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25 Cards in this Set
- Front
- Back
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Whats the difference between primary and secondary malnutrition?
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primary malnutrition is due to things being missed from the diet (improper intake)
secondary malnutrition is due to adequate intake, but malabsorption or impaired usage/storage/ increased need |
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What does PEM stand for? what is it?
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this is Protein energy malnutrition
an impairment of anabolic processes |
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What does Marasmus affect more severely?
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this typically affects Somatic Protein compartment (skeletal muscle)
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What does Kwashiorkor affect more severely?
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this affects visceral protein compartment most (internal organs and plasma proteins)
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Moderate energy deficit with sever protein deficit produces what disease? what are its signs?
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this produces Kwashiorkor
(shows as edema with the maintenance of some subcutaneous fat tissue) |
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Severe energy and protein deficit produce what disease? what are the signs?
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this produces Marasmus
(shows and skin and bones, with little to no sub cue fat) |
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How does marasmus develop? what does the body do to react? (RMR, protein synthesis)
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This develops slowly over time due to severe diet restriction (both protein and others)
the slow onset allows for adaptation- Low RMR, Low muscle protein synthesis, but normal plasma protein levels |
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How is Marasmus diagnosed?
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this is done by physical and history, as lab results are unremakable.
albumin may be reduced less O2 consumption due to low RMR |
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What are the two principle factors that lead to Kwashiorkor?
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Insufficient protein and marginal caloric intake
acute onset- triggered by infection or parasites which activate stress response (increased RMR) |
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How do TNF-alpha (Tumor Necrosis Factor- alpha) and IL-6 (interluken 6) lead to kwashiorkor?
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these inhibit the action of insulin, which stimulates protein degradation, and gluconeogenesis
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What does Insufficient amino acids due to PEM result in? (when considering Kwashiorkor)
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Edema- from low albumin synthesis
Decreased immune function Skin lesions and poor wound healing Random hyperpigmentation Hair changes |
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What causes fatty liver in Kwashiorkor?
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this is caused by IL-6 and TNF-a mediated insulin resistance and insufficient amino acids.
The insulin resistance leads to hyperglycemia, which leads to de novo FA synthesis. (from acetyl CoA)- Low amino acids reduces B100 production needed for VLDL synthesis (reduced export) |
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What are the major symptoms of Kwashiorkor
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Edema
immune dysfunction poor wound healing fatty liver skin and hair changes little fat is lost, due to acute onset |
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What is used to Diagnose Kwashiorkor?
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Albumin of below 2.8 gm/dL (with no weight loss)
AND one of these: Lymphopenia (1500/ul or less) Impaired wound healing Edema Easy Hair Pluckability |
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What causes cachexia?
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this is caused by a high RMR and anorexia (not eating)
leads to excessive weight loss and severe muscle wasting |
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How do Cytokine influence cachexia?
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these increase muscle wasting by reducing the transcription and translation of myosin
also high alpha MSH, and low NPY and AgRP produce anorexia |
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How does cortosol and epi afffect cachexia?
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these increase muscle wasting (more ubiquintin mediated system)
hyperglycemia (gluconeogenesis) high RMR decreased LPL increased lipolysis |
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what is Enteral Nutrition? when is it used?
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This delivers food to the upper GI tract, used when pt has normal absorptive capacity, but ingestion/digestion problems
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what is Parenteral nutrition? when is it used?
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this delivers nutrients to the blood stream, used with GI is non functional.
may use central or peripheral vein |
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Who needs nutritional support?
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people who have expected or present malnutrition
(sepsis, burns, trauma) |
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when is parenteral nutrition used in cachexia?
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in general it is not used, unless pt is expected to die of starvation before dying of the disease
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What is the preferred route of nutrition administration? why?
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Enteral administration (feeding tube) is preferred, as it keeps the GI alive.
CCK and gastrin stimulate intestinal growth/normal function |
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what type of entral tube is used if going for longer than 2 weeks?
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a PEG tube (percutaneous endoscopic gastrostomy) tube
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what kind of tonicity do parentral solutions have?
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these are hypertonic, so they must be put in large veins, for dillution
placed in large central veins (TPN/ Total Parenternal nutrition) short term (peripheral parenteral nutrition PPN) |
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How does tight insulin regulation help pts on paraenteral nutritional support?
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this reduces mortality, reduces bacteremia, excessive inflammation, organ failure, and polyneuorpathy
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