Gi Week 2 Objective 6

Front 1

What is the difference between acute and chronic pancreatitis?

Back 1

a) Acute pancreatitis: acute injury to significant portion of the pancreas, self-limited and non-progressive, gland histologically and functionally returns to normal afterwards.
b) Chronic pancreatitis: permanent structural damage with impaired exocrine and endocrine function, progressive patchy fibrosis, can by asymptomatic, often not preceded by acute pancreatitis or can exist simultaneously with acute pancreatitis, ddx is malignancy.

Front 2

What are the most common causes of acute pancreatitis?

Back 2

Alcohol and gallstones.

Front 3

Other causes of acute pancreatitis

Back 3

Mechanical: sludge, tumour
Metabolic: hyperlipidemia, hypercalcemia
Drugs: azathioprine/6-MP
Infection: virus, bacteria, parasite
Trauma/post-procedure: ERCP
Congenital/genetic: pancreas divisum, CFTR, familial
Vascular: ischemia, vasculitis
Idiopathic

Front 4

What is the most common cause of chronic pancreatitis?

Back 4

Chronic alcohol abuse

Front 5

What are some other causes of chronic pancreatitis?

Back 5

Hereditary: trypsin and protease inhibitor mutations
Duct obstruction: stone, tumour, trauma
Cystic fibrosis
Autoimmune (rare)
Idiopathic

Front 6

Which infectious agents cause pancreatitis?

Back 6

Virus: mumps, coxsackie
Bacteria: Mycoplasma pneumoniae

Front 7

What is the mechanism of pathogenesis caused by infectious agents?

Back 7

Inappropriate activation of digestive enzymes causes inflammation (autodigestion)

Front 8

Outline the pathogenesis of infectious pancreatitis.

Back 8

1. Infection stimulates release of intracellular proenzymes and lysosomal hydrolases.
2. Activation of enzymes occurs
3. Trypsin activates other proenzymes (prophospholipase and proelastase)
4. Activated enzymes damage the acinar cells.
5. Causes interstitial inflammation and edema, proteolysis (protease), fat necrosis (lipase, phospholipase) and hemorrhage (elastase).

Front 9

Outline the pathogenesis of alcoholic pancreatitis.

Back 9

1. Alcohol increases protein concentration in pancreatic juice.
2. Secretion of thickened protein-rich pancreatic fluid.
3. Leads to deposition of protein plugs in the pancreatic ducts.
4. Protein plugs turn into calculi (calcium carbonate precipitates)
5. Calculi obstruct small pancreatic ducts.
6. Accumulation of enzyme-rich interstitial fluid and autodigestion occurs
7. Induction of local inflammatory response by injured tissues.
8. Causes interstitial edema through leaky microvasculature, impaired blood flow and ischemia.
9. Alcohol also induces oxidative stress which generates free radicals and cause acinar cell necrosis, inflammation and fibrosis.

Front 10

What other pathological mechanism contributes to chronic pancreatitis?

Back 10

Reduced bicarbonate secretion by defective CFTR in cystic fibrosis.

Front 11

What causes pancreatic duct obstruction?

Back 11

Gallstones (acute pancreatitis)
Periampullary tumours
Pancreas divisum (congenital)
Biliary sludge
Parasites (Ascaris lumbricoides)
Pseudocysts (chronic pancreatitis)

Front 12

How is pancreatic duct obstruction identified on imaging?

Back 12

Plain films: calcifications.
Ultrasound, CT, MRI: calcifications, ductal dilation, pseudocyst.
ERCP/MRCP/Endoscopic ultrasound: beading duct and ectatic branches (chain of lakes), ductal calculi

Front 13

What other mechanism can account for the development of chronic pancreatitis?

Back 13

Necrosis-fibrosis: acute pancreatitis initiates a sequence of perilobular fibrosis, duct dilation and altered pancreatic secretions.
Over time and with multiple episodes of acute pancreatitis, there is loss of pancreatic parenchyma and fibrosis.