Pancreas Function/Disorders Flashcards

1
Q

which arteries supply the pancreas?

A

celiac and SMA

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

exocrine pancreas is ___% pancreatic mass

exocrine pancreas makes ______

A

85%

digestive enzymes, water, bicarb –> duodenum

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

pancreatic embryology

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

common variations in pancreatic duct anatomy

A

90%- Santorini and major duct connected

10% - fusion does no occur = pancreas divisium –> higher risk for pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

regulation of pancreas secretion

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what determines bicarb secretion from the pancreas?

A

duodenal pH >4.5 - sensed in s/secretin cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how does the pancreas avoid digesting itself?

A

pancreatic enzymes are stored in pancreas and secreted into duodenum as PROENZYMES. Enterokinase at brush border in duodenum converts trypsinogen –> trypsin. Trypsin makes the other zymogens –> active enzymes.

amylase and lipase are stored in active forms b/c there is no starch or TG in the pancreas to be digested

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

5 protective mechanisms in the pancreas

A
  1. synthesis of enzymes as inactive zymogens
  2. trypsin inhibitor packaged in zymogen granules
  3. segregation of enzymes in membrane bound compartments
  4. enterokinase restricted to small intestine
  5. acidic pH w/in zymogen inactivates Trypsin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Labs in acute pancreatitis

A

WBC: often elevated

Amylase: leaks from inflamed pancreas. high sensitivity, low specificity

Lipase: sensitive as amylase, but more specific , and remainvs elevated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Atlanta criteria for Acute pancreatitis

A

two or more of the following:

  • ​abdominal pain consistent w/ acute pancreatitis: sudden onset upper abdominal pain, often radiating to upper back. steady pain w/ “boring” quality.
  • elevated amylase or lipase >3x normal
  • confirmatory finding on CT
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

normal amylase, high lipase - interpretation?

A

delayed presentation of acute pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how do gallstones cause pancreatitis?

A

migrate to the cystic duct –> common duct –> can obstruct the ampulla of vater –> pancreatitis and/or cholangitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

which pancreatic hormone is most specific in dx pancreatitis?

A

lipase

lots of things can cause elevation of amylase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do you assess the severity of pancreatitis?

A

Bedside eval

BISAP >2

  • BUN>25, impaired mental status, SIRS, Age>60, pleural effusions

BUN >22

CRP >125 @48 hrs

SIRS persisting through 48 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is SIRS?

A

presence of at least 2

  • pulse >90 BPM
  • RR >20 or PCO2<32mm Hg
  • T> 100.4 or <96.8
  • WBC> 12K or <4K
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are these and prognosis for each

A

left = interstitial

  • very low mortality and infection (<1%)

right = necrotizing

  • high infection rate (30-50%)
  • mortality 10-30%
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what causes acute pancreatitis?

A
  1. alcohol
  2. gallstones
  3. idiopathic
  4. other: high TGs, autoimmune, drugs, IBD, infectious, neoplasm, toxic, iatrogenic (ERCP), trauma, scorpion
18
Q

inherited causes of pancreatitis

A

altered enzyme activity: trypsinogen mutations

abnormal ion movement: CFTR mutation

metabolic: familial hypertriglyceridemia (TGs <1000)

19
Q

tx for acute pancreatitis

A

nothing to tx underlying pathophys

supportive care: IV fluids/lytes (EARLY and w/ Lactate Ringers), montioring, analgesia + antiemetics

other txs: Abx, NG tube, nutritional support, urgent ERCP (if gallstones)

20
Q

systemic complications of acute pancreatitis

21
Q

local complications of acute pancreatitis

A

fluid collection

necrosis

infection

ascites

erosion into adjacent structures

GI obstruction

hemorrhage

22
Q

what is a pancreatic pseudocyst?

A

localized collection of pancreatic fluid that develops >4 wks after pancreatitis onset

how to distinguish from true pancreatic cysts: absence of epithelial lining

23
Q

how to prevent infection in acute pancreatitis pt?

A

enteral feeding through jejunal tube! - to maintain gut barrier function

*abx use is controversial for prophylaxis

24
Q

causes of death in acute pancreatitis

A

early <1 wk: SIRS, multiorgan failure

late: multiorgan failure, pancreatic infections/sepsis

25
features of chronic pancreatitis
* pain * calcification * pancreatic insufficiency
26
what causes chronic pancreatitis?
* cystic fibrosis * hereditary pancreatitis (same conditions as acute) * hypertriglyceridemia * autoimmune * fibrocalcific (equatorial countries)
27
course of chronic pancreatitis
gradually progressive pain at presentation. decreases w/ longstandng disease. calcification, malabsorption, and diabetes increase w/ progression \*increased risk of pancreatic cancer
28
name 5 causes of pain in chronic pancreatitis
* ischemia * pseudocyst * inflammation (general and neural) * duodenal and common duct obstruction * PD obstruction --\> increased pancreatic pressure
29
at what point does pancreatic enzyme deficiency cause steatorrhea?
\<10% lipase output
30
calcifications in chronic pancreatitis
31
tx for chronic pancreatitis
enzyme replacement and H2 blockers pain tx: narcotics, neuro-modulators (antidepressants), anti-inflammatory drugs, somatostatin
32
surgical tx of chronic pancreatitis pain
lateral pancreaticojejunostomy
33
mild acute pancreatitis aka edematous or interstitial pancreatitis separation of pancreatic lobules from eachother b/c edema. no evidence of necrosis in acinus.
34
severe acute pancreatitis acinar tissue is totally necrotic and gone
35
acute pancreatitis w/ pseudocyst: area of pancreas has become liquefied and necrotic. no epithelial lining
36
wall of pseudocyst
37
chronic inflammation, fibrosis in chronic pancreatitis atrophy of acinar tissue
38
pathogenesis of pancreatitis
* ​injury of acinar cells: activation of proenzymes * duct obstruction w/ increased intraductal pressure --\> leakage of pancreatic enzymes * activation of trypsin and other proenzymes
39
necrosis-fibrosis hypothesis
one theory about pathogenesis of chronic pancreatitis repeated episodes of acute pancreatitis --\> focal necrosis, patchy scarring, duct distortion this is probably happening in chronic alcoholics
40
PRSS1
mutant cationic trypsogen gene --\> elimate trypsin last-resort off-switch high incidence of pancreatic carcinoma
41
CF and pancreatitis
defect in electrolyte transport --\> viscous material accumulates in ducts --\> obstruction
42
lab findings, histology and tx in autoimmune pancreatitis
Labs: autoantibodies or high IgG histology: CP w/ ductitis tx: steroids NOT SURGERY