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ACEM Primary VIVA > VIVA: Pathology - Liver, biliary tract and pancreas > Flashcards

VIVA: Pathology - Liver, biliary tract and pancreas Flashcards

1
Q

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?

A
  • 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

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2
Q

How may hepatitis B lead to upper gastrointestinal bleeding?

A

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
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3
Q

What are the other complications of hepatitis-B-induced cirrhosis?

A

3 to pass:
- Jaundice
- Hepatorenal and hepatopulmonary syndrome
- Hepatic encephalopathy
- Ascites, pleural effusions
- Splenomegaly
- Hypogonadism (testicular trophy, amenorrhoea etc)
- Hepatocellular carcinoma

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4
Q

In general how may a patient acquire hepatitis B?

A

2 to pass:
- Congenital (i.e. vertical; most common worldwide)
- Contaminated blood products (e.g. IVDU, transfusions, needlestick injury)
- Bodily fluids (e.g. sexual)

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5
Q

What are the other possible outcomes of hepatitis B exposure?

A

2 to pass:
- Asymptomatic
- Acute hepatitis
- Non-progressive chronic hepatitis
- Carrier state

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6
Q

Describe the pathological features of the liver in alcoholic liver disease

A
  1. Hepatic steatosis*:
    - Fatty change
    - Perivenular fibrosis
  2. Hepatitis*:
    - Liver cell necrosis
    - Inflammation
    - Mallory bodies
    - Fatty change
    - Fibrosis
  3. Cirrhosis*:
    - Extensive fibrosis
    - Hyperplastic nodules
  4. Hepatocellular carcinoma*
  • needed to pass
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7
Q

Which of the pathological features of alcoholic liver disease are reversible?

A
  • Steatosis and hepatitis are reversible
  • Cirrhosis irreversible
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8
Q

What are the possible sequelae of cirrhosis?

A
  • Portal hypertension*
  • GIT bleeding
  • Hepatic failure
  • Coagulopathy
  • Hepatocellular carcinoma
  • Hepatorenal syndrome
  • Hepatopulmonary syndrome
  • Encephalopathy
  • Infection

*needed to pass + 3 others

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9
Q

Describe the pathogenesis of acute calculous cholecystitis

A

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

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10
Q

What are the complications of cholecystitis?

A
  • Bacterial infection (cholangitis, sepsis)*
  • Perforation and localised abscess
  • Rupture and peritonitis
  • Biliary fistula
  • Porcelain gallbladder (calcification)

*needed to pass + 2 others

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11
Q

What is the causative agent of hepatitis A?

A

Hepatitis A virus*:
- Small unenveloped ssRNA picornavirus
- Icosahedral capsid

*needed to pass

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12
Q

How is hepatitis A transmitted?

A

Faecal oral spread

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13
Q

How do the clinical outcomes of hepatitis A differ from hepatitis B?

A

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%

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14
Q

How is hepatitis A diagnosed serologically?

A
  • Acutely IgM anti-HAV*
  • Followed by appearance/persistence of IgG anti-HAV

*needed to pass

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15
Q

What type of virus causes hepatitis C?

A

Flaviviridae* family RNA* virus

*1/2 needed to pass

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16
Q

What are the risk factors for acquiring hepatitis C?

A
  • 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

17
Q

What is the natural course of hepatitis C?

A
  • 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

18
Q

What are the causes of jaundice?

A

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

19
Q

Apart from jaundice, what are the clinical features of liver failure?

A

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)

20
Q

What are some causes of pancreatitis?

A
  • 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
21
Q

What is the likely pathogenesis of acute pancreatitis?

A
  • 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

22
Q

What are the acute complications of severe pancreatitis?

A

3 to pass:
- Haemolysis
- DIC
- Fluid sequestration
- ARDS
- Diffuse fat necrosis
- Peripheral vascular collapse
- Shock
- Acute renal tubular necrosis

23
Q

What are the morphological features of chronic pancreatitis?

A

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

24
Q

What are the clinical consequences of chronic pancreatitis?

A

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)

25
Q

What are the causes of portal hypertension?

A

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

26
Q

What are the clinical consequences of portal hypertension?

A

2/4 to pass:
- Ascites (with potential for infection)
- Porto-systemic shunts: varices, haemorrhoids, spider naevi, caput medusae
- Congestive splenomegaly: thrombocytopaenia/pancytopaenia
- Hepatic encephlopathy

27
Q

What mechanisms are involved in the formation of ascites?

A

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

ACEM Primary VIVA (45 decks)

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