List the causes of acute pancreatitis.

Metabolic- alcohol*, hyperlipidaemia, hypercalcaemia, drugs, genetic Mechanical- trauma, gallstones*, iatrogenic (eg ERCP, perioperative) Vascular- shock, atheroembolism, polyarteritis nodosa

Infectious- Mumps, Coxsackievirus, Mycoplasma

Pass: Require Et0H, gallstones + 2 others

Outline the pathogenesis of acute pancreatitis.

Final common pathway of Autodigestion of pancreas by inappropriately activated pancreatic enzymes (esp trypsinogen to trypsin *)

  1. Activation of enzymes – caused by pancreatic duct obstruction with accumulation of enzyme rich fluid. Interstitial oedema, ischaemia and acinar cell injury
  2. Primary acinar cell injury esp in infectious and traumatic causes, drugs and alcohol- release of proenzymes and lysosomal hydrolases
  3. Defective intracellular transport of proenzymes to lysosomal compartment within acinar cells esp in metabolic, alcohol and duct obstruction

Alcohol- causative mechanism not established- increases in secretion, spasm of sphincter of Oddi, direct toxic effect on acinar cells, or causes protein rich fluid that plugs and obstructs small ducts

Pass: * required


What causes portal hypertension?

Pre-hepatic: obstructive thrombosis, portal vein narrowing, splenomegaly

Intrahepatic: cirrhosis (most common), schisto, fatty change, sarcoid/TB, nod hyperplasia

Post-hepatic: RVF, constrictive pericarditis, hepatic vein outflow obstruction

Pass: At least one of each required

What are the clinical consequences of portal hypertension?

Ascites, portosystemic venous shunts (eg varices, haemorrhoids, spiders), congestive splenomegaly, hepatic encephalopathy
Pass: Shunts + 1 other required


What are the causes of pancreatitis?

  • Gallstones
  • Alcohol
  • Iatrogenic
  • Viral
  • Hyperlipoproteinaemia
  • Hypercalcaemia
  • Drugs
  • Trauma
  • Shock
  • Vasculitis
  • Genetic mutations
  • Scorpion bite
  • Atheroembolism
  • Duct obstruction (tumour, parasites etc)

Pass Criteria:

  • Bold + 1

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

Pass Criteria:

  • Bold to pass

What are the acute complications of severe pancreatitis?

  • Haemolysis
  • Disseminated Intravascular Coagulation
  • Fluid Sequestration
  • Acute respiratory distress syndrome
  • Diffuse fat necrosis
  • Peripheral vascular collapse
  • Shock
  • Acute renal tubular necrosis

Pass Criteria:

  • 3 answers to pass


What conditions can lead to infarction of bowel?

  • Acute arterial obstruction
    • Atherosclerosis
    • Aortic aneurysm
    • Hypercoagulable state
    • OCP use
    • Embolism
  • Intestinal hypoperfusion
    • Cardiac failure
    • Shock
    • Dehydration
    • Vasoactive drugs
  • Systemic vasculitis
    • Henoch-Schonlein Purpura
    • Wegener’s granulomatosis
  • Mesenteric venous thrombosis
    • Hypercoagulable state
    • Invasive neoplasm
    • Cirrhosis
    • Trauma
    • Abdominal masses
  • Miscellaneous
    • Radiation
    • Volvulus
    • Stricture
    • Amyloid
    • Diabetes

Pass Criteria:

  • Bold to pass
  • Minimum 2 from each bolded group
  • 2 from non-bolded

What are the clinical features of ischaemic bowel?

  • Severe pain, may be transient
  • Tenderness
  • Peritonism
  • Nausea
  • Vomiting
  • Bloody diarrhoea
  • Melaena
  • Shock
  • Hyper/hypothermia
  • Sepsis

Pass Criteria:

  • Bold + 3 features

What parts of the bowel are most susceptible to ischaemic injury and why?

  • Watershed zones
    • Splenic flexure, sigmoid colon, rectum
    • Located at end of arterial supply
  • Surface epithelium: villi more at risk than crypts. Intestinal capillaries run from crypts up villi to surface.

Pass Criteria:

  • Must be able to explain why watershed zones are most at risk.


Describe the pathological effects on the liver long-term alcohol ingestion.

PROMPT – Please describe the morphological features.

  1. 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)

Pass Criteria:

  • Bold with 3 morphologic features of each to pass

Which of these conditions are reversible?

  • Steatosis and Hepatitis are reversible
  • Cirrhosis irreversible

Pass Criteria:

  • Bold to pass 

What are the possible sequelae of cirrhosis?

PROMPT – Complications?

  • Portal Hypertension
  • GIT Bleeding
  • Hepatic Failure
  • Coagulopathy
  • Hepatocellular Cancer
  • Hepatorenal Syndrome
  • Hepatopulmonary Syndrome
  • Encephalopathy
  • Infection

Pass Criteria:

  • Bold plus 3


Describe the pathogenesis of acute calculous cholecystitis.

  • Chemical irritation of obstructed gallbladder
    • Mucosal phospholipases hydrolyse luminal lecithins to toxic lysolecithins
    • Protective glycoprotein mucous layer disrupted
    • Allows bile salts to have detergent action of exposed mucosal epithelium
    • PGs contribute to inflammation
    • Gallbladder dysmotility develops
    • Distension and increased intraluminal pressure decreases mucosal blood flow.

Pass Criteria:

  • Bold + 2/6

What are the complications of cholecystitis?

  • Bacterial infection – cholangitis/sepsis
  • Perforation and localised abscess
  • Rupture and peritonitis
  • Biliary fistula
  • Porcelain gallbladder

Pass Criteria:

  • Bold + 2/4


What types of liver disease may result from chronic excessive alcohol consumption?

  • Hepatocellular steatosis (fatty change) – reversible
  • Alcoholic hepatitis – reversible
  • Cirrhosis – non reversible
  • Hepatocellular carcinoma – non reversible

Pass Criteria:

  • 1 reversible and 1 non reversible

What are the morphological features of cirrhosis?
Prompt: What happens to liver cells when chronically exposed to toxins or injurious agent?

  • Occurs diffusely throughout liver
  • Parenchymal nodules (regenerating hepatocytes) surrounded by dense bands of fibrous scar
  • Disorganised architecture
  • Variable degrees of vascular/portosystemic shunting
  • Elements of progression and regression

Pass Criteria:

  • 3 of 5 Bold to pass

What is the possible sequelae of cirrhosis?

  • Portal hypertension
  • GIT bleeding
  • Hepatic failure
  • Coagulopathy
  • Hepatocellular cancer
  • Hepatorenal syndrome
  • Hepatopulmonary syndrome
  • Encephalopathy
  • Infection

Pass Criteria:

  • Bold + 3 others


Biochemistry Results:

Bicarb   6

eGFR 31 mL/min

Creatinine 151 umol/L

Bilirubin 32 umol/L

Albumin 22 g/L

ALT 1778 U/L

AST 5314 U/L

ALP 272 U/L

GGT 471 U/L

Please interpret these biochemistry results.
Prompt: What is the pattern of the liver enzyme abnormality?

  • Bicarb – metabolic acidosis
  • eGFR/creatinine – moderate-severe renal impairment
  • Bilirubin – reduced excretion
  • Albumin – reduced synthesis, mild hepatic impairment
  • Abnormal liver enzymes c/w hepatitis

Pass Criteria:

  • Must recognize renal failure and hepatic LFTs to pass + bold


What is the causative agent of Hepatitis A?

  • Hep A virus
  • Small unenveloped single stranded RNA picornavirs
  • Icosahedral capsid

Pass Criteria:

  • Bold

How is hepatitis A transmitted?

  • Faecal-oral spread

Pass Criteria:

  • Bold

How do clinical outcomes of Hepatitis A differ from Hepatitis B?
Prompt: How are the long term outcomes different?

  • Self-limiting illness
  • No carrier state
  • No chronic stae
  • No association with hepatocellular carcinoma
  • Rarely leads to fulminant disease
  • Low fatality rate of 0.1%

Pass Criteria:

  • 3 of 6 to pass

How is Hepatitis A diagnosed serologically?

  • Acutely IgM-anti HAV
  • Followed by appearance/persistenc of IgG-anti HAV

Pass Criteria:

  • Bold to pass


How may Hepatitis B lead to upper GI bleeding?

  • Cirrhosis and portal hypertension with development of oesophageal varices
  • Coagulopathy due to loss of synthetic function (unable to produce coagulation proteins)

Pass Criteria:

  • 2 out of 3 bold to pass

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

  • Jaundice
  • Hepatorenal syndrome
  • Hepatic encephalopathy
  • Ascites
  • Pleural effusions
  • Splenomegaly
  • Hypogonadism (testicular atrophy, ammenorrhoea etc.)
  • Hepatocellular carcinoma

Pass Criteria:

  • 3 complications to pass.

In general, how may a patient acquire Hepatitis B?

  • Congenital (ie. vertical – most common form of transmission worldwide)
  • Contaminated blood products (ie. IVDU, blood transfusions, needlestick injury)
  • Bodily fluids (ie. sexual transmission)

Pass Criteria:

  • 2  to pass.

What are the other possible outcomes of Hepatitis B exposure?
Prompt: Apart from progressive chronic hepatitis

  • Asymptomatic
  • Acute hepatitis
  • Non progressive chronic hepatitis
  • Carrier state

Pass Criteria:

  • 2  to pass.

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