ASPEN ch 17 - PN complications Flashcards
categories of PN complications?
mechanical, metabolic, infectious
most common complication associated with PN
hyperglycemia
why hyperglycemia?
stress associated, excess CHO admin
recommend target BG concentration between _____ mg/dL
140-180
PN should be initiated at ___ of estimated energy needs for first 24 hrs
half
CHO admin NOT exceed rate of _____mg/kg/min or ____kcal/kg/d in acutely ill
4-5; 20-25
giving subsequent dose of insulin too soon is referred to as:
stacking
rare reason for hyperglycemia?
chromium deficiency (makes insulin less effective)
hyperglycemia associated with these worsened clinical outcomes:
^ risk infection, poor healing, inability gain wt
why hypoglycemia?
excess insulin admin
abrupt PN d/c associated with:
rebound hypoglycemia
how to prevent rebound hyperglycemia?
1-2hr taper down of infusion
clinical manifestation of EFAD?
scaly dermatitis, alopecia, hepatomegaly, thrombocytopenia, fatty liver, anemia
a triene:tetraene ratio > ___ indicates EFAD
0.2
why PN need exogenous source of fat?
hypertonic dextrose infusion causes insulin secretion and reduction in lipolysis
__ based ILEs associated with immunosuppressive effects, exaggerated SIRS, reticuloendothelial system dysfunction
soy
how come certain LCFA impaire immune fxn?
interfere w/ phagocytosis and chemotaxis, ^ risk for infection
how does hypertriglyceridemia occur?
dextrose overfeeding or rapid admin rates ILE > 0.11g/kg/h
probs of hyperlipidemia?
impaire immune response, alter pulmonary hemodynamics, ^ risk pancreatitis
ILE intake should be restricted to < ___% energy or ___g/kg/d
30; 1
pancreatitis due to ILE hyperlipidemia rare unless serum TG > ___mg/dL
1000
when pro admin excess, metabolic demand of disposing of byproducts of pro metabolism ^, thus ___ can result
azotemia
prerenal azotemia result from:
dehydration, excess pro, inadequate nrg from nonpro sources
intolerance to protein load is characterized by____
^BUN
crystalline a.a. prevents ___ risk
hyperammonemia
why pt receiving both PN and warfarin need close monitoring?
vit K in the preparation interacts with warfarin –>therapeutic failure
pt with hx prolonged poor diet intake should have supplemental __ and __
thiamine; folic acid
vitamin that undergo degradation after addition to PN?
vit A
trace element deficiencies that may occur?
zinc, selenium
decrease ____ dosing in pt with hepatobiliary disease cuz impairs excretion
copper; manganese
adverse effects of metabolic and physio shifts of fluid/electrolytes/vit/min in aggressive nutr support or repletion of malnourished pt
refeeding syndrome
at refeeding risk ___ days after start of support
2-5
mechanism of refeeding?
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
why liver disease common in PN?
intestinal failure
3 types of hepatobiliary disorders associated with PN:
steatosis, cholestasis, gallbladder sludge/stones
what is steatosis?
hepatic fat accumulation
steatosis presents as modest elevations of serum ___
aminotransferase
condition of impaired secretion of bile or frank biliary obstruction that occurs predominantly in children
PNAC (PN-associated cholestasis)
PNAC typically presents as:
elevated alkaline phosphates, gamma-glutamyl transpeptidase, conjugated bilirubin [ ] w/ jaundice
elevated serum ))) considered prime indictator for cholestasis
conjugated bilirubin
gallbladder stasis during PN may lead to development of _____ with subsequent ____
gallstones/sludge; cholecystitis
gallbladder stasis has more to do with ____ than PN infusion
lack of enteral stim (v CCK and impaired bile flow)
biliary sludge may progress to ____ in the absence of gallstones, referred to as ____ cholecystitis
acute cholecystitis; acalculous
infection associated with ____
cholestasis
risk factors for liver disease:
SIBO, massive resection of intestine
development of steatosis in PN primarily cuz of:
excess nrg (promote hepatic fat deposition by stim insulin release, ^ lipogenesis and v f.a. oxidation)
why dextrose-based PN containing little/no fat implicated in steatosis?
excess CHO deposit as fat, and may result in EFAD which lead to impaired lipoprotein formation and TG secretion
CHO content not exceed ____g/kg/d for adults
7
high lvl ___ exposure may lead to develop cholestasis
aluminum
probs of phytosterols/
inefficiently metabolized, impaire bile flow and cause sludge/stones
primary ___ deficiency associated with steatosis
carnitine
why maybe supplement choline?
conversion of methionine to choline may be less efficient when methionine given PN instead of PO
this type of PN shown reduce serum liver enzyme and conjugated bilirubin
cyclic
form of bile acid used to treat various chronic cholestatic liver diseases
ursodiol
most common form of metabolic bone disease characterized by low bone mass, compromised bone strength, deterioration of bone tissue/architecture
osteoporosis
___ is characterized by softening/bending of bones that occurs cuz bones contain osteoid tissue that failed to calcify
osteomalacia
risk factors for bone loss?
post menopause, long term PN, endocrine disease, GI disease, malignancy, meds, genetic disease, immobilization, alcohol, anorexia nervosa, roux en y
calcium supplementation in PN limited by minerals’ physical compatibility with ___
P
inadequate ___ dose may ^ urinary Ca excretion
P
higher ___ doses associated ^ urinary Ca excretion
protein
correction of acidosis with ___ in PN can reduce urinary calcium excretion
acetate
cyclic or continuous more Ca losses?
cyclic
why vit D excess cause bone disease?
suppress PTH secretion and promote bone resorption
only allowed to have up to ___mcg aluminum/L
25
___ is a prominent manifestation of Mg deficiency
hypocalcemia
Mg deficiency results in v mobilization of Ca from bone thru these mechanisms:
^ 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
magnesium deficiency can lead to hypophosphatemia how?
^ P excretion
copper deficiency can impair ___ formation, causing ____
bone; osteoporosis
meds that decrease bone resorption:
bisphosphonates, raloxifene, calcitonin, estrogen, monoclonal antibody denosumab
only FDA approved med that stim bone formation
teriparatide
avoid adding ___ to reduce osteoporosis risk
heparin
most common deficiencies
selenium, linoleic acid, Zn, Cu, Chromium, fat/water sol vitamins
symptoms o hypophosphatemia:
parasthesia, muscular weakness, confusion, convulsions, coma
