gilbert syndrome, hepatitis including viral / drug-induced / AI, cirrhosis)
Predominantly conjugated*:
- Impaired bile flow (e.g. cholangiopathy, biliary stricture, malignancy, choledocolithiasis)
- Deficiency of canalicular membrane transporters (e.g. Dubin-Johnson syndrome, Rotor syndrome)
*needed to pass + 1 example of each
Apart from jaundice, what are the clinical features of liver failure?
5 to pass:
- Icterus
- Pruritis
- Fetor hepaticus
- Palmar erythema
- Spider angiomata
- Hypogonadism
- Gynaecomastia
- Encephalopathy (asterixis)
- Coagulopathy
- Hepatorenal syndrome
- Hepatopulmonary syndrome
- Portal hypertension (varices, ascites, caput medusae)
What are some causes of pancreatitis?
- Gallstones*
- Alcohol*
- Iatrogenic
- Viral
- Hyperlipoproteinaemia
- Hypercalcaemia
- Drugs
- Trauma
- Shock
- Vasculitis
- Genetic mutations
- Scorpion bite
- Atheroembolism
- Duct obstruction (tumour, parasites, etc)
- needed to pass + 1 other
What is the likely pathogenesis of acute pancreatitis?
- Autodigestion of the pancreatic substance by inappropriately activated pancreatic enzymes* (e.g. trypsinogen)
- Causes interstitial inflammation and oedema, proteolysis, fat necrosis and haemorrhage
*needed to pass
What are the acute complications of severe pancreatitis?
3 to pass:
- Haemolysis
- DIC
- Fluid sequestration
- ARDS
- Diffuse fat necrosis
- Peripheral vascular collapse
- Shock
- Acute renal tubular necrosis
What are the morphological features of chronic pancreatitis?
3 to pass:
- Parenchymal fibrosis
- Reduced number and size of acini with relative sparing of islets of Langerhans
- Variable dilation and blockage of pancreatic ducts
- Destruction of exocrine parenchyma and in later stages destruction of endocrine parenchyma
- Calcification
What are the clinical consequences of chronic pancreatitis?
Irreversible impairment of pancreatic function including (3 to pass):
- Diabetes mellitus
- Steatorrhoea
- Malabsorption
- Pseudocyst
- Disease may be silent (amylase, lipase may not rise in chronic attack)
- Chronic attack not immediately life-threatening but long term outlook poor (50% 20-25yr mortality)
What are the causes of portal hypertension?
Increased resistance to portal blood flow, may be:
1. Prehepatic
- Portal vein thrombosis or narrowing
2. Hepatic (most important):
- Cirrhosis*
- Massive fatty change
- Schistosomiasis
- Granulomatous disease (e.g. sarcoid/TB)
3. Post-hepatic:
- Severe RHF
- Constrictive pericarditis
- Hepatic vein occlusion
*needed to pass + 1 each from other groups
What are the clinical consequences of portal hypertension?
2/4 to pass:
- Ascites (with potential for infection)
- Porto-systemic shunts: varices, haemorrhoids, spider naevi, caput medusae
- Congestive splenomegaly: thrombocytopaenia/pancytopaenia
- Hepatic encephlopathy
What mechanisms are involved in the formation of ascites?
Starling forces:
- Increased hydrostatic pressure (sinusoidal hypertension)*
- Decreased oncotic pressure (hypoalbuminaemia)*
- Increased formation of hepatic lymph, exceeding the capacity of the thoracic duct and percolating into peritoneum*
Splanchnic vasodilation with decreased BP -> renal retention of sodium and water due to secondary hyperaldosteronism*
*2/4 to pass
