Pancreas I: Acute and Chronic Flashcards

1
Q

What are the four protective mechanisms of acinar cell?

A

Inactive proenzymes
membrane enclosed
separate pathways
trypsin inhibitor

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2
Q

What are the four signals that act on the acinar cell to trigger zymogen release?

A

VIP, Secretin, Ach, CCK

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3
Q

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

A

the conversoin of pancreatic zymogens to their active forms within the acinar cell

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4
Q

What are the mechanisms of injury in acute pancreatitis?

A

blockage of secretion
co-localization of ZG and lysosomes
- premature zymogen activation
- autodigestion from within acinar cell

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5
Q

Explain the relationship of cytokines and acute pancreatitis?

A

proteases activate complement, C3A AND C5A recruit pmns and macrophages
inflammatory cells release cytokines (TNFa, IL1 PAF AND NO)
vascular injury and inflammatory responses

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6
Q

What are the local effect of acute pancreatitis?

A
autodigestion of pancreas
pancreatic sweeling (edema)
fat necrosis and hemorrhage

this leads to pain, n/v and abdom and radiating back pain (because retroperitoneal)

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7
Q

In acute pancreatitis where is the fat necrosis?

A

between lobules

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8
Q

What is the first radiographic sign of acute pancreatitis?

A

edema

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9
Q

How does the body respond to pancreatitis?

A

Circulating a1-antitrypsin and a-macroglobulin (binds to circulating trypsin and facilitates monocyte clearnace of macroglobulin-trypsin complexes)

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10
Q

What happens in inflammatory failure of containment to severe pancreatitis?

A

TNFa and IL6 leading to malaise fever and confusion

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11
Q

What happens in vascular failure of containment to severe pancreatitis?

A

kallikrein activation, thrombin activation, elastase chymotrypsin, leading to hypotension, dic hemorrhage

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12
Q

What happens in respiratory failure of containment to severe pancreatitis?

A

phospholipase a2 which degrades surfactant

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13
Q

What happens in metabolic failure of containment to severe pancreatitis?

A

fat saponification leading to hypocalcemia (bad for heart)

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14
Q

Describe the pathophysiology of acincar cell injury

A

insult to pancreas (i.e. etoh, obstruction)
intracellular activation of zymogens
cell necrosis and autodigestion

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15
Q

describe pathophy of local inflammatory response

A

cytokines and chemokines released by acinar cells
inflammatory cells recruited
inflammatory mediators released (tnfa il1)
pancreatic and vascular injury

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16
Q

describe pathophys of systemic response

A

circulating inflammatory mediators

sirs

17
Q

What are clinical causes of acute pancreatitis

A

gallstones and alcohol

18
Q

what are the main symptoms of acute pancreatitis?

A

abdominal pain, nausea vomiting

19
Q

How can you dx acute pancreatitis

A

elevated serum amylase and lipase, inflamed pancreas on ct

20
Q

What are the main causes of pancreatitis?

A

alcohol or gallstones

21
Q

What do you need to dx acute pancreatitis?

A

two of three:
abdominal pain, n/v
elevated serum amylase and lipase more than 3x upper limit of normal
ct imaging showing pancreatic inflammation

22
Q

What are risk factors for gallstones?

A

> 50 female with amylase over 4000, ast over 100, alk phosph over 300

23
Q

What are main predictors of poor outcome from acute pancreatitis?

A

hematocrit over 44% (from dehydration) bun over 25 mg/dl

24
Q

What is more common: interstitial pancreatitis or necrotizing?

A

interstitial (85%) with inflammation and edema

25
Q

37 yo wf with etoh prob and abdominal pain with increased amylase and ast and alt. Dilated cbd with no gallstones on CT. Dx?

A

gallstone pancreatitis because alcohol will not dilate the CBD

26
Q

Chronic Pancreatitis pathophys?

A

recurrent injury with tissue destruction and fibrosis. ie chronic alcohol ingestion
leads to abnormal secretion then protein plugs and ductal obstruction then to calcifications

27
Q

What are symptoms of chronic pancreatitis?

A

chronic abdominal pain, diabetes, steatorrhea

28
Q

Chronic pancreatitis is caused by

A

alcohol!!!!!!!!!!!!!!!80% gallstones don’t cause chronic pancreatitis

29
Q

What happens to stellate cells?

A

after recurrent bouts of pancreatitis and injury, stellate cells (which normally store vit. d.) become collagen producing cells.

30
Q

What do you see on histology in chronic pancreatitis?

A

little dark blue dots everywhere (lymphocytes), ducts are present but empty

31
Q

What does the pancreas become after chronic pancreatitsi?

A

fibroadipose tissue with preservation of islets of langherans

32
Q

why are islets of lagerhans preserved in chronic pancreatitis?

A

they don’t autodigest because they are endocrine. with severe pancreatitis though, they may be casualties.

33
Q

What are causes of pain in chronic pancreatitis?

A

increased pressure
biliary strictures and acute focal pancreatitis
and neural inflammation

34
Q

At what point do you see steatorrhea and diabetes in chronic pancre?

A

end-stage

35
Q

Why does steatorrhea occur in cp?

A

lipase deficiency

36
Q

Does lipase and proteinase deficiency occur first in cp?

A

lipase

37
Q

57 yo male adb pain diarrhea and weight loss. CT shows pan calcific and cystic stritures. increased amylase and glucose. next step?

A

address issues of alcohol ingestion