Pancreatitis Flashcards

1
Q

What is acute pancreatitis?

A

acute inflammation of pancreas and associated adjacent organs without evidence of chronic pancreatitis –> “intraabdominal burn”

  • Atlanta criteria 2/3: pain, radiography, amylase/lipase elevated
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2
Q

Severe acute pancreatitis will not occur without _____

A

retroperitoneal fat around it

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3
Q

Clinical features of acute pancreatitis

A

severe steady band-like upper abdominal pain, radiating to back –> 10-20 mins onset, lasts several days, 90% vomit/fever, 5-10% painless

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4
Q

What is the nature of most late complications of acute pancreatitis?

A

infection

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5
Q

Charcot’s triad

A

fever, jaundice, right upper quadrant pain: cholangitis

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6
Q

Pathophysiology of acute pancreatitis

A

trypsin activates zymogens in pancreas –> autodigestion of pancreatic cells –> autocascade –> inflammation/polys –> release of neutrophil lactase –> IL1,6 –> leaky capillaries, thrombosis, necrosis –> fluid in lungs –>system response –> hypotension, bowel shutdown, kidney shutdown (all due to blood rushing to pan creas)

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7
Q

How do cardiac arrhythmias occur due to pancreatitis?

A

fat digestion –> tgs converted to AA –> attract calcium/magnesium –> saponification –> hypocalcemia –> arrhythmia

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8
Q

Most common manifestation of pancreatitis?

A

mild/interstitial: <1% mortality

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9
Q

Most severe manifestations of pancreatitis?

A
  1. infected necrotizing pancreatitis (late): 50% mortality

2. necrotizing/severe pancreatitis (20% of cases): 20 % mortality

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10
Q

2 most common causes of acute pancreatitis

A

alcohol and gallstones

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11
Q

What kind of effect is pancreatitis?

A

cholinergic

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12
Q

M or F: Biliary pancreatitis

A

F

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13
Q

Biliary pancreatitis clinical marker

A

elevated ALT (not entirely sensitive so can’t rely on this)

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14
Q

Mechanism of alcohol pancreatitis

A

damages mitochondria, lysosome instability –> ROS, abnormal blood flow and secretion, sensitization to CCK resulting in zymogen activation

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15
Q

M or F alcohol pancreatitis

A

M

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16
Q

How high to TG have to be to get pancreatitis?

17
Q

How high do amylase/lipase have to be to get pancreatitis?

A

no threshold…can be normal!

18
Q

Is pancreatitis a response to high or low glucose?

A

high glucose –> high TG –> pancreatitis

19
Q

What is the R122 mutation?

A

mutation in autodigestion portion of trypsin that leaves it constitutively active

20
Q

What molecule can activate trypsin?

21
Q

What mutation prevents inhibition of trypsin?

A

loss of both copies of SPINK1

22
Q

Does this enhance trypsin activation? high pH

A

no –> low pH does

23
Q

Does this enhance trypsin activation? bile

24
Q

Does this enhance trypsin activation? low calcium

A

no –> high calcium does

25
Does this enhance trypsin activation? triglycerides
yes
26
Does this enhance trypsin activation? CCK
yes
27
Does this enhance trypsin activation? gastric distension
yes
28
Does this enhance trypsin activation? SPINK1
no --> inhibitor
29
Does this enhance trypsin activation? somatostatin
no --> inhibitor
30
Tx of acute pancreatitis
NPO (bowel rest), iv fluids, pain control, ultrasound bladder, CT, surgery, antibiotics
31
What is chronic pancreatitis?
permanent damage with fibrosis, exocrine/endocrine dysfunction/loss
32
Features of chronic pancreatitis
calcifications, duct stones, irregular dilated duct without mass, beads on a string dilated side branches, atrophy without mass
33
Best test for early pancreatitis?
secretin stimulation test/direct test of pancreatic function--> do it b/c damage starts before pain happens so pancreatitis is already underway upon clinical presentation give secretin and see bicarb production: >80 is normal
34
T/F cancer risk increases along spectrum of chronic pancreatitis
T
35
3 theories of pathophysiology of chronic pancreatitis
1. ductal obstruction from calcifications/protein precipitates activate trypsin causing upstream damage 2. oxidative stress from alcohol/cck/smoking leads to stellate cell activation and fibrosis 3. acute inflammatory attacks lead to necrosis and cytokine release that lead to chronic damage and fibrosis
36
Consequences of chronic pancreatitis
diabetes, steatorrhea, pain, cancer, b12 def, biliary obstruction
37
Type 3 diabetes
pancreatogenic diabetes: development can indicate cancer, no glucagon/somatostatin so hypoglycemia, usually no ketoacidosis, very insulin sensitive