Starvation and Malnutrition Flashcards

1
Q

How does your body get its energy in the fed state?

A

glycolysis, aerobic respiration

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2
Q

How does your body get its energy fasting b/w meals?

A

4-6 hours gluconeogenesis begins
glycogenolysis persists until 10-18 hours after meal

a little bit of FFA release from adipose tissue

**glucagon and epinephrine stimulate

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3
Q

What is the main source of energy after fasting 1-3 days?

A

Fatty Acids

also get some glucose (solely from gluconeogenesis) and ketone bodies

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4
Q

Starving after 5 days, what is the main energy source?

A

adipose–ketone bodies

also some glucose and fatty acids

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5
Q

Once again, when are the glycogen stores depleted?

A

after 1 day

really after 10-18 hours

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6
Q

Main source of energy for brain and muscles:
1 day of fasting
2 days of fasting
5 days of fasting

A

1 day of fasting: brain-glucose, muscles–mainly fatty acids, some glucose
2 days of fasting: brain-glucose, some ketone bodies, muscles–mainly fatty acids, some ketones
5 days of fasting: brain-ketone bodies, muscle–mainly fatty acids, some ketone bodies

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7
Q

Once again, when does the ketone body formation begin?

A

after 2 days of fasting

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8
Q

What is the one part of the body that can’t use ketones?

A

RBCs, lack mitochondria

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9
Q

Describe the circumstances that favor ketone formation?

A

oxaloacetate has been all used up b/c of gluconeogenesis

so now acetyl CoA can’t enter TCA. Instead, it goes on to make ketone bodies.

Acetyl CoA increases b/c of beta oxidation of fatty acids

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10
Q

Describe ketogenesis.

A

Fatty Acids and amino acids–>acetoacetate + beta hydroxybutyrate

Rate limiting enzyme: HMG CoA synthase

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11
Q

What type of ketone does the urine test detect?

A

only detects acetoacetate

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12
Q

Why does a patient in diabetic ketoacidosis have fruity breath?

A

b/c of acetoacetate–>acetone (fruity smell)

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13
Q

Why does EtoH on an empty stomach set you up for fasting hypoglycemia?

A

b/c alcohol causes the formation of NADH.
the increase in NADH favors the formation of pyruvate–>lactate and oxaloacetate–>malate
these then can’t be used for gluconeogenesis.

Basically, the liver can only metabolized ETOH or give body glucose. not both. Fasting hypoglycemia.

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14
Q

What are 4 possible fates of acetyl CoA?

A

TCA cycle
Fatty acid synthesis
cholesterol synthesis
ketone synthesis

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15
Q

What are the important features of kwashiorkor?

A

FLAMES
fatty liver (b/c of lack of ApoB100)
anemia
malnutrition (of protein, may have adequate calories)
Edema (distended abdomen)
Skin lesions and depigmentation of hair and skin

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16
Q

What are the key features of marasmus?

A

muscle wasting
totally energy malnutrition
also get variable edema, and loss of subcutaneous fat

17
Q

What is refeeding syndrome?

A

happens after 5 days of fasting
start low and go slow!!

cells gobble up all the new ions and nutrients etc–get serum depletion of potassium, magnesium. Can get arrhythmias and neuro problems.

depletion of ATP phosphorylating things inside the cell

**during fasting–cells sacrificed their ions for the good of the serum oncotic pressure.