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ACEM Primary Written > Gastrointestinal: Pathology - The pancreas > Flashcards

Gastrointestinal: Pathology - The pancreas Flashcards

1
Q

What % of the pancreas is endocrine vs exocrine?

A

80-85% exocrine
1-2% endocrine

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2
Q

How many litres are secreted by the pancreas daily?

A

2-2.5L/day

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3
Q

What are the cell types of the exocrine and endocrine pancreas?

A

Exocrine: acinar cells
Endocrine: insulin-secreting B cells, glucocagon-secreting a cells, somatostatin-secreting d cells

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4
Q

What % of cells in the endocrine pancreas are B, a or d?

A

B (insulin-secreting): 68%
a (glucagon-secreting): 20%
d (somatostatin-secreting): 10%

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5
Q

What is the effect of somatostatin on release of insulin and glucagon from pancreatic B and a cells?

A

Inhibits

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6
Q

Which pancreatic enzymes are NOT secreted as proenzymes?

A

Lipase
Amylase

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7
Q

Seven pancreatic proenzymes

A

Trypsinogen
Chymotrypsinogen
Procarboxypeptidase
Proelastase
Kallikreinogen
Phospholipase A
Phospholipase B

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8
Q

What % of acute pancreatitis is caused by alcohol and biliary tract disease?

A

80%

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9
Q

Seven broad causes of acute pancreatitis, with specific examples

A
  1. Obstruction (e.g. neoplasm, parasites)
  2. Medications (e.g. furosemide, thiazide diuretics, sulfonamides, azathioprine, methyldopa)
  3. Infection (e.g. mumps)
  4. Metabolic disorders (e.g. hypertriglyceridaemia, hypercalcaemia)
  5. Ischaemia (e.g. due to shock, thrombosis, thromboembolism, vasculitis)
  6. Trauma (blunt or iatrogenic, e.g. ERCP)
  7. Hereditary
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10
Q

Three pathogenic mechanisms of acute pancreatitis

A
  1. Duct obstruction: accumulation of enzymes in interstitium -> inflammatory response -> interstitial oedema -> impaired blood flow -> ischaemia -> acinar cell injury
  2. Primary acinar cell injury: e.g. in setting of infection, drugs, trauma -> release of proenzymes and lysosomal hydrolases -> enzyme activation -> acinar cell injury
  3. Defective intracellular transport of proenzymes: delivery of proenzymes to lysosomal compartment -> intracellular activation -> acinar cell injury
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11
Q

What is the common final pathogenic pathway for acinar cell injury and pancreatic inflammation?

A

Whether duct obstruction, primary acinar cell injury, or defective intracellular transport of proenzymes: all lead to pancreatic autodigestion via:
- Proteolysis (proteases)
- Fat necrosis (lipase, phospholipase)
- Haemorrhage (elastase)

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12
Q

What is the mechanism of pancreatic injury due to alcohol consumption?

A

Chronic EtOH causes secretion of protein-rich pancreatic fluid
Forms protein plugs which obstruct small pancreatic ducts

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13
Q

Five morphological features of pancreatitis

A
  1. Microvascular leakage causing oedema
  2. Fat necrosis by lipolytic enzymes
  3. Acute inflammation
  4. Proteolytic destruction of pancreatic parenchyma
  5. Destruction of blood vessels leading to interstitial haemorrhage
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14
Q

What is the difference in histological features seen with increasing severity of pancreatitis?

A

Mild (acute interstitial pancreatitis): inflammation, oedema, focal areas of fat necrosis
Severe (acute necrotising pancreatitis): acinar, ductal tissues, and islets of Langerhans are necrotic; intraparenchymal haemorrhage
Most severe (haemorrhagic pancreatitis): extensive parenchymal necrosis with dramatic haemorrhage

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15
Q

What are two clinical signs which may be seen in acute necrotising pancreatitis?

A

Periumbilical bruising (Cullen’s sign)
Flank bruising (Grey Turner’s sign)

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16
Q

Eight early sequelae of acute pancreatitis

A
  1. Acute renal tubular necrosis -> acute renal failure
  2. Hypocalcaemia (due to precipitation of Ca2+ in necrotic fat)
  3. Fluid sequestration, ARDS
  4. CV collapse, shock
  5. Sepsis (usually GNRs from GIT)
  6. DIC, haemolysis
  7. Transient hyperglycaemia
  8. Glycosuria
17
Q

What % of patients with severe necrotising pancreatitis develop sepsis?

A

40-60%

18
Q

Five later (week 2-4) sequelae of acute pancreatitis

A
  1. Pancreatic necrosis
  2. Haemorrhage from erosion into nearby arteries (e.g. UGIB)
  3. Pancreatic ascites, pleural effusion (fluid high in amylase)
  4. Pancreatic abscess and pseudocyst
  5. Fistula
19
Q

What are the four possible longterm outcomes of acute pancreatitis?

A

Most commonly there is full recovery with no longterm sequelae
May get recurrence (especially if ductal damage incurred)
Pancreatic insufficiency (both exocrine -> malabsorption, and endocrine -> DM)
Death in 5% of patients with severe necrotising pancreatitis (from shock, within first week of illness)

20
Q

Outline Ranson’s criteria

A

> /= 3 of the following, within 48hrs of admission, confers increasing risk of morbidity/mortality:
- Age >55yrs
- BSL >10mmol/L (with no history of diabetes)
- WCC >15 x 10^9 L
- LDH >600IU/L
- AST >200u/L
- Corrected Ca2+ <2.0mmol/L
- BUN >16mmol/L (with no improvement with IVT)
- Decreasing Hct
- Arterial pO2 <60mmHg
- Metabolic acidosis
- Serum albumin <32g/L

21
Q

Describe the mortality risk with increasing numbers of positive Ranson’s criteria

A

0-2: <5%
3-4: 20%
5-6: 40%
7-8: 100%

22
Q

What increases first in acute pancreatitis: serum amylase or lipase levels?

A

Amylase increases first, within 24hrs
Lipase follows, within 72-96hrs

23
Q

In what % of cases of acute pancreatitis is glycosuria present?

A

10%

24
Q

What defines chronic (as opposed to acute) pancreatitis?

A

Defined by IRREVERSIBLE loss of exocrine pancreatic parenchyma (and endocrine parenchyma in late stages)

25
Q

What is the prevalence of chronic pancreatitis?

A

0.04-5%

26
Q

What is the most common cause of chronic pancreatitis and what % of cases does this account for?

A

Longterm alcohol abuse
60-80% of cases

27
Q

Six causes of chronic pancreatitis. Which is most common? What % of cases are “idiopathic”? Which of these causes confers an increased risk of pancreatic cancer?

A
  1. Longstanding obstruction (e.g. by pseudocyst, calculi, trauma, neoplasm, divisum)
  2. Tropical pancreatitis
  3. Hereditary pancreatitis (increased risk of pancreatic cancer)
  4. CFTR mutations
  5. “Idiopathic” (40%)
28
Q

Two genes implicated in hereditary chronic pancreatitis

A

PRSS1
SPINK1

29
Q

Describe the three pathogenic mechanisms underlying chronic pancreatitis

A
  1. Ductal obstruction by concentrations (increased protein concentrations in pancreatic juices leads to ductal plugging and calcification via precipitation of calcium carbonate)
  2. Direct toxic effects (e.g. alcohol)
  3. Oxidative stress
30
Q

Five morphological features of chronic pancreatitis

A
  1. Parenchymal fibrosis
  2. Decreased number and size of acini
  3. Variable dilation of pancreatic ducts
  4. Relative sparing of islets of Langerhands
  5. Chronic inflammation
31
Q

How can chronic pancreatitis present?

A

May be silent
May present with recurrent attacks of pain (precipitated by alcohol, overeating, or medications that increased the tone of the spincter of Oddi, e.g. opioids)

32
Q

What is the 20-25yr mortality rate of chronic pancreatitis?

A

50%

33
Q

Seven complications/sequelae of chronic pancreatitis

A
  1. Death
  2. Severe chronic pain
  3. Pancreatic pseudocysts
  4. Increased risk of pancreatic cancer with hereditary pancreatitis only
  5. Exocrine insufficiency (malabsorption, steatorrhoea)
  6. Endocrine insufficiency (DM)
  7. Ascites, pleural effusion (with high amylase content in fluid)
34
Q

What % of cases of chronic pancreatitis result in formation of pseudocyst?

A

10%

35
Q

What are pancreatic pseudocysts? How big are there?

A

Localised collections of necrotic-haemorrhagic material rich in pancreatic enzymes, surrounded by non-epithelial fibrous granulation tissue
May be 2-30cm in diaemeter

36
Q

What % of pancreatic cysts are pseudocysts?

A

75%

37
Q

What is the typical location of a pancreatic pseudocyst?

A

Commonly involves lesser omental sac or lies in retroperitoneum
Less commonly in substance of pancreas

38
Q

Four longterm outcomes of pancreatic pseudocyst

A
  1. Spontaneous resolution
  2. Secondary infection
  3. Compression of adjacent structures
  4. Perforation into adjacent structures

ACEM Primary Written (160 decks)

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