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msk exam 1 spring 2015 > Biochemistry - Heck > Flashcards

Biochemistry - Heck Flashcards

1
Q

absorptive state

A

after a meal - immediate

blood glucose level increases

insulin released
glycogen synthesis
protein synthesis
triglyceride synthesis

brain and RBCs - insensitive to insulin

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2
Q

post-absorptive state

A

during fast - 12 hours or overnight

glucagon released

glycogenolysis in liver
AA uptake for gluconeogenesis

epinephrine released

  • muscle - AA to blood
  • adipose - FA to blood
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3
Q

liver

A

maintain blood glucose

synthesize ketones from acetyl CoA

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4
Q

adipose

A

take up FA and convert to TGs for long term storage

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5
Q

resting skeletal muscle

A

release AA to blood

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6
Q

active skeletal muscle

A

fast twitch - anaerobic glycolysis from glycogen

slow twitch - oxidative metabolism of glycogen
-after several hours - switch to lipolysis

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7
Q

muscle contraction

A

activates the TCA cycle

via:
increase in Ca
increase in ADP
decreased NADH/NAD ration

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8
Q

high intensity level of exercise

A

increased lactate dehydrogenase

  • convert pyruvate to lactate
  • with anaerobic metabolism
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9
Q

NADH dehydrogenase

A

in ETC complex 1

increases with high intensity exercise

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10
Q

anaerobic muscle metabolism

A

high intensity exercise

need for ATP - exceeds mito capacity for ox phos

lactate production - increased NADH/NAD ratio directs pyruvate into lactate

H production - decreased pH, causing pain and fatigue
-lactic acid dissociates to lactate and H

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11
Q

aerobic muscle metabolism

A

low intensity exercise

rate of ATP utilization is lower

increased CO2 - complete oxidation of glucose to CO2

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12
Q

TCA cycle

A

generates NADH and FADH2

-driving force for ETC

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13
Q

NAD and FAD

A

from ETC

increase activity of TCA cycle

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14
Q

myosin ATPase

A

stimulates ADP

-increases activity of isocitrate DH (rate limiting of TCA cycle)

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15
Q

isocitrate DH

A

produces NADH - driving ETC

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16
Q

buildup of NADH

A

inhibit TCA cycle

-inhibit alpha-KG DH and isocitrate DH

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17
Q

muscle contraction

A

increase Ca

stimulates - isocitrate DH and alpha-KG DH - increased TCA cycle activity

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18
Q

citrate

A

with buildup - unable to proceed through TCA cycle

inhibits acetyl CoA entering TCA cycle

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19
Q

aerobic metabolism supplements

A

probably no immediate benefit

rate limiting factor - O2 availability, not cycle intermediates

CoQ, succinate, riboflavin, niacin, pantothenate

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20
Q

exercise

A

increases skeletal m capacity and efficiency for fuel ox

over time:

  • more TCA cycle enzymes
  • more ETC components
  • more mitochondria - size and productivity

also more vasodilatory and lymphatic drainage

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21
Q

major metabolic source in anorexic

A

fuel for skeletal muscle - is fatty acids

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22
Q

ketone bodies

A

made in liver

-fuel for brain and skeletal m

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23
Q

elevated ammonia in blood

A

liver failure

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24
Q

elevated ketones in blood

A

during starvation

from FA produced by liver

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25
Q

severe hypoglycemia

A

passing out

unresponsive

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26
Q

starvation

A

prolonged fasting 2 days

glucagon and epinephrine elevated

  • muscle - FA
  • brain - ketones and glucose
  • RBCs - glucose

decrease in body temp, BP, and HR - so don’t burn much glucose

27
Q

epinephrine

A

stimulates muscle glycogenolysis

28
Q

glucagon

A

stimulate switch to lipolysis

29
Q

skeletal muscle pain in anorexic

A

pH and lactic acid

  • skeletal m - anaerobic metabolism
  • this is because iron deficiency anemia - inhibit O2 delivery to tissue
  • also - messes up ETC**
30
Q

amenorrhea

A

body fat >22%

reduced LH and FSH production

31
Q

death by starvation

A

40% ideal body weight lost
20-50% body protein lost
70-95% body fat stores lost

32
Q

starvation

A

depletion of muscle glycogen
depletion of adipose TAGs
depletion of glucose from liver glycogen

33
Q

vitamin deficiency

A

also seen in starvation

sx - fatigue, nausea, loss of appetite

riboflavin, niacin, thiamine, pantothenate

34
Q

riboflavin

A

for FAD and FMN

-part of ETC

35
Q

niacin

A

precursor to NAD+

36
Q

thiamine

A

for alpha-KG DH

37
Q

pantothenate

A

precursor to CoA

38
Q

iron deficient anemia and ETC

A

non-heme iron proteins

function in electron transport

causes fatigue

39
Q

metabolic sources of energy

A

glucose, AAs, FAs - to acetyl CoA

acetyl CoA to TCA cycle

40
Q

glucagon

A

phosphorylation of rate-limiting enzymes

41
Q

insulin

A

dephosphorylation of rate-limiting enzymes

42
Q

insulin independent

A

brain and RBCs

43
Q

RBC

A

utilize glucose anaerobically

44
Q

released in postabsorptive state

A

glucagon and epinephrine

45
Q

marked elevation of epinephrine and glucagon

A

starvation - prolonged fasting

46
Q

liver fuel

A

glucose and AA - well fed

FA - fasting

47
Q

skeletal m fuel

A

glucose well fed

FA, ketone - fasting

48
Q

cardiac m fuel

A

FA - well fed

FA, ketone -fasting

49
Q

synthesis of ketones

A

in liver

50
Q

fast twitch fibers

A

anaerobic glycolysis

51
Q

slow twitch fibers

A

oxidative

52
Q

postnatal period

A

switch to beta-ox of FAs in cardiac muscle

53
Q

citric acid cycle

A

oxidation of acetyl CoA to CO2

releases energy as NADH, FADH2, and GTP

54
Q

isocitrate DH regulation

A

inhibited by NADH and ATP

stimulated by ADP

55
Q

alpha-ketoglutarate DH regulation

A

requires thiamine, lipoic acid, CoA, FAD, and NAD

lack of thiamine slow oxidation of acetyl CoA

56
Q

succinyl CoA synthetase

A

catalyzes phosphorylation of GDP to GTP

57
Q

ATP synthase

A

F0 component - proton flow

F1 component - ATP synthase - phosphorylate ADP

58
Q

cyanide poisoning

A

irreversible binding of cytochrome a/a3 in ETC

59
Q

carbon monoxide

A

binds cytochrome a/a3 less tightly than cyanide

60
Q

citrate

A

carries acetyl CoA to cytoplasm for FA synthesis

61
Q

lesch nyhan disease

A

purine salvage enzyme deficiency
-hypoxanthine guanine phosphoribosyl pyrophosphate transferase - HPRT

CNS deteriration, mental retardation, spastic cerebral palsy, self mutilation

62
Q

orotic aciduria with megaloblastic anemia

A

OMP synthase deficiency

63
Q

purine salvage pathway enzyme

A

HGPRT

deficient - lesch nyhan

msk exam 1 spring 2015 (21 decks)

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