MITSOURA Q's [PDH & TCA Cycle & Their Regulation, ETC & Oxidative Phosphorylation, Oxygen Toxicity & Oxidative Stress] Flashcards

1
Q

what are the 3 symptoms of niacin deficiency?

A

dermatitis, diarrhea, dementia

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2
Q

what are the symptoms of riboflavin deficiency?

A

dermatitis, cheiliosis, glossitis

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3
Q

[HIGH YIELD] which cofactor does E1 of PDH require?

A

thiamine pyrophosphate (TPP) factor

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4
Q

[HIGH YIELD] which cofactor does E2 of PDH require?

A

lipoid acid cofactor (target of arsenic poisoning) & CoA cofactor

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5
Q

[HIGH YIELD] which cofactor does E3 of PDH require?

A

FAD & NAD+ cofactors

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6
Q

[HIGH YIELD] what are the 5 cofactors of PDH?

A
  • TPP, lipoid acid, FAD

- diffusible: NAD+, CoA

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7
Q

what are the common symptoms of PDH deficiency?

A

lactic acidosis and neurological symptoms

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8
Q

what are the treatments for PDH deficiency?

A
  • ketogenic diet (low carbohydrate/high fat)
  • thiamine administration
  • muscle relaxants & anti-convulsants
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9
Q

which diseases does thiamine (vitamin B1) deficiency cause?

A

Beriberi, Wernicke encephalopathy, Korsakoff syndrome, Wernicke-Korsakoff syndrome

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10
Q

[HIGH YIELD] which enzymes does thiamine (vitamin B1) deficiency affect?

A

PDH, HMP, alpha-ketoglutarate dehydrogenate

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11
Q

wet Beriberi

A

edema, cardiovascular symptoms (cardiac failure)

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12
Q

dry Beriberi

A

peripheral neurologic dysfunction

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13
Q

Wernicke encephalopathy

A

REVERSIBLE

-ataxia, confusion, nystagmus

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14
Q

Korsakoff syndrome

A

IRREVERSIBLE

-deficits in memory, hallucinations

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15
Q

[HIGH YIELD] what are the 5 cofactors of alpha-ketoglutarate dehydrogenase?

A

same as PDH:

-TPP, lipoid acid, FAD, NAD+, CoA

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16
Q

[HIGH YIELD] what is the energy production of the TCA cycle (for full turn of ONE pyruvate)?

A

1 GTP, 3 NADH, 1 FADH2

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17
Q

[HIGH YIELD] what is the energy production of the TCA cycle (for full turn of ONE glucose)?

A

2 GTP, 6 NADH, 2 FADH2

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18
Q

where does TCA cycle occur?

A

mitochondria

19
Q

oxidation

A

loss of electrons

20
Q

reduction

A

gain of electrons

21
Q

what kind of rxn does dehydrogenase carry out?

A

redox rxn

22
Q

what are the biologically active forms of niacin/nicotinic acid (vitamin B3)?

A

NAD+ & NADP+

23
Q

what do you call niacin deficiency?

A

pellagra

24
Q

prosthetic group

A

permanently attached to enzymes

25
Q

examples of prosthetic groups

A

TPP, lipoid acid, FAD

26
Q

what are the biologically active forms of riboflavin (vitamin B2)?

A

FAD & FMN

27
Q

what do you call riboflavin deficiency?

A

ariboflavinosis

28
Q

what type of run is PDH rxn (conversion of pyruvate to AcCoA)?

A

oxidative decarboxylation

29
Q

what are the subunits of PDH?

A

E1, E2, E3 (catalyic subunits)

& PDH Kinase & Phosphatase (regulatory subuints)

30
Q

what determines the direction of LDH rxn?

A

pyruvate/lactate ratio

31
Q

how is PDH activity regulated?

A

1) allosteric effectors on PDH catalytic subunits

2) regulation of catalytic subunits by PDH kinase & PDH phosphatase

32
Q

what activates PDH?

A

PDH phosphatase (dephosphorylates)

33
Q

what inactivates PDH?

A

PDH kinase (phosphorylates)

34
Q

how are PDH kinase & PDH phosphatase regulated?

A

allosteric effectors & insulin

35
Q

what does deficiency in CoA and pantothenic acid cause?

A

burning foot syndrome

36
Q

what inhibits citrate synthase?

A

citrate and ATP

37
Q

what inhibits isocitrate dehydrogenase?

A

NADH

38
Q

what stimulates isocitrate dehydrogenase

A

ADP & NAD+

39
Q

what inhibits alpha-ketoglutarate dehydrogenase?

A

succinyl-CoA, NADH ATP

40
Q

what causes biotin deficiency?

A

eating raw eggs (avidin)

41
Q

what are the symptoms of biotin symptoms?

A

dermatitis, glossitis, loss of appetite

42
Q

A 10-year-old boy has suffered from slowly progressing ataxia (poor motor coordination) since the age of 5. a blood test shows abnormal elevation of lactic acid levels after an oral glucose load. deficiency of which of the following enzymes or transporters is the most likely cause of the boy’s condition?

A

pyruvate dehydrogenase

43
Q

the primary function of the TCA cycle is to:

A

produce reduced nucleotides (NADH & FADH2) from metabolic fuels to permit oxidative phosphorylation

44
Q

an uncoupler of oxidative phosphorylation:

A

allows electron transport to proceed without ATP synthesis