Feb8 M2-Starvation Weight Loss Frailty Flashcards

1
Q

name of disease caused by chronic starvation

A

protein-energy malnutrition (PEM) (also starvation disease or hunger disease)

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2
Q

weight loss in prolonged starvation is due to what

A

loss of body cell mass mostly

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3
Q

% fat loss and % BCM lost in prolonged starvation

A

70% fat lost

25% BCM lost (but muscle is denser than fat) so accounts for more weight

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4
Q

how BCM loss and weight loss are related in prolonged starvation

A

proportions are similar. if lose 23% body weight, lose 23% BCM (most body weight loss is BCM)

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5
Q

what increases in prolonged starvation and consequence

A

ECF volume increased. leads to frank edema (hunger edema). may hide extent of lean tissue loss

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6
Q

what happens eventually in prolonged starvation

A

body adapts (metabolic adaptation) and reaches new equilibrium where energy balance and N balance = 0

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7
Q

how is an energy balance of 0 reached in prolonged starvation

A
  1. lower BMR (changes in TH metab and SS activity)
  2. less BCM
  3. less NEAT (do less work, less EE)
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8
Q

how is a N balance of 0 reached in prolonged starvation

A
  1. loss of BCM (need less protein
  2. more efficient protein turnover
  3. increased retention of dietary aa
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9
Q

main costs of starvation adaptation

A
  • loss of insulating fat
  • loss of muscle mass and physical power
  • easier hypothermia (generating less heat)
  • loss of central (organs: heart, intestines, etc.) muscle mass
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10
Q

in a person with a negative N balance, why do we attribute the protein loss and BCM loss to a loss of muscle mass

A

because to sustain central protein mass, aa from degradation of muscle are used

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11
Q

systemic inflammation link with adapted starvation

A

are opposed. systemic inflammation increases TEE and aa catabolism. may induce death in starvation adapted person

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12
Q

marasmus def

A

PEM (protein energy metabolism) in a child

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13
Q

marasmus charact

A

high ECF, low albumin, good fat store, liver fat

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14
Q

kwashiorkor def

A

more dangerous form of PEM.

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15
Q

kwashiorkor cause

A

inflammatory response to infection in infants and children in existing PEM combined with vitamin and mineral deficiencies

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16
Q

frailty def

A

deterioration of body function with age

17
Q

most important modifiable contributor to frailty and name for this

A

muscle atrophy (sarcopenia = muscle atrophy with age)

18
Q

frailty charact + is it only in old people?

A

less muscle mass, less immune system regulation, impaired balance and agility, impaired mental cognition (mildly)
younger people can be frail too

19
Q

to what extent sarcopenia can be stopped and how

A

life-long lifestyle, physical activity, nutrition (can minimize but not halt sarcopenia)

20
Q

sarcopenic obesity def

A

condition of obese patients with muscle atrophy

a patient CAN be frail and obese

21
Q

how to evaluate frailty and common charact

A
  • physical fct, gait speed and cognition

- charact: slow walking, exhaustion on normal tasks, less voluntary activity

22
Q

3 causes of diminished muscle mass in frail people

A
  • sarcopenia
  • disuse muscle atrophy
  • PEM
23
Q

prevention and treatment of frailty

A

focus on exercise (formal and NEAT): increases food consumption and muscle mass bc increases TEE

24
Q

fasting def and metabolic charact of long term fasting

A

diet devoid of protein, carbs or fat.

long term fasting leads to ketosis

25
Q

how energy is provided to the brain in fasting and consequent wastes

A
  1. glucose from glycerol and aa from muscle
  2. FAs oxidized but some not completely and yield acetoacetic acid, acetone and beta-hydroxybutyric acid (3 ketone bodies)
26
Q

why ketone bodies increase in prolonged fasting

A

liver takes FAs, converts them to ketone bodies and puts ketone bodies back in blood

27
Q

how serum glucose changes in prolonged fasting

A

mild decrease even though liver releases much less glucose bc glucose uptake and metab by tissue is decreased

28
Q

ketoacidosis def

A

ketosis severe enough to lower serum bicarb

29
Q

ketoacidemia possible in prolonged fasting?

A

no but possible in diabetes bc ketoacidosis in diabetes is much more important

30
Q

syndrome nondiabetic ketoacidemia occurs when + glucose levels

A

protracted (prolonged) vomiting, volume depletion in binge drinkin + no food consumption
NORMAL glucose levels

31
Q

NDKA vs diabetic ketoacidemia

A

NDKA often less severe bc glucose levels are normal

32
Q

prolonged fasting labs

A

low glucose, low insulin, moderate ketosis

33
Q

ketoacidosis of severe diabetes associated with what (and why it differs from NDKA)

A
  1. hyperglycemia
  2. volume depletion
  3. hypermetabolic state
  4. severe ketosis