Protein Energy Malnutrition (Look @ handout) Flashcards

1
Q

If negative energy balance…

A

obligatory negative Nitrogen balance

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2
Q

Masamus

A

Severe wasting, due to energy deficiency

Slower onset, better adaptation

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3
Q

Kwashiorkor

A

Edematous PEM, generally w/o wasting
Protein deficiency (+ metabolic stress + micronutrient deficiency/imbalance)
Rapid onset, “mal-adaptation”

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4
Q

Starvation

A

pure caloric deficiency

Organism adapts to conserve lean body mass & increase fat metabolism

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5
Q

cachexia

A

associated w/ inflammatory or neoplastic conditions

Not reversed by feeding; anorexia

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6
Q

Sarcopenia

A

subnormal amount of skeletal muscle, w/o weight loss

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7
Q

Causes of PEM

A
Social & economic factors
Poverty
Inadequate breastfeeding
Ignorance
Inappropriate weaning/CF
Monotonous/restricted diets, plant-based	

Biologic factors: maternal under-nutrition, low birth weight infants – persistence of effects (epigenetic?)

Environmental factors: overcrowding, infectious burden, agricultural patterns, etc

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8
Q

Who is at risk for PEM?

A

Infants (0-12 mo): marasmus/severe wasting most common
Older infants (12 - 24 mo): esp kwashiorkor; voluntary restrictive/alternative feeding
Acute weight loss: e.g. anorexia nervosa, s/p bariatric surgery, intentional restriction, social deprivation
Chronic illnesses: alcoholism, pancreatitis, HIV/AIDS, malabsorption
Elderly: wasting/loss of LBM (sarcopenia)

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9
Q

underweight definition

A

-low weight for age
->2 SD below median (50th percentile)
-

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10
Q

Stunting

A

“chronic malnutrition”
-Length for age (% of median)

Normal 95 - 105 %
Mild 90 - 94 %
Moderate 85 - 89 %
Severe:

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11
Q

Wasting

A

decreased weight relative to length (approx equal to BMI)

“ideal body weight”
50th % wt/ht

%IBM
90-110 Normal weight
80-89 Mild wasting
75-79 Moderate

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12
Q

Fuel utilization during starvation

A

blood sugar drops some and levels
mobilization of fat stores
ketone bodies rise

Blood sugar remains in normal range: gluconeogenic aa + glycerol

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13
Q

Marasmus

A

“normal” response to starvation

Muscle: increase utiliz of triglycerides/fa
brain: inc utiliz of ketones
liver: decreased gluconeogenesis
muscle: decreased protein deg (increased recycing aa, but contiues esp skel muscle)
liver/kidney: decreased urea production and excretion

result:Utilization of fat stores, minimize muscle wastingleading to decreased Basal Metabolic Rate

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14
Q

Other “normal” responses to starvation

A

Dec Physical activity/ ↑ resting
Decreased Basal Metabolic Rate:
Hypothermia, hypotension, bradycardia

Endocrine changes:
dec insulin, dec thyroid, ↑ epinephrine & corticosteroid
GI tract: mucosal atrophy, decreased secretions, decreased motility
Myocardial atrophy, decreased cardiac output;

Loss of functional reserve & physiologic responsiveness to stress

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15
Q

Kwashiorkor: “abnormal” adaptive response

A

Classic etiologic description:
protein deficiency (qualitative &/or quantitative) w/ adequate energy
Current description: + Infectious stress, cytokine release, + micro-nutrient deficiency, oxidative damage, (“dysbiosis”?)
** Hypoalbuminemia & edema **
increased insulin, decreased lipolysis (esp. w/ continued CHO )
increased hepatic fatty acid syn (inc CHO & dec lipolysis, dec protein) –> fatty, enlarged liver

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16
Q

Signs of kwashiorkor

A

misery, edema, hepatomegaly

  • erythematous, hyperpigmentation, “flaky paint”
  • dry, brittle, depigmented “flag sign”

Rash looks like pelagra (“pelagroid”)

“moon facies” (swollen cheeks)

17
Q

sx more in marasmus

A

Weight loss, loss of muscle, loss of fat, diarrhea

18
Q

sx more in kwashiorkor

A

edema, psychologic changes, anorexia, hepatomegaly, infections, diarrhea, skin lesions, hair changes, moon facies

19
Q

Principles of tx for Severe PEM

A

GO SLOWLY!!
Resolve life-threatening conditions (e.g. infections)
Restore nutritional status w/o abruptly disrupting homeostasis / “adapted state”
Ensure nutritional rehabilitation (Macronutrients & micronutrients)

20
Q

Refeeding syndrome

A

Broad range of metabolic consequences occurring due to rapid reinstitution of nutrients (& energy/substrate) in pt w/ PEM; can result in sudden death
Catabolic state –> anabolic state:
Fluid shifts –> heart failure
Requires E, nutrients, enzymes
Common derangements: K+, P+, Mg,++ Thiamine (look at slide for specifics)

21
Q

Management of refeeding syndrome

A

Refeed slowly (start w/ 50-75% of basal needs)
Avoid fluid overload (enteral vs IV)
Monitor levels – supplement as necessary (K, P, Mg); provide micronutrients
Monitor vital signs
Monitor physical exam (e.g. edema, rash)
Resolution of edema before full feeding (wt loss first w/ edematous PEM)