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