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Biochem review USMLE > glucose metabolism > Flashcards

glucose metabolism Flashcards

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USMLE® Step 1 flashcards
1
Q

malate-aspartate shuttle (location, ATP yield)

A

heart and liver

32 ATP

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2
Q

glycerol-3-phosphate shuttle (location, ATP yield)

A

muscle

30 ATP

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3
Q

hexokinase (when used, where, affinity/vmax, regulated by)

A

when glucose is low
ubiquitous
high affinity, low Vmax
feedback inhibition by glucose-6-P, not affected by insulin

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4
Q

glucokinase (when used, where, affinity/vmax, regulated by)

A

when glucose is high
liver, pancreatic B cells
low affinity, high Vmax
induced by insulin

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5
Q

glucokinase mutation leads to

A

MODY (maturity onset DM of young)- decreased B-cell metabolism of glucose leads to decreased insulin secretion, DM is worse in pregnancy

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6
Q

2 steps of glycolysis that require ATP

A

glucose –> glucose-6-P (by hexokinase)

fructose-6-P –> fructose-1,6-bisP (PFK-1)

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7
Q

regulators of PFK-1

A

(+) fructose-2,6-bisP, AMP

(-) ATP, citrate

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8
Q

regulators of pyruvate kinase

A

(+) fructose-1,6-bisP

(-) alanine, ATP

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9
Q

effect of pyruvate kinase deficiency

A

decreased ability to convert PEP –> pyruvate
RBCs are most vulnerable
decreased ability to make ATP + decreased activity of Na/K ATPase = cell swelling/lysis = hemolytic anemia

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10
Q

fate of fructose-2,6-bisP in the fasting state

A

fasting = increased glucagon levels = increased cAMP = increased protein kinase A = phosphorylate and activate fructose-2,6-bisphosphatase= removes P to form fructose-6-P –> gluconeogenesis (decreased glycolysis)

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11
Q

fate of frucotose-6-P in fed state

A

fed = high insulin = decreased cAMP/protein kinase A = active PFK-2 = increased fructose-2,6-bisP = increased PFK-1 activity (increased glycolysis)

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12
Q

5 cofactors required for pyruvate dehydrogenase complex

A 
TPP
lipoic acid
CoA
FAD
NAD
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13
Q

mnemonic for 5 cofactors fo PDH complex

A

TLC For Nobody

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14
Q

effect of arsenic

A

inhibits lipoid acid= rice water stools, garlic breath

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15
Q

what other enzyme complex uses same 5 cofactors at PDH complex?

A

a-ketoglutarate dehydrogenase

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16
Q

3 factors that increase activity of PDH-C

A

high calcium
high ADP
high NAD+/NADH

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17
Q

effects of pyruvate dehydrogenase deficiency

A

backup of pyruvate and alanine, leading to lactic acidosis

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18
Q

cause of pyruvate dehydrogenase deficiency

A

X-linked (gene for E1-alpha subunit) or acquired (thiamin def in alcoholism)

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19
Q

symptoms of pyruvate dehydrogenase deficiency

A

neurologic defects starting in infancy

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20
Q

treatment for pyruvate dehydrogenase deficiency

A

ketogenic diet (high fat, increased lysine, leucine)

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21
Q

2 purely ketogenic amino acids

A

lysine, leucine

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22
Q

4 fates of pyruvate

A

1) alanine via ALT (transfer of amino groups to liver)
2) oxaloactate via pyruvate carboxylase (gluconeogensis)
3) lactate via lactic acid dehydrogenase
4) actely-CoA via pyruvate dehydrogenase (TCA cycle)

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23
Q

lactate dehydrogenase deficiency

A

symptoms pronounced in times of decreased O2 (anaerobic exercise), inability to regenerate NAD+, leads to muscle breakdown

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24
Q

3 irreversible enzymes in TCA cycle

A

citrate synthase
isocitrate dehydrogenase
a-ketoglutarate dehydrogenase

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25
Q

NADH enters ETC at

A

complex I- NADH dehydrogenase

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26
Q

FADH2 enters ETC at

A

complex II- succinate dehydrogenase

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27
Q

other name of complex III

A

cytochrome bc1

28
Q

other name of complex IV

A

cytochrome C oxidase

29
Q

other name of complex V

A

ATP synthase

30
Q

inhibitors of complex I (3)

A

rotenone
amytal
MPP

31
Q

inhibitor of complex III (1)

A

antimycin A

32
Q

inhibitors of complex IV (4)

A

CN
CO
H2S
N3-

33
Q

inhibitor of complex V (1)

A

oligomycin

34
Q

uncoupling agents (3)

A

aspirin, thermogenic, 2,4-DNP

35
Q

effect of uncoupling agents

A

increase permeability of the inner membrane, leads to dissipation of the H gradient and decreased ATP synthesis/increased heat production

36
Q

4 irreversible enzymes of gluconeogenesis, sites of action

A

1) pyruvate carboxylase- mitochondria
2) PEP carboxykinase- cytosol
3) fructose-1,6-bisphosphatase- cytosol
4) glucose-6-phosphatase- ER

37
Q

where does gluconeogenesis occur? (3)

A

mainly liver, also kidney and intestinal epithelium

38
Q

what fatty acids can contribute to gluconeogenesis?

A

odd chain FA- yield 1 propionyl-CoA during metabolism which will enter the TCA cycle as succinyl-CoA –> oxaloacetate –> gluconeogenesis

39
Q

3 products of HMP shunt (oxidative)

A

2 NADPH
CO2
ribulose-5-P

40
Q

3 products of HMP shunt (non-oxidative)

A

ribose-5-P
glycerol-3-P
Fructose-6-P

41
Q

how will the cell accommodate a high demand for NADPH?

A

convert fructose-6-P to glucose-6-P for use in HMP shunt

42
Q

describe the consequences of G6PD deficiency

A

G6PD is used to make NADPH
NADPH is important for the regeneration of reduced glutathione (GSH) from oxidized glutathione (GSSG)- GSH is used by glutathione peroxidase to neutralize H2O2 and prevent oxidative damage to cells = without G6PD, cells are increasly vulnerable to oxidate stress = hemolysis

43
Q

triggers for hemolysis in G6PD(6)

A 
fava beans
INH
sulfa drugs
dapsone
primaquine
nitrofurantoin
44
Q

inheritance for G6PD deficiency

A

X-linked recessive

45
Q

survival advantage for G6PD deficiency

A

malaria resistance

46
Q

blood smear findings in G6PD deficiency

A

heinz bodies- precipitation of oxidized hemoglobin

bite cells - from removal of heinz bodies by splenic macrophages

47
Q

what are the steps that lead to glycogenolysis?

A
  • fasting state leads to increased glucagon and epinephrine
  • stimulate adenylate cyclase = increase cAMP –> increase protein kinase A
  • protein kinase A phosphorylates glycogen phosphorylase kinase (active state) –> phosphorylates glycogen phosphorylase (active) = glycogenolysis
48
Q

what are the steps that stop glycogenolysis?

A
  • fed state leads to increased insulin
  • insulin binds to tyrosine kinase receptor= dimerizes
  • protein phosphatase is activated which removes phosphate from BOTH glycogen phosphorylase kinase and glycogen phosphorylase = stopping glycogenolysis
49
Q

alternative route for glycogenolysis stimulation in muscle

A

calcium and calmodulin can activate glycogen phosphorylase kinase

50
Q

bonds in glycogen (2)

A

a1,4- linear molecule

a1,6- branches

51
Q

use of glycogen in muscle

A

used during exercise to supply muscle only

52
Q

use of glycogen in liver

A

used to maintain blood glucose

53
Q

what is the substrate for glycogen synthesis?

A

UDP-glucose (made by UDP-glycogen pyrophosphorylase)

54
Q

cofactor required for glycogen phosphorylase

A

B6

55
Q

role of deb ranching enzyme

A

at 4 glucoses away from branch point, deb ranching enzyme moves all glucose of the branch (except one) to the end, allowing glycogen phosphorylase to continue

56
Q

alternative site for glycogen degradation, enzymes

A

in lysosomes using a1,4 glycosides

57
Q

enzyme deficit in von gierke disease

A

glucose-6-phosphatase

58
Q

symptoms of von gierke disease

A

severe fasting hypoglycemia
increased blood lactate
increased glycogen in the liver/hepatomegaly

59
Q

enzyme deficit in pompe disase

A

lysosomal a1,4-glucosidase

60
Q

symptoms of pompe disease

A

cardiomegaly

organomegaly

61
Q

2 forms of pompe disease

A

infantile- more severe

adult- slow onset weakness, death from respiratory failure

62
Q

enzyme deficit in cori disease

A

debranching enzyme

63
Q

symptoms of cori disease

A

similar to von gierke, but less severe because it does not affect gluconeogenesis
no increase in blood lactate

64
Q

enzyme deficit in McArdle’s disease

A

skeletal muscle glycogen phosphorylase

65
Q

symptoms of McArdle’s disease

A

increased glycogen in muscle

painful cramps, myoglobinuria with strenuous exercise

Biochem review USMLE (11 decks)

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