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Pathology - Pancreas > Pancreatitis > Flashcards

Pancreatitis Flashcards

1
Q

What is the most common cause of acute pancreatitis?

A

Gallstones, present in 35-60% of cases of pancreatitis

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2
Q

What percentage of patients with gallstones develop pancreatitis?

A

5%

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3
Q

What potential causes of pancreatic duct obstruction can lead to pancreatitis?

A
  • Gallstones and biliary sludge (most common)
  • Periampullary neoplasm
  • Choledochocele
  • Parasites (particularly Ascaris lumbricoides and Clonorchis sinensis)
  • Pancreas divisum (possibly)
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4
Q

What is the mechanism of pancreatitis from duct obstruction?

A

Duct obstruction → increased intrapancreatic ductal pressure → accumulation of enzyme-rich fluid in the interstitium → most enzymes are inactive zymogens but lipase is produced in an active form → fat necrosis → ‘danger’ signals are produced by the necrosis which stimulates periacinar myofibroblasts and leukocytes to release pro inflammatory cytokines → interstitial oedema → oedema further compromises local blood flow → vascular insufficiency and ischaemic injury to acinar cells

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5
Q

Other than duct obstruction, what are two mechanisms can lead to acinar cell injury thereby causing enzyme activation and acute pancreatitis?

A
  1. Alcohol, drugs, trauma, ischaemia, viruses and hypercalcaemia → PRIMARY ACINAR CELL INJURY → release of digestive enzymes, inflammation and autodigestion of pancreatic tissues
  2. Metabolic injury, alcohol and duct obstruction can lead to DEFECTIVE INTRACELLULAR TRANSPORT OF PROENZYMES WITHIN ACINAR CELLS. In normal acinar cells, digestive enzymes and lysosomal hydrolyses are transported in separate pathways, but if the pancreatic proenzymes are inappropriately delivered to the intracellular compartment containing lysosomal hydrolyses then the proenzymes will be activated, the lysosomes disrupted and the activated enzymes are released.
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6
Q

What are the three main genes implicated in hereditary pancreatitis?

A

PRSS1
SPINK1
CFTR

All mutations increase/sustain the activity of trypsin

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7
Q

What is the lifetime risk of patients with hereditary pancreatitis developing pancreatic cancer?

A

40%

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8
Q

What are the causes/triggers of acute pancreatitis?

A

Pancreatic duct obstruction (gallstones)
Excess alcohol intake
Genetic factors (PRSS1, SPINK1, CFTR)
Traumatic injuries (including iatrogenic - ERCP)
Medications (eg. azathioprine)
Infections (eg. mumps)
Metabolic disorders leading to hypercalcaemia and hyperlipidaemia
Ischaemia (shock, atheroembolism, vasculitis)

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9
Q

What are the basic morphologic alterations that are demonstrated in acute pancreatitis?

A
  1. Microvascular leak and oedema
  2. Fat necrosis
  3. Acute inflammation
  4. Destruction of pancreatic parenchyma
  5. Destruction of blood vessels and interstitial haemorrhage
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10
Q

What are the histologic alterations in acute interstitial pancreatitis (the milder form)? What colour are the fat cells?

A
  • Mild inflammation
  • Interstitial oedema
  • Focal areas of fat necrosis in the pancreas and the peripancreatic fat

Fat necrosis results from the enzymatic activity of lipase
The released fatty acids combine with calcium to form insoluble fat salts that impart a granular blue microscopic appearance to the fat cells

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11
Q

What are the morphologic alterations in acute necrotising pancreatitis (the more severe form)?

A
  • Necrosis of acinar and ductal tissues as well as the islets of Langerhans
  • Vascular injury leads to haemorrhage into the pancreatic parenchyma
  • Macroscopically, the pancreatic substance is red-black from haemorrhage and contains interspersed foci of yellow-hits, chalky fat necrosis
  • Focal fat necrosis can also occur in the omentum and mesentery
  • Serous, slightly turbid, brown tinged peritoneal fluid containing globules of fat
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12
Q

What is the most severe form of pancreatitis?

A

Haemorrhagic pancreatitis - extensive parenchymal necrosis accompanied by dramatic haemorrhage within the substance of the gland

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13
Q

What are the typical symptoms of acute pancreatitis?

A

Epigastric pain with radiation to the back
Anorexia, nausea and vomiting

Severe pancreatitis is a medical emergency: sudden calamitous onset of an acute abdomen, shock (due to SIRS) and acute renal tubular necrosis

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14
Q

Lab findings in pancreatitis?

A 
Leukocytosis
Elevated amylase and lipase
DIC (in severe)
Acute renal impairment
Hypocalcaemia (due to precipitation of calcium soaps in necrotic fat)
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15
Q

Treatment of acute pancreatitis?

A

Total restriction of oral intake
Supportive therapy - IV fluids, analgesia
Addressing underlying cause

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16
Q

What percentage of patients with severe pancreatitis die within the first week?

A

5%

17
Q

What is chronic pancreatitis?

A

Prolonged inflammation of the pancreas associated with irreversible destruction of exocrine parenchyma, fibrosis and in the late stages, the destruction of endocrine parenchyma.

18
Q

What are the causes of chronic pancreatitis?

A
  • Long-term alcohol abuse (more common)
  • Recurrent bouts of acute pancreatitis
  • Long-standing obstruction of the pancreatic duct by calculi or neoplasms
  • Autoimmune injury to the gland (IgG4)
  • Hereditary pancreatitis (up to 25% of chronic pancreatitis has a genetic basis)
19
Q

Which two fibrogenic cytokines predominate in chronic pancreatitis?

A
  1. Transforming growth factor beta (TGF-beta)
  2. Platelet-derived growth factor (PDGF)

Induce the activation and proliferation of periacinar myofibroblasts (pancreatic stellate cells) → deposition of collagen and fibrosis

20
Q

What are the morphologic features of chronic pancreatitis?

A
  1. Fibrosis
  2. Atrophy and dropout of acini
  3. Variable dilation of the pancreatic ducts

Chronic pancreatitis caused by alcohol abuse is characterised by ductal dilatation and intraluminal protein plugs and calcifications

  • Chronic periductal and perilobular chronic inflammatory infiltrate
  • Ductal epithelium may be atrophied, hyperplastic or may show squamous metaplasia
  • Acinar loss is a constant feature
  • Relative sparing of the islets of Langerhans, which become embedded in the sclerotic tissue and may fuse and appear enlarged, but in advanced disease the islets are also lost
21
Q

What are the morphologic features of autoimmune pancreatitis?

A
  1. Duct-centric mixed inflammatory cell infiltrate
  2. Venulitis
  3. Increased numbers of IgG4-secreting plasma cells
22
Q

What are the clinical manifestations of chronic pancreatitis?

A
  • Intermittent or persistent abdominal pain
  • Pancreatic exocrine insufficiency → chronic intestinal malabsorption → hypoalbuminaemia → weight loss and oedema
  • Diabetes mellitus

Pathology - Pancreas (3 decks)

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