191b - Starvation and Metabolic Adaptation Flashcards

1
Q

What is the difference in the cause of Marasmus vs. Kwashiorkor?

A
  • Marasmus = not enough calories
    • -> Very low body weight, wasted appearance
  • Kwashiorkor = not enough protein
    • -> Low or normal body weight, edema, distended abdomen
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2
Q

What is the difference between total parenteral nutrition and peripheral parenteral nurition?

A
  • Total parenteral nutrition
    • High osmolality => must be administered into vena cava
    • Can meet energy and protein needs
  • Peripheral parenteral nutrition
    • Lower osmolality => can be infused in a peripheral vein
    • Usually cannot completely meet energy/protein needs
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3
Q

Describe the differences in the presentation of Marasmus vs. Kwashiorkor

A
  • Marasmus (calorie deficiency)
    • Very low body weight
    • Wasted appearance (loss of fat and muscle)
    • Normal liver function
    • Dry, inelastic skin
  • Kwashiorkor (protein deficiency)
    • Low or normal body weight
    • Edema -> may appear normal weight
    • Distended abdomen
    • Dysfunctional liver; marked hypoalbuminemia (-> edema)
    • Flaky paint rash, depigmentation of hair
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4
Q

Which tissues can use ketone bodies in late starvation? (2)

A

Brain

Muscle

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5
Q

What behavior changes occur in normal volunteers during starvation? (5) (Keys et al)

A
  • Preoccupation with food
  • Hoarding and stealing food
  • Bing eating if opportunity
  • Abnormal taste preferences
  • Depression, apathy, irritability, other personality changes
    • Cannot psychologically rehabilitate until nutritionally rehabilitated
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6
Q

Which tissues use FFAs in late starvation? (2)

A

Muscle

Liver

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7
Q

How does muscle metabolism change during starvation?

A

Muscles become more efficient

=> Fewer calories burned, conserves energy

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8
Q
A

Major burn

  • Protein loss through open wounds
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9
Q
A

2-3 months

(but varies with starting adiposity)

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10
Q

Which tissues use glucose in late starvation? (3)

A

Brain

RBCs

Renal medulla

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11
Q

What is metabolic adaptation (after weight loss)?

A

Changes in metabolism/hormones that occur after weight loss; evolutionarily, they are aimed at preventing death from starvation

In short, BMR decreases

  • Decreased:
    • Leptin
    • Energy expenditure T3/T4
  • Increased
    • Ghrelin
    • Muscular efficiency (-> decreased calorie burn)
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12
Q

How can refeeding syndrome be prevented?

A
  • Replete electrolytes before calories
  • Go slowly with calories
  • Replete thiamine
    • Cofactor for pyruvate dehydrogenase - needed to metabolize glucose/carbohydrates

Monitor and continue repleting as necessary!

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13
Q

How long does metabolic adaptation to weight loss persist?

A

Forever (many years)

  • This means that even YEARS after a pt has lost weight, their body will be trying to conserve energy because it thinks its starving
    • BMR continues to slow
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14
Q

Describe the pathogenesis of refeeding syndrome

A

Glucose intake

  • Electrolyte shift into cells
  • Low blood electrolytes
  • Arrhythmia, decreased contractility

Simultaneous fluid -> exacerbation of heart failure

Prevent by repleting electrolytes prior to nutrition, go slow with nutrition

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15
Q

How many grams of dietary carbohydrates/day will suppress ketosis and glucogneogenesis?

A

100 g

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16
Q
A

C

  • This is Kwashiorkor (caused by marked protein deficiency)
    • Very hypoalbuminemic
    • Skin and hair changes
    • Distended abnomen
    • Fatty/dysfunctional liver
17
Q

How does metabolism change in ilness? (2)

A
  • Increased energy expenditure
    • Increased BMR
  • Markedly increased protein metabolism
    • (Glucose no longer suppresses protein catabolism)
18
Q

Is leptin indicated as a weight loss supplement?

A

No!

Exogenous leptin -> pts develop antibodies to endogenous leptin

Leptin is only used to treat people with genetic leptin deficiency

19
Q

What are the substrates for gluconeogenesis during starvation (5)

Which one can only be used by the kindey?

A
  • Lactate
  • Pyruvate
  • Alanine
  • Glycerol
  • Glutamine