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NUTR 442 > ASPEN ch 28 pancreatitis > Flashcards

ASPEN ch 28 pancreatitis Flashcards

1
Q

__ released in acinar cytoplasm activates ____

A

trypsin; TNFa, IL1+6, pro-inflam cytokines

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2
Q

cascade of inflam peaks ___ h after inciting event, can lead to ___

A

24-36; organ failure

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3
Q

poorer outcomes associated with:

A

alcoholism, starvation, undernutrition, chronic inflammation (obesity)

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4
Q

risk of severe acute pancreatitis is ___x higher in obese

A

2-3

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5
Q

why alcohol abuse common associated with pancreatitis?

A

ethanol sensitize pancreas to injury

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6
Q

pancreatitis with alcohol/gene etiology commonly associated with:

A

ductal stones, strictures, outflow obstruction

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7
Q

90% of AP caused by:

A

alcohol abuse, gallstones, idiopathic

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8
Q

other causes AP?

A

drugs, autoimmune/tropical disease ,infection, hypertriglyceridemia, herediatry, malignancy

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9
Q

what is the sentinel acute pancreatitis event (SAPE) hypothesis?

A

virtually any etiology of AP if severe enough may lead to scarring and end organ damage

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10
Q

autoimmune induced pancreatitis usually associated with:

A

less severe acute attacks, small duct disease, silent disease–> chronic pancreatitis with malabsorption

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11
Q

ppl with hereditary pancreatitis , particularly ___ mutations, have increased risk of ____

A

PRSS1; pancreatic cancer

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12
Q

__ lvls ^ in first hours of AP, then ___

A

amylase; serum lipase

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13
Q

why amylase/lipase presence not specific?

A

cleared by kidneys so could be ^ if secretion impaired, many organs produce these

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14
Q

^ liver enzymes, or if liver enzymes wax and wane with bouts of ab pain, suggest ___etiology

A

biliary

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15
Q

nonbiliary causes of AP associated with:

A

pain steadily ^ then constant

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16
Q

to optimally manage pt and prevent complications, clinicians need to determine:

A

severity of acute event ASAP

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17
Q

how to determine disease severity?

A

CT scans assess necrosis, Ranson, Imrie, Apache 2 scores, SIRS criteria, blood tests for CRP

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18
Q

among scoring methods , ____ is more predictive of both severity and clinical outcomes

A

APACHE 2

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19
Q

early recognition of SIRS can prompt adequate management with __

A

intravascular volume replacement (prevent ischemic end organ damage)

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20
Q

why end organ damage

A

hypoperfusion, changes in microvascular blood flow induced by inflamm cascade

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21
Q

most beneficial management strategies for SAP:

A

ICU, delay CT, early EN, avoid prophylactic antibiotics, treat local complications

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22
Q

___ scans are used therapeutically as well as for dianosis

A

EUS and ERCP

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23
Q

why stones in common bile duct and pancreatic cysts often misssed?

A

artifacts from overlying gas and fluid filled bowel

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24
Q

__ scans used to grade AP:

A

CT

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25
Q

what is grade B pancreatitis?

A

focal/diffuse enlargement of pancreas

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26
Q

what is grade C pancreatitis?

A

pancreatic gland abnormalities accompanied by mild parapancreatic inflamm changes

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27
Q

what is grade D pancreatitis?

A

fluid collection in single location, usually in anterior pararenal space

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28
Q

what is Grade E pancreatitis?

A

2+ fluid collections near pancreas or gas either within pancreas or within parapancreatic inflam

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29
Q

grade A-E score is coupled with score for degree of ___ to see if ^ mortality risk

A

necrosis

30
Q

endoscopic procedure providing ultrasound exam of pancreas thru gastric wall

A

EUS (after AP attack)

31
Q

___ provides direct cannulation of pancraes and biliary ducts

A

ERCP

32
Q

ERCP beneficial to treat pt with ____

A

ascending cholangitis or retained common duct stones

33
Q

ERCP with ____ highly beneficial for manage pancreatic ascites and pleural effusions

A

stenting of pancreatic duct disruptions

34
Q

ERCP with measurement of presssure at ___ useful determine cause of idiopathic

A

sphincter of Oddi

35
Q

major indication for endoscopic therapy?

A

need for long term relief of bile duct strictures that occur as complication of fibrosis from chronic pancreatitis

36
Q

are prophylactic antibiotics useful?

A

nope

37
Q

mild vs severe nutr concerns?

A

wt loss from muscle catabolism minimal vs. hypermetabolic similar to sepsis (ox stress, catabolism SIRS)

38
Q

nutr decline in AP can result from reduced oral intake due to:

A

ab pain, nausea, vomiting, ileus, pancreatic rest

39
Q

why malabsorb and maldigest?

A

v enzyme output

40
Q

why excess pro loss?

A

steatorrhea, pancreatic fistulas, inflamm of peritoneal/retroperitoneal surface

41
Q

hyperglycemia risk relate to:

A

degree of pancreatic inflam, necrosis, obesity, prediabetes

42
Q

damage to inflam islet cells leads to decreased ___ production and impaired __ metabolism, resulting in hypertriglyceridemia from inadequate glucose control and v of lipoprotein lipase

A

insulin; lipid

43
Q

why v calcium?

A

v PTH, ^ calcitonin, v magnesium

44
Q

why EN?

A

maintain fut integrity, stim bloood flow to gut, stim secretory IGA and bile salts (prevent bacteria adherece), maintain gut-associated lympohid tissue, support commensal bacteria, lessen disease severity, v ox stress, faster resolution, reduce complications

45
Q

in SAP, pt on EN have increases in ___ capacity, faster decreases in ___ levels, and faster resolution of ____ when compared with PN pt

A

antioxidant; CRP; SIRS

46
Q

3 bad possibilities of early use of EN?

A

1) clinically silent ^ in pancreatic enzyme output 2) uncomplicated exacerbation of symptoms 3) significant exacerbation of symptoms and ^ in SIRS

47
Q

when EN indicated , ___ access easier than ___

A

gastric; jejunal

48
Q

pt who will not tolerate EN:

A

severe ileus or gastroparesis

49
Q

polymeric formulas infused distal to ___ inhibited pancreatic secretions better than PN

A

ligament of Treitz

50
Q

most common causes of diarrhea

A

sorbitol containing meds and C difficile

51
Q

if quantity of lipids in PN limited to less than ____and ____ control maintained, hypertriglyceridemia during PN diminished

A

1g/kg; glucose

52
Q

how to assess for readiness resume oral?

A

reduction in pain, absence of vomiting, CT, biochem markers

53
Q

in CP, gland has ____ changes including irreversible loss of _____ and ___ mass with replacement of stroma by ___ tissue, with or without lymp inflam cell infiltrate

A

ultrastructural; exocrine; endocrine; fibrous

54
Q

___ quadruples pt risk of AP progressing to CP

A

tobacco smoking

55
Q

why smoking cause CP?

A

vasoconstrictive nicotine, ox stress, toxic effects

56
Q

ppl at risk for hypertriglyceridemia induced pancreatitis:

A

hyperlipoproteinemia, DM, alcohol abuse, obesity, pregnancy

57
Q

fear of pain w/ eating

A

sitophobia

58
Q

complications of CP

A

diabetes, malabsorption, bile duct stricture, portal hypertension, duodenal stricture, pseudocysts, fistulas and ascites

59
Q

exocrine insufficiency occurs ____ yrs after onset of CP

A

10-12 (asini destruction)

60
Q

exocrine insufficiency manifests as:

A

diarrhea, steatorrhea, malassimilation

61
Q

what is steatorrhea?

A

quantitative appearance of >7 g fat/day after consuming 100g diet fat

62
Q

reliable, pt friendly, relatively inexpensive way to find out if ppl have steatorrhea

A

fecal elastase 1 test

63
Q

vitamin deficiencies common in CP?

A

fat sol, vit B12

64
Q

alcohol abuse contributes to ____ deficiencies

A

thiamin, folate, Mg, Zn

65
Q

major late sequelae of CP and independent risk factor for mortality

A

diabetes

66
Q

hallmark clinical symptom of CP

A

pain

67
Q

categories of pain:

A

nocioceptive (normal), neuropathic, psychogenic

68
Q

long term EN through ___

A

PEG

69
Q

enteric coated preparations of pancreatic enzymes resist degradation by gastric acid and require luminal pH greater than ___

A

5

70
Q

if use uncoated enzymes, prevent inactivation with ____

A

gastric acid suppression

NUTR 442 (34 decks)

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