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Study Flashcards

1
Q

Steps to treat hyperemesis gravidarium

A
  • IVF with multivitamins and B vitamins
  • antiemetics
  • avoidance of PO
  • EN if unable to take PO after 24-48 hrs
  • PN if EN trial failed
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2
Q

failed EN trial for hyperemesis is

A
  • n/v/d exacerbation
  • significant gastric residuals
  • tube displacement
  • associated with >5% weight loss
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3
Q

Infusion of phosphate should not exceed

A

7 mmol/hr

can cause thrombophlebitis and metastatic calcium-phosphate deposition with potential of organ dysfunction

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4
Q

most common complication with PN administration

A

hyperglycemia

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5
Q

cause of hyperglycemia in the stressed patient

A

 increased insulin resistance
 increased gluconeogenesis and glycogenolysis
 suppressed insulin secretion

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6
Q

glycemic target for critically ill adult

A

 140-180 mg/dL
 110-140 in some cases if can be safely achieved
 <110 not recommended due to adverse effects of hypoglycemia

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7
Q

components of basal-bolus regimen

A

o Basal insulin
o Nutritional component prior to meals
o Correctional insulin

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8
Q

Glutamine dipeptides in parenteral solutions improve…

A

 Improve water solubility
 Improve stability during heat sterilization
 Improve capability for prolonged shelf life

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9
Q

is free glutamine stable in PN

A

no

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10
Q

is parenteral or enteral glutamine more beneficial

A

parenteral - enteral is protein bound and difficult to determine exact content

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11
Q

factors associated with PN prescribing errors

A

o Inadequate knowledge regarding PN therapy
o Certain patient characteristics – ex. age, impaired renal fnx
o Miscalculation of PN dosages
o Specialized PN dosage formulation
o Prescribing nomenclature

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12
Q

how to order PN ingredients

A

o Amounts/day for adults
o Amounts/kg/day for pediatric and neonatal
o Limits confusion of conversion from amounts/L, % concentration, and volume

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13
Q

High output fistula is

A

> 500 ml/day

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14
Q

Is PN routine in Chron’s

A

no

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15
Q

preferred nutrition intervention in acute pancreatitis

A

EN

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16
Q

When to use PN in burn patients

A

only if unable to feed enterally

linked with increased mortality

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17
Q

when may an adult cancer patient benefit from PN preoperatively

A

when severely malnourished and the therapy is to continue 7-10 days postoperatively

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18
Q

PICC

A

a catherter inserted via peripheral vein whose distal tip lies in the vena cava
o Cephalic or basilic vein is often the insertion site

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19
Q

PICC disadvantages

A

 High rate of malposition
 Limited arm mobility
 Limited ability to perform daily self-care due to availability of only one hand

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20
Q

PICC advantages

A

 No risk of pneumothorax
 Available as double, single, triple lumen
 Does not require repeated skin puncture

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21
Q

CDC recommendations regarding PICCs

A

 Do not routinely place to prevent infection
 Catheter replacement at scheduled intervals has not shown decrease in catheter related infections
 Catheter insertion with guidewire is associated with less discomfort and mechanical complication
• Replacement during bacteremeia should not be done over a guidewire
 Remove PICC only if it is suspected or known to be the source of the infection

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22
Q

central line

A

catheters with the distal tips in either the superior or inferior vena cava

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23
Q

common complication of bedside central line placement

A

misplacement including pneumothorax

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24
Q

when can you start infusion after central line placement

A

immediately if placed with fluoroscopy

if not must radiographically confirm first

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25
Q

can you auscultate to confirm central line tip placement

A

no

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26
Q

Institute for Healthcare Improvement central line bundle

A

 Group of evidence-based interventions that results in better outcomes when implemented together
 Recommends avoiding central venous access devices with high risk for infection, such a femoral catheters, when other access is available

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27
Q

preferred central line site

A

subclavian

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28
Q

peripheral line osmolarity

A

up to 900 mOsm/L

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29
Q

osmolarity of 10% dextrose

A

500

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30
Q

osmolarity of 3% amino acid

A

300

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31
Q

1 g AA contributes how much osmolarity

A

10 mOsm

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32
Q

1 g dextrose contributes how much osmolarity

A

5 mOsm

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33
Q

how does increased amino acid affect calcium phosphate precipitation

A

reduces risk by forming soluble complexes with calcium reducing free calcium ions available and lowers pH improving calcium phosphate solubility

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34
Q

does CaCl or calcium gluconate dissociate more readily

A

CaCl

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35
Q

Increased temp affect on dissociation of calcium salts

A

increases dissociation increasing risk of precipitation

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36
Q

in what order should Ca and Phos be added to reduce risk of precipitate

A

phos first and ca near end - not back to back

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37
Q

when does calcification occur in pn

A

serum calcium level multiplied by serum phos level exceeds 55 mg/dl

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38
Q

when are branched chain amino acids indicated in encephalopathy

A

o Only indicated in chronic encephalopathy for those who cannot tolerate at least 1 gm/kg/day of standard protein despite optimal phamacotherapy

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39
Q

EFAD may be caused by

A

Failure to provide at least 2-4% of total caloric intake as linoleic acid and 0.25-0.5% as alpha linolenic acid may lead to deficiency

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40
Q

adult lipids to prevent EFAD

A

500 mL 10% or 250 ml 20% twice weekly

500 ml 20% once weekly

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41
Q

infant lipids for EFAD prevention

A

05-1 g/kg/day

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42
Q

lab to test for EFAD

A

triene to tetraene ratio >0.2

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43
Q

EFAD can occur within ___ of exclusive PN without fat emulsion

A

1-3 weeks

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44
Q

lipid infusion rate in adults

A

no more than 0.11 gm/kg/hr

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45
Q

lipid infusion rate in children

A

no more than 0.15 gm/kg/hr

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46
Q

lipid infusion rate in neonates

A

no more than 0.17 gm/kg/hr

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47
Q

is 10 or 20% lipid emulsion better

A

20%

allows more efficient triglyceride clearance

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48
Q

10% lipid emulsion is less ideal than 20% because

A

has increased phospholipid content which is associated with plasma lipid alterations

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49
Q

avoid triglyceride of

A

 >400 in adults

 >200 in peds

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50
Q

physical mixture (lipids)

A

emulsion of two or more oils

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51
Q

structure lipid

A

created through hydrolysis of triglycerides and transesterification of fatty acids to form composite triglyceride molecule with various propotions of MCFA and LCFA
 Advantage over physical mixture because slower rate of release and utilization of MCFA

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52
Q

what should be reduced in hepatobiliary disease PN due to impaired excretion

A

manganese

copper

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53
Q

aluminum contamination from parenteral nutrition causes

A

aluminum toxicity

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54
Q

sources of PN aluminum contamination

A

 Calcium and phosphate salts
 Heparin
 Albumin
o No clear evidence that insulin is source

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55
Q

daily aluminum should not exceed

A

5 mcg/kg/day

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56
Q

how is manganese excreted

A

90% via bile into feces

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57
Q

Manganese toxicity

A

can occur on long term PN

accumulates in brain affecting CNS

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58
Q

monitor manganese by

A

MRI brain imaging

erythrocyte or whole blood assessment (60-80% in RBCs)

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59
Q

what may increase risk of manganese toxicity

A

cholestasis and biliary obstruction

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60
Q

early phase of manganese toxicity

A

weakness
anorexia
headache
apathy

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61
Q

 only transfer, measuring, and mixing manipulations with closed or sealed packaging systems performed promptly and attentively

A

low contamination risk

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62
Q

 compounding PN using manual or automated devices with multiple injections, detachments, and attachments of nutrient source products to the device or machine to deliver to final sterile container

A

medium contamination risk

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63
Q

 using nosterile ingreadient or nonsterile devices prior to terminal sterilization

A

high contamination risk

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64
Q

extemporaneously compounded L-glutamine for supplementation in PN formulation

A

high contamination risk

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65
Q

cracking - emulsion destabilization

A

 small lipid particles coalesce to form large droplet
 signs
• yellow brown oil droplets near TNA surface
• continuous layer of yellow-brown liquid at the surface
• marbling streaking of oil throughout
 clinical danger

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66
Q

creaming - emulsion destabilization

A

 occurs almost immediately once IVFE mixed with other chemical constituents
 cream layer visible at surface as translucent band separate from remaining dispersion
 common, not significant determinant of infusion safety except in extreme cases

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67
Q

PN CHO intake should not exceed

A

4 mg/kg/min

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68
Q

rapid infusion of phosphate can result in

A

tetany due to abrupt decrease in serum calcium concentration

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69
Q

metabolic alkalosis can be caused by

A
  • NG suctioning
  • volume depletion
  • diuretic use
  • excess acetate
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70
Q

markers of metabolic alkalosis

A

increased pH
normal PaCO2
increased serum bicarb

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71
Q

ex of metabolic bone disease

A

osteomalcia
osteoporosis
osteopenia

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72
Q

aluminum toxicity can cause what (in terms of bone health)

A

osteomalacia by…
• Impairing calcium bone fixation
• Inhibiting the conversion of vit d
• Reducing PTH secretion

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73
Q

aluminum toxicity is worsened by

A

renal insufficiency

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74
Q

most important contributor to metabolic bone disease

A

negative calcium balance

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75
Q

hypocalcemia occurs from

A
  • Decreased calcium intake

* Increased calcium urinary excretion

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76
Q

hypercalcemia occurs from

A
  • Excessive calcium and inadequate phos supplementation
  • Excessive protein in PN
  • Cyclic PN infusion s
  • Chronic metabolic acidosis
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77
Q

protein should not exceed what to help prevent hypercalcemia

A

o Ideally will not exceed 1.5g/kg/day

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78
Q

what is used to dx metabolic bone disease

A

bone mineral density

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79
Q

risk factors for metabolic bone disease

A

chron’s
cancer
short bowel
hyperthryoidism

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80
Q

chron’s contributes to metabolic bone disease because of

A

 Malabsorption of Ca and vit D

 Use of corticosteroids

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81
Q

short bowel contributes to metabolic bone disease because of

A

renal wasting of Ca

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82
Q

PNALD is reduced by

A

o Cycling PN
o Supplementing with enteral
o Adding ursodiol
o Increasing omega 3:omega 6 ratio

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83
Q

3 basic types of hepatobiliary disorders associated with PN

A

steatosis
cholestasis
gallbladder sludging/stone

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84
Q

steatosis

A 
•	Mild elevation in 
o	Minotransferases
o	Serum alkalin phosphatase
o	Bilirubin concentraton 
o	Complication of overfeeding
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85
Q

cholestasis from PN is primarily in

A

children

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86
Q

cholestasis

A
  • Impaired biliary secrection
  • Elevation conjugated bilirubin levels, alkalin phos, gamma glutamyltransferase
  • > 2 mg/dL serum conjugated bilirubin is indicator
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87
Q

gallbladder sludging in PN is result of

A

lack of enteral stimulation

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88
Q

hypertonic hyponatremia

A

o Hyperglycemia causes shift of water out of cells into EC space, diluting serum sodium

not true sodium or water imbalance

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89
Q

for every 100 mg/dL increase in serum glucose above 100 mg/dL, serum sodium is expected to

A

decrease by approximately 1.6 mEq/L

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90
Q

causes of hyperglycemia in patient receiving PN

A
  • CHO >4-5 mg/kg/min or 20-25 kcal/kg/day
  • stress associated sepsis
  • obesity
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91
Q

 Develops when fibrin build up inside of vein causes the vascular access device to adhere to the vessel wall

A

mural thrombus

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92
Q

 Layer of fibrin that develops around the outside of a central venous catheter secondary to aggregation of fibrin from the presence of a central venous catheter within a vein

A

fibrin sheath

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93
Q

fibrin sheath often results in

A

withdrawal occlusion

fibrin acts as a one-way valve

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94
Q

fibrin sheath is a

A

thombotic catheter occlusion

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95
Q

fibrin tail

A

 Fibrin build up on the CVC tip

 Allows infusion through but prevents withdrawal of blood

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96
Q

intraluminal thrombus

A

 Clot within the catheter lumen
 Caused by inadequate flushing and blood reflux
 Inability to infuse and aspirate without resistance

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97
Q

pinch off syndrome

A

 Catheter is compressed between first rib and clavicle causing intermittent compression and pinching

pain relived by raising or lowering the arm

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98
Q

pinch off syndrome leads to

A
  • intermittent occlusion of infusion and aspiration

* increased risk of catheter fracture

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99
Q

treatment of pinch off syndrom

A

removal of catheter and reinsertion at more lateral position in subclavian vein or placement in internal jugular vein

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100
Q

central venous thrombosis

A

 arm, shoulder, or neck swelling, limb, jaw, ear pain, dilated collateral veins over arm, neck, or chest

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101
Q

O.1N hydrochloric acid for clearing

A

• Crystalline occlusion because its acidic pH is favorable for calcium and phosphate solubility

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102
Q

sodium bicarb for clearing

A

• Precipitates associated with medication in high pH range such as tobramycin and phenytoin

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103
Q

70% ethanol for clearing

A

lipid reside

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104
Q

Groshong CVC

A

 Three-position, pressure sensitive valve that restricts blood backflow and air embolism by remain closed when not in use

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105
Q

Groshong CVC eliminate

A

needs for heparin flushes for patency

should be flushed with NS after med admin or blood aspiration to ensure closed

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106
Q

Systematic approach to prevent unnecessary catheter removals and/or unnecessary instillationsof compounds to relive the catheter occlusion

A

Obtain thorough hx of signs/symptoms of catheter malfunction from patient
 Double-check cather function for patency and blood aspitation
 Check for mechanical causes and assess if occlusion nis related to postural changes
• Clamps, kinked tubing, tigh sutures
 Obtain thorough hx of recent flushing techniques, medication ninfusion, and blood aspiration
 Assess for physical signs of edema, redness, pain, or dilated vessels

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107
Q

refeeding

A

sodium retension
hypophosphatemia
hypokalemia
hypomagnesemia

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108
Q

Na retention in refeeding leeds to

A

fluid overload
pulmonary edema
cardia decompensation

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109
Q

hypophosphatemia in refeeding leads to

A

respiratory failure and seizures

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110
Q

hypokalemia in refeeding leads to

A

cardiac arrhythmias and neuromuscular effects

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111
Q

hypomagnesemia in refeeding leads to

A

cardiac arrhythmias and neuromuscular effects

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112
Q

Max PN components

A

o 30-40 ml/kg/day of fluid
o 7 gm/kg/day CHO
o 2.5 gm/kg/day fat
o 2 gm/kg/day protein

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113
Q

clinical exit site infection

A

 Erythema, tenderness or purulence within 2 cm of catheter exit site

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114
Q

management of clinical exit site infection

A
  • Culture of drainage
  • Blood culture
  • Topical antimicrobial agent if no purulence and no clinical signs of sepsis
  • Systemic antimicrobial if purulenc is present or if topical is unsuccessful
  • Removal if systemic fails or patient has clinical signs of sepsis
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115
Q

most common infection for tunneled central venous catheter

A

contamination of catheter hub

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116
Q

most common infection for nontunneled central venous catheter

A

extraluminal colonization of catheter or intraluminal colonization of hub and lumen

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117
Q

how to decrease risk of catheter-associated sepsis

A

 Use of full-barrier precutions during catheter insertion
 Skin prep with chlorhexidine
 Avoid prophylactic use of antibiotic ointment at catheter exit site to not encourage resistant flora growth
 No evidence that antibiotic prophylaxis reduces incidence
 Do educate health care personelle on how to maintain

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118
Q

Malassezia furfur

A

 Associated with superficial infections of the skin and associated sutures
 Yeast
 Cause of catheter-related blood stream infection
 Most common in premature infants and patients receiving IVFE

119
Q

treatment of Malassezia furfur

A
  • Discontinue IVFE
  • Remove catheter
  • Antifungal therapy
120
Q

refractory hypokalemia can be due to

A

hypomagnesemia due to accelerated renal potassium loss or impairment of Na-K pump activity

121
Q

respiratory acidosis

A

o Decreased pH
o Elevated PaCO2
o Normal sodium bicarb

122
Q

respiratory acidosis is related to

A

overfeeding

123
Q

check blood glucose for diabetics getting PN

A

every 2-6 hours

124
Q

max CHO infusion rate

A

4 g CHO/kg/min

125
Q

how much insulin/gm dextrose

A

0.05-0.1 units

then increase by adding 2/3 previous days sliding scale insulin requirement

126
Q

standard formulas are what % free water

A

85

127
Q

osmolarity of gastric secretions

A

300 mOsm

128
Q

osmolarity of 1 kcal/ml formula

A

300-350

is istonic

129
Q

osmolarity of 1.2 kcal/ml

A

400-450

130
Q

osmolarity of 1.5 kcal/ml

A

500-650

131
Q

osmolarity of 2 kcal/ml

A

700-800

132
Q

nitrogen output

A

losses + 2 g for insensible losses

133
Q

hold TF for abdominal distension when girth exceeds baseline measurement by

A

8-10 cm

134
Q

NPH is

A

intermediate

135
Q

NPH/regular is

A

intermediate

136
Q

insulin glargine is

A

long acting

137
Q

tube feeding syndrom

A

related to high protein TF without adequate fluid leads to azotemia, hypernatremia, and dehydration

138
Q

EN formula label should contain

A 
o	Patient identifiers
o	Product name
o	Enteral access delivery site
o	Administration method
o	Time/date the formula was prepared and hung
139
Q

optimal sodium concentration o fORS

A

90-120 mEq/L

140
Q

gastric residual check

A

every 4 hrs for the first 48 hours

141
Q

when to use promotility agents with GRVs

A

2 checks > or = 250 ml

142
Q

do not introduce cows milk before

A

12 months

143
Q

iron requirements in infants

A

2-4 mg/kg/day

144
Q

increased intake of juice, soda, and SSB put children at risk for

A

magnesium and calcium deficiency

145
Q

how much milk for adequate calcium in kids age 4-8

A

3 - 8 oz glasses/day

146
Q

how much milk for adequate calcium intake for teens

A

4 - 8 to 10 oz glasses/day

147
Q

85th to 94th percentile

A

overweight

148
Q

> 95%ile

A

obese

149
Q

precocious puberty is associated with

A

advanced bone age

150
Q

genetic short stature typically have bone age

A

similar to chronological age

151
Q

hypothyroidism causes what in children regarding bone health

A

delayed bone age

152
Q

growth hormone causes what in children regarding bone health

A

delayed bone age

153
Q

cushing syndrome causes what in children regarding bone health

A

delayed bone age

154
Q

fenton growth chart

A

allows comparison for preterm infants from 22 weeks gestastional age up through 10 weeks post term age

155
Q

Z-score

A

express how far a child’s weight falls from median on growth charts

156
Q

below -3 z score

A

severely wasted

157
Q

below -2 z score

A

wasted

158
Q

above 2 z score

A

overweight

159
Q

above 3 z score

A

obese

160
Q

potassium for children

A

2-4 mEq/kg

161
Q

Holliday segar

A

estimates caloric expenditure in fixed weight categories

assumes for each 100 calories metabolized, 100 ml h20 is required

162
Q

calculation for Holliday segar

A
  • 1st 10kg – 100 ml/kg/day
  • 2nd 10kg – 50 ml/kg/day
  • Each additional kg – 20 ml/kg/day when <50kg
  • Or 15 ml/kg when >50 kg
163
Q

Mosteller’s formula

A

body surface area fluid calculation

the square root of height cm x weight kg divided by 3600, this is then multiplied by 1500ml/day

164
Q

Vitamin D deficient rickets

A 
	Low or normal serum calcium
	Low or normal serum phosphorus
	High alkaline phosphatase
	Increased PTH
	Low 25OH vit D levels 
	1,25 OH vit D low to normal
165
Q

Vitamin D dependent rickets

A

 1,25 OH vit D will be elevated

166
Q

renal tubular acidosis

A

 Abnormal serum creatinine

 Abnormal anion gap

167
Q

osteogenesis imperfecta

A

 Genetic disease characterized by multiple bone fractures, short stature
 Diagnosed by physical exam
 Labs WNL

168
Q

acute diarrhea

A

<14 days

169
Q

persistent diarrhea

A

14 days or longer

170
Q

chronic diarrhea

A

longer than 30 days

171
Q

zinc for children with diarrhe

A

20 mg/day for 10-14 days

172
Q

zinc for infants <6 mo with diarrhea

A

10 mg/day for 10-14 days

173
Q

infant vitamin D requirement

A

400 IU

174
Q

contraindications to NG feeding in baby

A

 Upper airway secretions
 Nasal polyps
 Recurrent sinusitis
 Otitis

175
Q

galactosemia

A

 Inborn error of metabolism that affects ability to metabolize galatose
 Only treatment is to eliminate galatose

176
Q

There is a higher concentration of galactose in

A

lactose free milk

177
Q

infant formula osmolarity

A

<460 mOsm/kg

178
Q

standard infant formula Kcal @ 20 Kcal/oz and osmolarity

A

200-380

179
Q

osmolarity of infant protein hydrolysate

A

330-370

180
Q

standard infant formula at 30 Kcal osmolarity

A

450

181
Q

CHO modular impact on osmolarity

A

increases

182
Q

fat modular impact on osmolarity

A

none

183
Q

preterm formulas contain how much lactose vs glucose

A

40-50% lactose

50-60% glucose

184
Q

preterm formulas contain what % MCT

A

40-50% - easier to absorb than the long chain in regular

185
Q

when will regurgitation resolve

A

7-12 months

186
Q

max GIR in infant

A

14-18 mg/kg/min

187
Q

lipids for infants

A

0.5-1 g/kg/day

188
Q

essential AA in neonates

A

taurine

tyrosine

189
Q

give which AA in smaller amounts to neonate

A

phenylalanine
methionine
glycine

190
Q

pediatric selenium recommendation

A

2 mcg/kg/day

191
Q

energy needs of critically ill and postop neonate

A

significantly lower due to absence of growth, decreased activity, and reduction of insensible losses

192
Q

use how much pancreatic enzyme to reduce risk of fibrosing colonopathy

A

<10,000 units lipase/kg/day

193
Q

CF related diabetes is related to

A

mucus obstruction of pancreatic beta cell preenting insulin secretion and potentially leading to beta cell destruction

194
Q

meconium ileus

A
  • Intestinal obstruction, mass in right lower quadrant, abdominal
  • Most often in neonate
  • Not caused by high dose enzyme therapy
195
Q

Jejunum is primary site of absorption for…

A

water soluble vitamins with the exception of b12 which is in the ileum

196
Q

complete ileal resection precludes absorption of

A

vit b12 and bile acids - increases diarrhea

197
Q

PKU is deficiency in

A

phenylalanine hydroxylase

198
Q

PKU treatment

A

restrict phenylalanine and supplement tyrosine

199
Q

biliary atresia

A

atrophy of the bile ducts
causes obstruction of bile flow from the liver to the biliary system and small intestine causing malabsorption of fat and fat soluble vitamins

200
Q

cylothorax

A

accumulation of chyle in the pleural space due to thoracic duct damage

associated with cardiac surgery

201
Q

if burns are > than what %, needs cannot be met by PO alone

A

20%

202
Q

Ebb response lasts

A

3-5 days

203
Q

Ebb response includes

A 
o	Depressed ree
o	Hyperglycemia
o	Low plasma insulin
o	Loss of plasma volume
o	Decreased oxygen consumption
o	Decreased BP
o	Reduced cardiac output
o	Decreased body temperature
204
Q

flow response includes

A
  • Elevated catecholamine
  • Elevated or normal plasma insulin
  • Hyperglycemia
  • Elevated glucagon and glucocorticoids
  • High glucagon-to-insulin ratio
  • Catabolism
  • Increased body temp
  • Increased cardiac output
  • Redistribution of polyvalent cations such as zinc and iron
  • Mobilization of metabolic reserves
  • Increase urinary excretion of nitrogen, sulfur, magnesium, phos, and potassium
  • Accelerated gluconeogenesis
205
Q

flow response peaks

A

between day 6 and 10 following injury

206
Q

typically home PN is covered for patients with

A

 Less than or equal to 5 feet of small bowel beyond the ligament of Treitz
 Gastrointestinal losses exceeding 50% of oral intake
• 2.5-3 liters/day in and >1.25-1.5 liters/day out
 Bowel rest required for at least 90 days and 20-35 cal/kg/day prescribed

207
Q

special justification for home PN coverage when

A
  • Calorie outside of 20-35/day
  • Protein outside 0.8-1.5 G/kg/day
  • Lipid use >1500 Gm/month
208
Q

symptoms of hypocupremia

A 
	Anemia
	Leukopenia
	Foot numbness
	Gain difficulty 
	Dysfunction of spinal cord
209
Q

anemia associated with low copper

A

macro or normocytic

210
Q

symptoms of spinal cord disfunction from copper deficiency

A
  • Paresthesisa and numbness in lower extremities
  • Sensory ataxia
  • Spastic gait
211
Q

copper deficiency can look similar to

A

B12 deficiency

212
Q

Magnesium brain deposition can occur when IV administration is

A

1.1 mg/day

213
Q

what potentiates action of insulin

A

chromium

214
Q

symptoms of zinc deficiency

A
  • Loss of taste
  • Altered smell
  • Skin rash
  • Growth failure
  • Alopecia
  • Decreased muscle work capacity
  • Gonadal hypofunction leading to decreased plasma testosterone and fertility
215
Q

acute phase response for iron and ferritin

A

decreased iron

increased ferritin

216
Q

folate absorption

A

converted to monoglutamate by jejunal enzymes for entry into intestinal wall

then further reduced before portal circulation for reabsorption via enterohepatic circulation

217
Q

folate absorption limited by

A
  • Zinc deficiency
  • Chronic alcohol consumption
  • Changes in jejunal luminal pH
  • Impaired bile secretion
218
Q

choline is required for

A

lipid transport and metabolism

219
Q

0.85 RQ

A

mixed substrate

220
Q

<0.82 RQ

A

underfeeding

lipid catabolism

221
Q

> 1 RQ

A

overfeeding, lipogenesis, increased respiratory demand

222
Q

> 1 RQ indicates

A

excessive CO2 production

223
Q

stress phase lasts

A

24 hours

224
Q

catabolic phase lasts

A

7-10 days

225
Q

selenium status measured by

A

plasma glutathione peroxidase
erythrocyte content
blood levels

226
Q

signs of Vit D toxicity

A 
o	Nausea
o	Vomiting
o	Weakness
o	Fatigue
o	Diarrhea
o	Headache
o	Confusion
o	Tremor
o	Soft tissue calcification in long term
227
Q

signs of vit D deficiency

A

o Hypocalcemia
o Osteomalacia
o Osteoporosis

228
Q

ileal brake

A

 Inhibitor feedback which slows gastric emptying and intestinal transit
 Triggered by fat in distal ileum

229
Q

Swinamer equation

A

 Uses body surface area in addition to physiological variables to predict RMR
 Found to be predictive in ~55%

230
Q

SMOF

A

 30% soybean
 30% MCT
 25% olive
 15% fish

231
Q

SMOF omega6:3 ratio

A

2.5:1

232
Q

albumin half life

A

14-20 days

233
Q

retinol binding protein half life

A

12 hrs

234
Q

prealbumin half life

A

2-3 days

235
Q

transferrin half life

A

8-10 days

236
Q

acid base disorder from diuretic

A

metabolic alkalosis

loss of bicarb poor CL rich EC restricting EC volume
now same amount of bicarb in smaller volume

237
Q

short chain fatty acid chain length

A

2-4 carbons

238
Q

medium chain length

A

6-12 carbons

239
Q

long chain length

A

14-18 carbons

240
Q

butyric length

A

short

241
Q

lauric length

A

medium

242
Q

stearic length

A

long

243
Q

oleic length

A

long

244
Q

very long chain fatty acid length

A

20 carbon or more

245
Q

most enteral dietary lipids are ingested as

A

trglycerides

246
Q

fatty acids up to ___ can be absorbed directly via the villi of the intestinal mucosa

A

10 carbons

247
Q

long chain triglycerides require

A

bile salts for digestion and formation of micelles

248
Q

fatty acids are oxidize for ATP

A

in any cell with mitochondria

249
Q

linoleic and alpha linoleic acids require what to enter mitochondria

A

L-carnitine

due to long chain length

250
Q

carnitine is required as

A

cofactor for transformation of free long-chain fa into acylcarnitines and transport into the mitochondria

251
Q

majority of fat digestion occurs where

A

duodenum by pancreatic lipase

252
Q

what hydrolyzes fat in small intestine

A

pancreatic lipase
cholesterol ester hydrolase
phospholipase

253
Q

role of bile salts

A

emulsifiers in fat digestion

254
Q

oils rich in linoleic acid

A

corn
soybean
safflower

255
Q

oils rick in alpha linolenic

A

soybean

canola

256
Q

soybean lipid emulsion composition

A

55-60% linoleic

3-4% alpha linolenic

257
Q

body water females

A

50%

258
Q

body water males

A

60%

259
Q

TBW composition

A

2/3 IC

1/3 EC

260
Q

EC water compostion

A

1/4 intravascular

3/4 interstitial

261
Q

urea accounts for __% total urinary nitrogen loss

A

80%

262
Q

skeletal muscle contains how much glycogen

A

300-400 grams

<1560 Kcal

263
Q

Na cotransporters are required for what vitamins

A 
C
B6
E
D
B1
choline
264
Q

determine amount of N in protein

A

divide total grams protein by 6.25

265
Q

leucine in fasting

A

increase in bloodstream and in the muscle

oxidation in the muscle increases

266
Q

pyruvate oxidation in fasting

A

limited by acetyl coa production

267
Q

pyruvate and lactate in fasting

A

pyruvate reduced to lactate

both return to liver for gluconeogenesis

268
Q

AMDR have been established for

A

omega 3, 6, and total fat

269
Q

Hartnup’s syndrome

A

 Autosomal recessive disorder

 Basic amino acids are not absorbed

270
Q

hartnup’s may present as

A

pellagra like

  • dermatitis
  • diarrhea
  • dementia
271
Q

substrate for NO production

A

arginine

272
Q

increased pCO2 from pulmonary insufficiency

A

decreases pH

273
Q

increase pCO2 is greatest

A

with overfeeding

274
Q

loop diuretics cause

A

o Excess K and mag excretion – hypokalemia and hypomagnesemia
o Azotemia due to volume depletion

275
Q

iron absorbed

A

duodenum

276
Q

calcium absorbed

A

duodenum

277
Q

folic acid absorbed

A

proximal jejunum

278
Q

b12 absorbed

A

distal ileum

279
Q

wet beriberi

A

 Enlarged heart
 Nonspecific electrolyte abnormalities
 Vasodilation
 Peripheral neuritis

280
Q

which suppresses more acid

PPI or H2-blockers

A

PPI

281
Q

PPI requires what for absorption

A

50 cm of jejunum

use liquid in severe sbs

282
Q

small bowel bacterial overgrowth can lead to

A

metabolic acidosis

283
Q

Zinc is necessary for

A

 Synthesis of granulation ntissue
 Reepithelialization
 Anti-inflammatory
 Antimicrobial

284
Q

zinc deficiency seen in

A

 Diarrhea
 Malabsorption
 Hypermetabolic states

285
Q

zinc serum level in stress

A

falls as albumin primary transporter

286
Q

cyclosporine can cause

A

 Hyperkalemia
 Hypomagnesemia
 Hyperglycemia
 Hypercholesterolemia

287
Q

deficiencies common after gastric bypass

A 
	Thiamin
	Zinc
	Folate
	B12
	Iron 
	Copper
288
Q

copper deficiency can be a complication of

A

celiac disease

289
Q

conditionally indispensable AA include

A 
	arginine 
	cysteine
	glutamine
	glycine
	proline
	tyrosine
290
Q

SIADH

A

hyponatremia
 Inappropriate ADH release leading to increased total body water and dilutional hyponatremia
 Increased sodium concentration and osmolaltity in urine due to excessive water reabsorption

291
Q

small intestine length

A

300-600 cm

292
Q

need PN when small intestine

A

<120 cm

though can be as little as 60 cm if ileocecal valve present

293
Q

valoproic acid induces what type of deficiency

A

carnitine

CNSC (1 decks)

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