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NUTR 442 > ASPEN ch 17 - PN complications > Flashcards

ASPEN ch 17 - PN complications Flashcards

1
Q

categories of PN complications?

A

mechanical, metabolic, infectious

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2
Q

most common complication associated with PN

A

hyperglycemia

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3
Q

why hyperglycemia?

A

stress associated, excess CHO admin

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4
Q

recommend target BG concentration between _____ mg/dL

A

140-180

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5
Q

PN should be initiated at ___ of estimated energy needs for first 24 hrs

A

half

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6
Q

CHO admin NOT exceed rate of _____mg/kg/min or ____kcal/kg/d in acutely ill

A

4-5; 20-25

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7
Q

giving subsequent dose of insulin too soon is referred to as:

A

stacking

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8
Q

rare reason for hyperglycemia?

A

chromium deficiency (makes insulin less effective)

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9
Q

hyperglycemia associated with these worsened clinical outcomes:

A

^ risk infection, poor healing, inability gain wt

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10
Q

why hypoglycemia?

A

excess insulin admin

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11
Q

abrupt PN d/c associated with:

A

rebound hypoglycemia

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12
Q

how to prevent rebound hyperglycemia?

A

1-2hr taper down of infusion

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13
Q

clinical manifestation of EFAD?

A

scaly dermatitis, alopecia, hepatomegaly, thrombocytopenia, fatty liver, anemia

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14
Q

a triene:tetraene ratio > ___ indicates EFAD

A

0.2

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15
Q

why PN need exogenous source of fat?

A

hypertonic dextrose infusion causes insulin secretion and reduction in lipolysis

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16
Q

__ based ILEs associated with immunosuppressive effects, exaggerated SIRS, reticuloendothelial system dysfunction

A

soy

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17
Q

how come certain LCFA impaire immune fxn?

A

interfere w/ phagocytosis and chemotaxis, ^ risk for infection

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18
Q

how does hypertriglyceridemia occur?

A

dextrose overfeeding or rapid admin rates ILE > 0.11g/kg/h

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19
Q

probs of hyperlipidemia?

A

impaire immune response, alter pulmonary hemodynamics, ^ risk pancreatitis

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20
Q

ILE intake should be restricted to < ___% energy or ___g/kg/d

A

30; 1

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21
Q

pancreatitis due to ILE hyperlipidemia rare unless serum TG > ___mg/dL

A

1000

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22
Q

when pro admin excess, metabolic demand of disposing of byproducts of pro metabolism ^, thus ___ can result

A

azotemia

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23
Q

prerenal azotemia result from:

A

dehydration, excess pro, inadequate nrg from nonpro sources

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24
Q

intolerance to protein load is characterized by____

A

^BUN

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25
Q

crystalline a.a. prevents ___ risk

A

hyperammonemia

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26
Q

why pt receiving both PN and warfarin need close monitoring?

A

vit K in the preparation interacts with warfarin –>therapeutic failure

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27
Q

pt with hx prolonged poor diet intake should have supplemental __ and __

A

thiamine; folic acid

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28
Q

vitamin that undergo degradation after addition to PN?

A

vit A

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29
Q

trace element deficiencies that may occur?

A

zinc, selenium

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30
Q

decrease ____ dosing in pt with hepatobiliary disease cuz impairs excretion

A

copper; manganese

31
Q

adverse effects of metabolic and physio shifts of fluid/electrolytes/vit/min in aggressive nutr support or repletion of malnourished pt

A

refeeding syndrome

32
Q

at refeeding risk ___ days after start of support

A

2-5

33
Q

mechanism of refeeding?

A

reintroduction of CHO cause insulin release which uptakes lots of gluc/lytes/min/water to cells, CHO admin increases demand for intracell P to synth ATP (v P), ^ need for thiamine/K/Mg

34
Q

why liver disease common in PN?

A

intestinal failure

35
Q

3 types of hepatobiliary disorders associated with PN:

A

steatosis, cholestasis, gallbladder sludge/stones

36
Q

what is steatosis?

A

hepatic fat accumulation

37
Q

steatosis presents as modest elevations of serum ___

A

aminotransferase

38
Q

condition of impaired secretion of bile or frank biliary obstruction that occurs predominantly in children

A

PNAC (PN-associated cholestasis)

39
Q

PNAC typically presents as:

A

elevated alkaline phosphates, gamma-glutamyl transpeptidase, conjugated bilirubin [ ] w/ jaundice

40
Q

elevated serum ))) considered prime indictator for cholestasis

A

conjugated bilirubin

41
Q

gallbladder stasis during PN may lead to development of _____ with subsequent ____

A

gallstones/sludge; cholecystitis

42
Q

gallbladder stasis has more to do with ____ than PN infusion

A

lack of enteral stim (v CCK and impaired bile flow)

43
Q

biliary sludge may progress to ____ in the absence of gallstones, referred to as ____ cholecystitis

A

acute cholecystitis; acalculous

44
Q

infection associated with ____

A

cholestasis

45
Q

risk factors for liver disease:

A

SIBO, massive resection of intestine

46
Q

development of steatosis in PN primarily cuz of:

A

excess nrg (promote hepatic fat deposition by stim insulin release, ^ lipogenesis and v f.a. oxidation)

47
Q

why dextrose-based PN containing little/no fat implicated in steatosis?

A

excess CHO deposit as fat, and may result in EFAD which lead to impaired lipoprotein formation and TG secretion

48
Q

CHO content not exceed ____g/kg/d for adults

A

7

49
Q

high lvl ___ exposure may lead to develop cholestasis

A

aluminum

50
Q

probs of phytosterols/

A

inefficiently metabolized, impaire bile flow and cause sludge/stones

51
Q

primary ___ deficiency associated with steatosis

A

carnitine

52
Q

why maybe supplement choline?

A

conversion of methionine to choline may be less efficient when methionine given PN instead of PO

53
Q

this type of PN shown reduce serum liver enzyme and conjugated bilirubin

A

cyclic

54
Q

form of bile acid used to treat various chronic cholestatic liver diseases

A

ursodiol

55
Q

most common form of metabolic bone disease characterized by low bone mass, compromised bone strength, deterioration of bone tissue/architecture

A

osteoporosis

56
Q

___ is characterized by softening/bending of bones that occurs cuz bones contain osteoid tissue that failed to calcify

A

osteomalacia

57
Q

risk factors for bone loss?

A

post menopause, long term PN, endocrine disease, GI disease, malignancy, meds, genetic disease, immobilization, alcohol, anorexia nervosa, roux en y

58
Q

calcium supplementation in PN limited by minerals’ physical compatibility with ___

A

P

59
Q

inadequate ___ dose may ^ urinary Ca excretion

A

P

60
Q

higher ___ doses associated ^ urinary Ca excretion

A

protein

61
Q

correction of acidosis with ___ in PN can reduce urinary calcium excretion

A

acetate

62
Q

cyclic or continuous more Ca losses?

A

cyclic

63
Q

why vit D excess cause bone disease?

A

suppress PTH secretion and promote bone resorption

64
Q

only allowed to have up to ___mcg aluminum/L

A

25

65
Q

___ is a prominent manifestation of Mg deficiency

A

hypocalcemia

66
Q

Mg deficiency results in v mobilization of Ca from bone thru these mechanisms:

A

^ release mg ions at bone surface in exchange for ^ bone uptake of Ca ions from serum; inhibit PTH release, so low PTH lvls for degree of hypocalcemia, functional v bone response to PTH so functional hypoparathyroidism

67
Q

magnesium deficiency can lead to hypophosphatemia how?

A

^ P excretion

68
Q

copper deficiency can impair ___ formation, causing ____

A

bone; osteoporosis

69
Q

meds that decrease bone resorption:

A

bisphosphonates, raloxifene, calcitonin, estrogen, monoclonal antibody denosumab

70
Q

only FDA approved med that stim bone formation

A

teriparatide

71
Q

avoid adding ___ to reduce osteoporosis risk

A

heparin

72
Q

most common deficiencies

A

selenium, linoleic acid, Zn, Cu, Chromium, fat/water sol vitamins

73
Q

symptoms o hypophosphatemia:

A

parasthesia, muscular weakness, confusion, convulsions, coma

NUTR 442 (34 decks)

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