Protein Energy Malnutrition (Look @ handout) Flashcards
If negative energy balance…
obligatory negative Nitrogen balance
Masamus
Severe wasting, due to energy deficiency
Slower onset, better adaptation
Kwashiorkor
Edematous PEM, generally w/o wasting
Protein deficiency (+ metabolic stress + micronutrient deficiency/imbalance)
Rapid onset, “mal-adaptation”
Starvation
pure caloric deficiency
Organism adapts to conserve lean body mass & increase fat metabolism
cachexia
associated w/ inflammatory or neoplastic conditions
Not reversed by feeding; anorexia
Sarcopenia
subnormal amount of skeletal muscle, w/o weight loss
Causes of PEM
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
Who is at risk for PEM?
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)
underweight definition
-low weight for age
->2 SD below median (50th percentile)
-
Stunting
“chronic malnutrition”
-Length for age (% of median)
Normal 95 - 105 %
Mild 90 - 94 %
Moderate 85 - 89 %
Severe:
Wasting
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
Fuel utilization during starvation
blood sugar drops some and levels
mobilization of fat stores
ketone bodies rise
Blood sugar remains in normal range: gluconeogenic aa + glycerol
Marasmus
“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
Other “normal” responses to starvation
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
Kwashiorkor: “abnormal” adaptive response
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
Signs of kwashiorkor
misery, edema, hepatomegaly
- erythematous, hyperpigmentation, “flaky paint”
- dry, brittle, depigmented “flag sign”
Rash looks like pelagra (“pelagroid”)
“moon facies” (swollen cheeks)
sx more in marasmus
Weight loss, loss of muscle, loss of fat, diarrhea
sx more in kwashiorkor
edema, psychologic changes, anorexia, hepatomegaly, infections, diarrhea, skin lesions, hair changes, moon facies
Principles of tx for Severe PEM
GO SLOWLY!!
Resolve life-threatening conditions (e.g. infections)
Restore nutritional status w/o abruptly disrupting homeostasis / “adapted state”
Ensure nutritional rehabilitation (Macronutrients & micronutrients)
Refeeding syndrome
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)
Management of refeeding syndrome
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)
