Malnutrition Flashcards

1
Q

PEM definition

A
  • Protein energy malnutrition:
    • Multi-nutritional deficiency complex in which deficiency of energy is most commonly the outstanding deficit –> if negative energy balance, obligatory negative N balance
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2
Q

Causes of malnutrition (environmental and biological)

A
  • Environmental: overcrowded or unsanitary living conditions, agricultural patterns, droughts, floods, wars
  • Biological: maternal malnutrition (low birthweight infants), infectious diseases
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3
Q

Clinical consequences of malnutrition

A
  • Impaired immune and GI function
  • Leads to vicious circles of malnutrition, infection, and diarrhea
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4
Q

Energy/substrate metabolism in short term vs. long term starvation

A
  • Short term: gluconeogenesis
  • Long term: fatty acid oxidation –> production of ketone bodies
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5
Q

Marasmus: definition

A
  • Severe wasting of fat and muscle mass, due primarily to energy deficiency
  • Most equivalent to “simple” starvation
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6
Q

Marasmus: pathophysiology

A
  • Reduction in energy expenditure –> decreased physical activity, bradycardia, hypothermia
  • Decreased activity of sodium pump
  • Shift in fuel utilization to mobilization of body fat –> increased ketones, decreased gluconeogenesis
  • Muscle protein catabolism - but with increased overall protein turnover
  • Decreased inflammatory response and impaired immune function
  • Impaired function of GI tract (dysmotility, malabsorption)
  • Result: loss of functional reserve, loss of physiological responsiveness to stress
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7
Q

Kwashiorkor: definition

A
  • Edematous protein energy malnutrition
  • Without wasting
  • Due predominantly to protein deficiency and metabolic stress
  • Higher mortality than marasmus
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8
Q

Kwashiorkor: pathophysiology

A
  • Unknown, but thought to be failure of normal adaptive response of protein sparing usually seen in fasting state
  • Contributing factors: infectious stress, cytokine release, relative micronutrient deficiencies, possibly free radical exposure and oxidative damage
  • Fat reserves and muscle mass tend to be unaltered
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9
Q

Kwashiorkor: signs/symptoms

A
  • Skin lesions (“flaky paint”)
  • Hair texture and pigmentation changes (“flag sign”)
  • Hypoalbuminemia and enlarged fatty liver –> edema (“moon facies”)
  • Increased insulin, decreased lipolysis
  • Increased hepatic fatty acid synthesis
  • Increased permeability of biological cell membranes –> edema
  • Impaired sodium/potassium homeostasis (increased Na+, decreased K+)
  • Hypotransferrinemia (anemia)
  • Impairment of immune system (increased infection)
  • Protein deficiency (especially on a multiple choice test)
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10
Q

Marasmic kwashiorkor

A
  • Combination of chronic energy deficiency and chronic or acute protein deficit
  • Clinical evidence of both wasting and edema
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11
Q

Relationship between age and marasmus/kwashiorkor

A
  • 0-12 mo: marasmus/severe wasting most common form of PEM
    • Stunting common < 1 y/o
  • 12-24 mo: kwashiorkor/edematous PEM more common
  • Older children: stunting common; milder degree of wasting
  • Pregnant/lactating women: with PEM, effects are primarily on fetus, neonates, and infants
  • Elderly tend to suffer from PEM
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12
Q

Physical exam findings associated with marasmus

A
  • Weight loss ++++
  • Loss of muscle ++++
  • Loss of fat ++++
  • Psych impairment ++
  • Anorexia +/-
  • Associated infections ++
  • Diarrhea +++
  • Hair changes +/-

NO edema, hepatomegaly, or skin lesions

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13
Q

Physical exam findings associated with kwashiorkor

A
  • Weight loss ++
  • Loss of muscle +
  • Loss of fat +
  • Edema ++++
  • Psych impairment ++++
  • Anorexia ++++
  • Hepatomegaly ++
  • Associated infections ++++
  • Diarrhea ++
  • Skin lesions ++
  • Hair changes ++
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14
Q

General appropriate treatment approaches to PEM

A
  • Go slow
  • Resolving life-threatening conditions
  • Restoring nutritional status without abruptly disrupting homeostasis
  • Ensuring nutritional rehabilitation
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15
Q

Resolving life-threatening conditions in PEM

A
  • Enteral feeding preferred
  • Avoid overhydration
  • K+ and Mg++
  • Avoid excessive Na+
  • Treatment of infections
    • Signs/symptoms may be mild/absent
  • Avoid hypoglycemia
    • Preferably by small, frequent oral feeds
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16
Q

Restoring nutritional status in PEM (without disrupting homeostasis)

A
  • Slow
  • Small, frequent (q 4hr) feeds - liquid oral or nasogastric tube
  • Initial goal = maintenance protein and energy requirements
    • NOT catch-up amounts
  • Diet should be high protein, high fat
  • Fix micronutrient deficiencies
    • K, Mg, P, Zn, Vit A
17
Q

Ensuring nutritional rehabilitation in PEM

A
  • Gradually advance energy intakes to 1.5x normal and 3-4x protein needs
  • Usually begins 1-2 weeks after initial stabilization - after resolution of edema
  • Restoring appetite may take awhile
    • Especially in kwashiorkor
  • Familiar foods
  • Emotional and physical stimulation/exercise –> cardiorespiratory and skeletal function
18
Q

Metabolic derangements in refeeding syndrome

A
  • Acute shifts form extracellular to intracellular spcaes
  • Most common and potentially dangerous: K+, P, Mg++
    • Potassium: increased insulin secretion –> intracellular glucose and K+ –> decreased serum K+ –> altered nerve/muscle function
    • Phosphorus: increased insulin secretion –> intracellular P –> intracellular phosphorylated intermediates –> P trapped in intracellular space
    • Magnesium: increased requirements with increased metabolic rate –> co-factor for ATPase
  • Any one of these derangements, if severe, can cause sudden death