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Flashcards in Nutrition: Parenteral & Enteral Deck (81)
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31

What is the maximal oxidative capacity of glucose?

the max amount of glucose that is no longer needed to supply the energy needs of the body. the conversion of glucose into fat is an energy inefficient process that results in increased energy expenditure, increased O2 consumption and increased CO2 production

32

What should be done if there is unexplained CO2 retention?

decrease GIR, may have found maximum oxidative capacity; probably around 12-13; there are no good lab means for determining when this threshold has been exceeded

33

How can maximum oxidative capacity exacerbate respiratory course?

increased CO2 production

34

What are the advantages of IL administration?

prevention of essential fatty acid deficiency, normal growth and development, concentrated energy sources and a vehicle of the transport of the fat soluble vitamins

35

Why is 20% concentration preferred over 10% in all GA and wt classes?

decrease in risk of hypertriglyceridemia, hypercholesterolemia and hyperphospholipidemia; the phospohlipid content of 10% impedes plasma triglyceride clearance resulting in a increased tri and cholesterol serum concentration

36

How are IL prepared?

from soy and/or saffol oils, fatty acids, egg yolk. phospholipids and glycerin

37

What can happen if exogenous fats are not given?

fatty acid deficiency disorder can develop within 72h; can be prevented c as little as 0.5-1g/kg/d

38

The prevention of fatty acid deficiency can prevent what complications in the newborn?

decrease the incidence of complications a/w free radical formation such as BPD and ROP; manifests with dry, flaky skin

39

What are the fat soluble vitamins?

ADEK

40

How does IL fair in the peripheral vein?

relatively low osmolality and well tolerated; evidence to support that IL helps to maintain vessel latency

41

Where should your tri level be?

<150mg/dL

42

What is critical for brain development?

milk fat; specific fatty acids are required for myelin formation and neuronal growth, retinal development and as key complements for cell membranes

43

Why is the very preterm infant vulnerable to fatty acid supply insufficiency?

bc the major period for in utero fat secretion does not occur until the last trimester

44

What other additives can be found in TPN?

electrolytes, minerals, vitamins, trace elements and heparin

45

What are the special considerations for Na and K infusion?

we have daily needs for Na and K; do not add K until UOP has been est; other daily needs include acetate and Cl

46

What are the special considerations for mineral infusion?

Ca Gluconate, when considering how much to add, consider the route of administration- very caustic to the peripheral vein- limit Ca if giving PIV

47

What are the special considerations for vitamin infusion?

based on GA and current weight

48

What are the special considerations for trace element infusion?

neotrace: if pt has cholestasis, need to remove the copper and manganese (or decrease), if renal dysfx, then the chromium needs to be removed

49

Why is heparin added to the solution?

incudes lipoprotein lipase activity that enhances the clearance of triglycerides when administering IL, also decrease risk of thrombosis, decrease risk of catheter related sepsis and decrease phlebitis in peripheral lines and for PIV

50

How do you dose IL administration?

start at 0.5-1g/kg/d in a stable infant and increase by 0.5-1g/kg/d to 3g/kg/d

51

When does osmotic diuresis occur?

when spill a lot of glucose into the urine, and water follows

52

What are complications a/w protein administration?

metabolic acidosis with no other explanation (protein tolerance) and excessive elevation of BUN

53

What are complications a/w glucose administration?

osmotic diuresis, hyperosmolality, noter upper limits of glucose oxidative capacity, note lower limits of GIR in infants with hyperglycemia, if continued hyperglycemia, ensure that AA is being given, consider dc IL and consider insulin gtt

54

What are complications a/w IL administration?

lipid intolerance, altered glucose metabolism, increased free bilirubin concentrations, acute impaired pulmonary function and interference with immune function and plt fx

55

What are common complications of TPN?

nosocomial infx, hyperglycemia, metabolic bone dz and cholestatic jaundice

56

What are the most common nosocomial infx r/t TPN administration?

staph epi, staph aureus, candida albican and malessezia furfur

57

What is the pathoetiology of metabolic bone dz secondary to TPN?

caused by an imbalance of vitamin D, minerals and trace elements primarily due to inadequate Ca and Phosphorus and inadequate ratios of each

58

What is the pathoetiology of cholestatic jaundice secondary to TPN?

portal inflammation and bile duct proliferation, occurs in 7-10% of babies on prolonged TPN. enteral feeds stimulate bile flow and stimulate hormones that prevent cholestasis

59

Why can't glucose and calcium be maximized with peripheral vascular access?

bc of local irritation and the risk of infiltration

60

How should an infant be transitioned to enteral feds?

as soon as the baby's condition allows, enteral feeds are safer, more physiologic and cost effective, avoids s/e of parenteral nutrition and stimulates the development of the GI tract