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G.I & Nutrition > Pancreatitis > Flashcards

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?

A

> 1000

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?

A

calcium

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

A

yes

24
Q

Does this enhance trypsin activation? low calcium

A

no –> high calcium does

25
Q

Does this enhance trypsin activation? triglycerides

A

yes

26
Q

Does this enhance trypsin activation? CCK

A

yes

27
Q

Does this enhance trypsin activation? gastric distension

A

yes

28
Q

Does this enhance trypsin activation? SPINK1

A

no –> inhibitor

29
Q

Does this enhance trypsin activation? somatostatin

A

no –> inhibitor

30
Q

Tx of acute pancreatitis

A

NPO (bowel rest), iv fluids, pain control, ultrasound bladder, CT, surgery, antibiotics

31
Q

What is chronic pancreatitis?

A

permanent damage with fibrosis, exocrine/endocrine dysfunction/loss

32
Q

Features of chronic pancreatitis

A

calcifications, duct stones, irregular dilated duct without mass, beads on a string dilated side branches, atrophy without mass

33
Q

Best test for early pancreatitis?

A

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
Q

T/F cancer risk increases along spectrum of chronic pancreatitis

A

T

35
Q

3 theories of pathophysiology of chronic pancreatitis

A
  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
Q

Consequences of chronic pancreatitis

A

diabetes, steatorrhea, pain, cancer, b12 def, biliary obstruction

37
Q

Type 3 diabetes

A

pancreatogenic diabetes: development can indicate cancer, no glucagon/somatostatin so hypoglycemia, usually no ketoacidosis, very insulin sensitive

G.I & Nutrition (43 decks)

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