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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
what is grade B pancreatitis?
focal/diffuse enlargement of pancreas
26
what is grade C pancreatitis?
pancreatic gland abnormalities accompanied by mild parapancreatic inflamm changes
27
what is grade D pancreatitis?
fluid collection in single location, usually in anterior pararenal space
28
what is Grade E pancreatitis?
2+ fluid collections near pancreas or gas either within pancreas or within parapancreatic inflam
29
grade A-E score is coupled with score for degree of ___ to see if ^ mortality risk
necrosis
30
endoscopic procedure providing ultrasound exam of pancreas thru gastric wall
EUS (after AP attack)
31
___ provides direct cannulation of pancraes and biliary ducts
ERCP
32
ERCP beneficial to treat pt with ____
ascending cholangitis or retained common duct stones
33
ERCP with ____ highly beneficial for manage pancreatic ascites and pleural effusions
stenting of pancreatic duct disruptions
34
ERCP with measurement of presssure at ___ useful determine cause of idiopathic
sphincter of Oddi
35
major indication for endoscopic therapy?
need for long term relief of bile duct strictures that occur as complication of fibrosis from chronic pancreatitis
36
are prophylactic antibiotics useful?
nope
37
mild vs severe nutr concerns?
wt loss from muscle catabolism minimal vs. hypermetabolic similar to sepsis (ox stress, catabolism SIRS)
38
nutr decline in AP can result from reduced oral intake due to:
ab pain, nausea, vomiting, ileus, pancreatic rest
39
why malabsorb and maldigest?
v enzyme output
40
why excess pro loss?
steatorrhea, pancreatic fistulas, inflamm of peritoneal/retroperitoneal surface
41
hyperglycemia risk relate to:
degree of pancreatic inflam, necrosis, obesity, prediabetes
42
damage to inflam islet cells leads to decreased ___ production and impaired __ metabolism, resulting in hypertriglyceridemia from inadequate glucose control and v of lipoprotein lipase
insulin; lipid
43
why v calcium?
v PTH, ^ calcitonin, v magnesium
44
why EN?
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
in SAP, pt on EN have increases in ___ capacity, faster decreases in ___ levels, and faster resolution of ____ when compared with PN pt
antioxidant; CRP; SIRS
46
3 bad possibilities of early use of EN?
1) clinically silent ^ in pancreatic enzyme output 2) uncomplicated exacerbation of symptoms 3) significant exacerbation of symptoms and ^ in SIRS
47
when EN indicated , ___ access easier than ___
gastric; jejunal
48
pt who will not tolerate EN:
severe ileus or gastroparesis
49
polymeric formulas infused distal to ___ inhibited pancreatic secretions better than PN
ligament of Treitz
50
most common causes of diarrhea
sorbitol containing meds and C difficile
51
if quantity of lipids in PN limited to less than ____and ____ control maintained, hypertriglyceridemia during PN diminished
1g/kg; glucose
52
how to assess for readiness resume oral?
reduction in pain, absence of vomiting, CT, biochem markers
53
in CP, gland has ____ changes including irreversible loss of _____ and ___ mass with replacement of stroma by ___ tissue, with or without lymp inflam cell infiltrate
ultrastructural; exocrine; endocrine; fibrous
54
___ quadruples pt risk of AP progressing to CP
tobacco smoking
55
why smoking cause CP?
vasoconstrictive nicotine, ox stress, toxic effects
56
ppl at risk for hypertriglyceridemia induced pancreatitis:
hyperlipoproteinemia, DM, alcohol abuse, obesity, pregnancy
57
fear of pain w/ eating
sitophobia
58
complications of CP
diabetes, malabsorption, bile duct stricture, portal hypertension, duodenal stricture, pseudocysts, fistulas and ascites
59
exocrine insufficiency occurs ____ yrs after onset of CP
10-12 (asini destruction)
60
exocrine insufficiency manifests as:
diarrhea, steatorrhea, malassimilation
61
what is steatorrhea?
quantitative appearance of >7 g fat/day after consuming 100g diet fat
62
reliable, pt friendly, relatively inexpensive way to find out if ppl have steatorrhea
fecal elastase 1 test
63
vitamin deficiencies common in CP?
fat sol, vit B12
64
alcohol abuse contributes to ____ deficiencies
thiamin, folate, Mg, Zn
65
major late sequelae of CP and independent risk factor for mortality
diabetes
66
hallmark clinical symptom of CP
pain
67
categories of pain:
nocioceptive (normal), neuropathic, psychogenic
68
long term EN through ___
PEG
69
enteric coated preparations of pancreatic enzymes resist degradation by gastric acid and require luminal pH greater than ___
5
70
if use uncoated enzymes, prevent inactivation with ____
gastric acid suppression

NUTR 442 (34 decks)

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