Pancreas Path/Pathophys I Flashcards

1
Q

What are the four protective mechanisms of the acinar cell that prevent autodigestion?

A

Inactive proenzymes
membrane enclosed
Separate pathways
Trypsin inhibitor

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2
Q

What stimuli act through cAMP on the acinar cell?

A

VIP, Secretin

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3
Q

What stimuli act through Ca2+ signaling on the acinar cell?

A

ACh

CCK

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4
Q

What is the earliest event in the pathogenesis of acute pancreatitis?

A

Conversion of zymogens to active forms within the acinar cells

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5
Q

What are the two mechanisms of injury in acute pancreatitis?

A

Block secretion and/or co-localization of ZG and lysosomes

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6
Q

Explain the pathogenesis of cytokines/inflammation and acute pancreatitis

A
  • Proteases activate complement
  • C3a and C5a recruit PMNs and macros
  • Inflammatory cells release cytokines (TNF, etc)
  • Vascular injury and inflammation
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7
Q

What are the ‘local effects’ of acute pancreatitis?

A

Autodigestion
Pancreatic edema
Fat necrosis and hemorrhage

Produces pain, nausea, vomiting

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8
Q

What kind of necrosis does acute pancreatitis cause?

A

Fat AND coagulative

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9
Q

What are some microscopic pathology findings in acute pancreatitis?

A

Fat necrosis between lobules
hemorrhage
coagulative necrosis

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10
Q

What mechanisms does the body have to contain pancreatitis?

A

Circulating alpha-antitrypsin
(inactivates proteases)

Circulating alpha macroglobulin
(binds trypsin and facilitates monocyte clearance)

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11
Q

What substance is responsible for fever, malaise, and confusion in severe pancreatitis?

A

TNF-alpha, IL-6

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12
Q

What are some vascular pathological mediators of severe pancreatitis?

A

kallikrein >hypotension
thrombin > DIC, hemorrhage
elastase > hemorrhage
chymotrypsin > hemorrhage

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13
Q

Explain the respiratory pathogenesis of acute pancreatitis?

A

PLA2 causes hypoxemia

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14
Q

Explain why acute pancreatitis causes hypocalcemia

A

Fat saponification of calcium and lipids depletes plasma levels

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15
Q

What are the main causes of acute pancreatitis?

A

Gallstones

Alcohol

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16
Q

How do you diagnose acute pancreatitis (methods)?

A

Elevated serum amylase
Elevated lipase
Inflammed pancreas on CT

17
Q

What is the cause of hereditary pancreatitis?

A

Trypsinogen mutation

18
Q

Diagnostic criteria for acute pancreatitis?

A

2/3 of:
-Abdominal pain, N, V
-Elevated amylase and lipase > 3x normal
Ct imaging showing inflammation

19
Q

What are some risk factors for gallstones?

A
Age > 50
Female
High amylase
High AST
High Alk Phos
20
Q

What is involved in the supportive management of acute pancreatitis?

A
NPO
Very aggressive fluids
Pain relief
Nutrition
Antibiotics if biliary
21
Q

What are some predictors of poor outcome in acute pancreatitis?

A

Admit w/ HCT > 44% w fail to dec in 24h

Admit w/ BUN > 25 w inc after 24h fluids

22
Q

What is the cause of chronic pancreatitis?

A

Chronic alcoholism (also CF)

23
Q

What are S/S of chronic pancreatitis?

A

Chronic abdominal pain
Diabetes
Steatorrhea

24
Q

Chronic pancreatitis pathophysiology

A

Chronic alcohol ingestion leads to abnormal secretions that cause protein plugs and ductal obstruction. This leads to calcification, recurrent acute episodes, and pain. Recurrent episodes cause stellate cell activation leading to fibrosis and further pain. The fibrosis and recurrent pancreas injury together cause cell death, leading to malabsorption and diabetes.

25
Q

Elevated liver enzymes and dilated common bile duct suggest this cause of acute pancreatitis?

A

gallstones

26
Q

Describe the chronic pancreatitis pathology

A

End-stage replacement of exocrine acini and ducts with fibroadipose tissue, BUT preservation of islets of Langerhans (because not digesting themselves)

27
Q

What is the first type of malabsorption to begin in CP?

A

Fat before protein or carbohydrate

Due to lipase deficiency

28
Q

Describe diabetes in CP

A

Only in severe disease (>80% destruction)
Loss of BOTH insulin and glucagon makes difficult to control
Low insulin requirements
Ketoacidosis is rare