11c. Clinical Aspects of Acute and Chronic Pancreatitis Flashcards

1
Q

serum amylase: why is it relevant?
name several tissues that it comes from?
what does it do?

A
  • cornerstone to diagnosis of pancreatitis! leaks from inflamed pancreas, then is reabsorbed.
  • comes from pancreas, salivary glands, fallopian tubes, ovaries, prostate, lung
  • acts on starch to split alpha 1-4 glucosidic bonds
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2
Q

serum amylase lab: what is its sensitivity and specificity for pancreatitis? (relative, not numbers)

A

sensitivity is high, esp early in course

specificity is low, esp at lower elevations

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3
Q

serum lipase: why is it relevant?
how does it change with time?
other conditions that will make it elevated?

A
  • as sensitive for acute pancreatitis as amylase, but more SPECIFIC
  • elevated the first day of illness, remains elevated longer than amylase
  • other intra-abdominal probs and renal insuff can elevate it (usually only to levels less than 1000 u/L)
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4
Q

Atlanta Criteria for acute pancreatitis?

A

Two of these three:

  • abd pain clinically consistent with acute pancreatitis
  • elevated amylase/lipase greater than 3x upper limit of normal
  • confirmation via abdominal imaging
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5
Q

clinical diagnosis of acute pancreatitis?

A
  • symptoms and PE
  • lab tests
  • other conditions ruled out
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6
Q

role of imaging in diagnosing acute pancreatitis?

A
  • not essential
  • confirmatory
  • stages severity, indicates complications
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7
Q

protective mechanisms in the pancreas that prevent activation of zymogens? (this info is also in another deck, but just for repetition)

A
  • enzymes are synthesized/stored in inactive form
  • trypsin inhibitor is packaged in zymogen granule just in case
  • enzymes are segregated in membrane-bound compartments
  • enterokinase exists only in the small intestine
  • acidic pH in granules inhibits trypsin
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8
Q

serum levels of amylase and lipase over time with acute pancreatitis? what levels might be seen in a case with delayed presentation?

A

both initially rise quickly, then amylase falls more quickly than lipase.
in a delayed presentation, labs may show elevated lipase but normal amylase (since it returned to nl more quickly)

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9
Q

what other conditions may elevate both serum amylase and serum lipase?

A
  • intestinal ulceration, obstruction, ulceration or ischemia. intraluminal pancreatic enzymes are re-absorbed from gut back into bloodstream due to damaged intestinal mucosa.
  • elevated amylase and slightly elevated lipase are seen in biliary tract disease and renal failure
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10
Q

two types of acute pancreatitis? what does Benson think about these two types?

A

mild and severe acute pancreatitis

Bensen thinks they are very distinct from each other (apples/oranges)

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11
Q

what are a few ways to assess the severity of acute pancreatitis?

A
  • BISAP > 2
  • BUN > 22
  • CRP > 150 at 48h
  • SIRS persisting at 48h
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12
Q

what is BISAP?

A

5 elements, 2+ = severe acute pancreatitis:

  • BUN > 25
  • Impaired mental status
  • SIRS
  • Age > 60
  • Pleural effusion
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13
Q

what is SIRS?

A

systematic inflammatory response syndrome. defined by at least 2:

  • Tachycardia: pulse > 90
  • Pulm: RR > 20 or PCO2 < 32
  • Temp: T > 100.4 or < 96.8
  • Infection: WBC > 12,000 or < 4,000
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14
Q

what are Ranson’s Criteria of Severity (general overview)?

A

(not on exam, may still be on boards)
eleven criteria taken both at time of admission and after 48h that predict the severity of outcome (mild v severe) in acute pancreatitis.

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15
Q

what feature of a patient will worsen the prognosis of acute pancreatitis?

A

OBESITY.

increases both severity and complications

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16
Q

Prognosis of mild (interstitial) v severe (necrotizing) acute pancreatitis?

A

mild (interstitial): infection and mortality both < 1%

severe (necrotizing): infection 30-50%, mortality 10-30%

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17
Q

Causes of death in acute pancreatitis if death occurs early on (< 1 wk)?

A

*multiorgan failure

SIRS

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18
Q

Causes of death in acute pancreatitis if death occurs later on (> 1 wk)?

A

*pancreatic infections, sepsis, infectious complications

multiorgan failure

19
Q

2 most common causes of acute pancreatitis?

A

alcohol, gallstones

also idiopathic and ‘other’ causes

20
Q

mechanisms for gallstone causing acute pancreatitis?

A
  • stone obstructing the common opening of the common bile duct and pancreatic duct, allows reflux of bile into the pancreas
  • obstructed pancreatic duct, same reflux problem
21
Q

what are a few things included in the ‘other’ category of causes of acute pancreatitis?

A

(impt because some of these causes are reversible)

  • drugs, toxins
  • metabolic and structural issues
  • autoimmune
  • infectious
  • neoplastic
  • trauma
22
Q

how does a gallstone look on ultrasound?

A

white round/oval mass with characteristic acoustic ‘shadow’ – darkened area where US was blocked by stone

23
Q

how does microlithiasis/biliary sludge look on ultrasound?

A

dense layer of material in dependent area of gallbladder. does not cause an acoustic shadow like a gallstone will.

24
Q

what anatomical anomaly puts pts at higher risk for acute pancreatitis?

A

pancreas divisum

25
Q

inherited causes of acute pancreatitis?

A
  • altered enzyme activity: trypsinogen mutation
  • Cystic Fibrosis (may not be a mutation severe enough to cause CF, but can still cause reduction in CFTR function -> pancreatitis)
  • familial hypertriglyceridemia
26
Q

familial hypertriglyceridemia: what are serum triglyceride levels? mechanism of causing pancreatitis?

A
  • serum TG levels > 1000
  • reversible, can also be drug-induced
  • mechanism (theoretical): lipase continuously released from pancreas, TG hydrolysis generates short chain FAs that are toxic to the pancreas
27
Q

mechanism by which trauma can cause acute pancreatitis?

A
  • midline injury, panc compressed against spine
  • may sever pancreatic duct
  • may cause ductal leak
  • may cause a gradual obstructing stenosis of duct at site of trauma
28
Q

a cause of pancreatitis in south america?

A

scorpion bite! toxin can cause pancreatitis.

found in central and south america and the caribbean

29
Q

strategies for altering the severity of acute pancreatitis?

A

unfortunately there is very little data to show that interventions exist.
in severe gallstone pancreatitis ERCP seems to help (removal of the stone)

30
Q

supportive care for acute pancreatitis?

A

aggressive fluid and electrolyte replacement
monitoring
analgesia

31
Q

systemic complications of acute pancreatitis?

A
shock/multiorgan failure
coagulopathy
resp failure
renal failure
hyperglycemia
hypocalcemia
32
Q

a local complication of acute pancreatitis that may self-resolve?

A

acute fluid collection, around the pancreas. usually resolve spontaneously but may require drainage (if infected or symptomatic)

33
Q

what is a pancreatic pseudocyst?

A

localized pancreatic fluid collection with a well-defined, fibrous wall. not lined by epithelium (hence PSEUDOcyst).

34
Q

why is someone with acute pancreatitis at incr risk for infection?

A

in the critically ill pt there is a breakdown in the fut barrier function, allows translocation of gut bacteria

35
Q

nutrition issues in pancreatitis: what should I do in mild acute pancreatitis? severe acute pancreatitis? TPN vs enteral? composition of diet?

A
  • nutritional support not as impt in mild acute pancreatitis: early recovery is expected
  • severe acute pancreatitis: nutritional support will speed recovery, prevent nutritional depletion.
  • enteral is beneficial and safe for severe acute panc.
  • give low fat elemental diet into the jejunum
36
Q

cardinal clinical features of chronic pancreatitis?

A
  • pain
  • calcification (intraductal)
  • panc insufficiency (endo and exocrine)
  • eventually: malabsorption, diabetes
37
Q

western countries; most common cause of chronic pancreatitis? other causes?

A

alcoholism

other causes include CF, hereditary, hypertriglyceridemia, autoimmune

38
Q

causes of pain in chronic pancreatitis?

A
  • acute pancreatitis superimposed on chronic (inf, pseudocysts)
  • obstruction -> incr pressure
  • nerve inflammation
39
Q

how diminished does a person’s lipase reserve have to get before the pt will show signs of steatorrhea?

A
  • capacity of panc to secrete lipase must decr to 10% of normal level before excess fecal fat excretion (steatorrhea)
  • so, we have impressive reserves of lipase
  • also, when a pt with chronic pancreatitis presents with steatorrhea, it implies that 90% of their pancreas is destroyed
40
Q

what’s the best way to detect pancreatic calcifications?

A

CT: more sensitive than abd Xray, often used if the xray is negative

41
Q

in patients with fat malabsorption due to severe pancreatic insufficiency, what is a possible treatment?

A

pancreatic enzyme supplements. decreased fecal fat excretion by greater than 50%

42
Q

pain management for chronic pancreatitis? what is the role of narcotics, TCAs, anti-inflammatories, decreasing pancreatic stimulation?

A
  • narcotics are first line. AE = addiction, pain from narcotic bowel syndrome
  • TCAs help some patients (neuromodulation)
  • anti-inf not shown to be helpful
  • somatostatin analogs (octreotide) not very helpful
43
Q

what is a lateral pancreaticojejunostomy?

A
  • aka Puestow procedure.
  • reduces pain in chronic pancreatitis
  • main pancreatic duct is opened, jejunum anastomosed so that pancreatic duct drains directly into the jejunum.