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M&M Test 1 > B6-038 Gout & Hyperuricemia > Flashcards

B6-038 Gout & Hyperuricemia Flashcards

1
Q

the urate crystals present in tophi come from

A

purine breakdown

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2
Q

[….] is the only biochemical pathway that has urate as the end product

A

purine breakdown

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3
Q

the conversion of glutamine to glutamate is what type of reaction?

A

amidation

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4
Q

does amidation occur in purine or pyrimidine synthesis?

A

both :)

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5
Q

[…] provides the carbon backbones during the de novo synthesis of nucleotide bases

A

amino acids

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6
Q

synthesis of […] requires vitamin B9

A

purine bases

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7
Q

PRPP synthase is regulated by

A

purine and pyrimidine nucleotides (end product inhibition)

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8
Q

UTP inhibits […], which helps build the ring in pyrimidine synthesis

A

CAD complex

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9
Q

the first step of the salvage of purine bases is

A

addition of ribose

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10
Q

3 purine bases

A

hypoxanthine, adenine, guanine

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11
Q

loss of the enzyme HGPRT causes

A

Lesch-Nyhan syndrome

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12
Q

classic presentation: male child with motor symptoms, self-mutilation, gout

A

Lesch-Nyhan syndrome

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13
Q

Lesch-Nyhan syndrome is a defect in

A

purine salvage

causes excess de novo purine synthesis leading to excess uric acid

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14
Q

key enzyme in deoxynucleotide synthesis

A

ribonucleotide reductase

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15
Q

hydroxyurea and gemcitabine inhibit what enzyme?

A

ribonucleotide reductase

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16
Q

what enzyme is deficient in SCID?

A

adenosine deaminase

(involved in purine breakdown)

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17
Q

proper regulation of ribonucleotide reductase results in

A

the concentration of all four dNTPs in a cell being roughly equivalent

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18
Q

if dCTP is elevated, how might that effect ribonucleotide reductase?

A

dCTP would allosterically effect RNR resulting in increased production of ADP, UDP, and GDP

**always trying to ensure all four substrates are roughly equal in cell

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19
Q

primary hyperuricemia is caused by

A

in-born defects

**secondary is unrelated to genetics

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20
Q

in a patient with gout, prevalence of […] correlates with serum and urinary uric acid levels

A

nephrolithiasis

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21
Q

for the management of gout, the American College of Rheumatology recommends against

A

vitamin C supplementation

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22
Q

evidence of support for lifestyle/diet recommendations in the management of gout is [high or low]

A

low

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23
Q

standard of care diagnostic test for gout

A

synovial fluid aspirate

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24
Q

why do pre-menopausal females have lower serum uric acid levels than males?

A

estrogen impact activity of renal uric acid transporters

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25
Q

what part of the renal tubule regulates uric acid?

A

PCT

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26
Q

inhibits xanthine oxidase, directly reducing the production of uric acid

A

allopurinol

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27
Q

inhibits OAT transporters

A

probenecid

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28
Q

inhibits URAT1 transporter

A

lesinurad

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29
Q

inhibits reabsorption of urate from urine [2]

A

probenecid, lesinurad

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30
Q

inhibits ribonucleotide reductase, preventing the synthesis of deoxyribonucleotides

A

hydroxyurea

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31
Q

promotes degradation of urate in serum

A

pegloticase

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32
Q

third line treatment for persistent gout, very expensive

A

pegloticase

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33
Q

inhibits tubulin polymerization, used to treat inflammatory conditions

A

colchicine

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34
Q

inhibits de novo pyrimidine base synthesis preventing cell division making it useful in the treatment of rheumatoid disease

A

leflunomide

**not helpful for gout as it’s for pyrimidine synthesis, not purine

35
Q

hydroxyurea prevents

A

deoxyribonucleotide synthesis

36
Q

allopurinol and febuxostat MOA

A

purine breakdown

37
Q

key enzyme in purine breakdown
inhibition of this reduces the production of uric acid

A

xanthine oxidase

38
Q

is there strong evidence for managing gout with diet?

A

no

**despite this, remains “gold standard”. balance QOL with patient goals and evidence

39
Q

crucial enzyme for synthesis of all nucleotides

A

PRPP synthetase

**also involved in purine salvage pathway

40
Q

inhibits dihydrofolate reductase

A

methotrexate

41
Q

best treatment for acute nephrolithiasis caused by tumor lysis syndrome

A

pegloticase

42
Q

how does an in-born error in G6P cause an elevated risk of hyperuricemia?

A

glucose-6-phosphate builds up in liver –> shunts into PPP –> produces more nucleotides –> catabolized –> high levels of uric acid

43
Q

limited in use of treatment of gout due to impact on excretion of other drugs in kidney

A

probenecid

44
Q

inhibits reabsorption of uric acid by URAT1 in PCT

A

lesinurad

**no longer manufactured

45
Q

recombinant PEGylated-urate oxidase
converts urate to allantoin

A

pegloticase

46
Q

drugs for gout that do NOT impact nucleotide metabolism [3]

A

pegloticase
lesinurad (d/c)
probenecid

47
Q

inhibit xanthine oxidase to directly reduce uric acid production, specifically treating gout

A

allopurinol
febuxostat

48
Q

drugs that inhibit cell division by reducing nucleotide availability
used to treat autoimmune disorder and cancer, not necessarily gout [3]

A

lefunomide (arthritis)
hydroxyurea (cancer)
methotrexate

49
Q

transporters in PCT that may be responsible for association of gout and high fructose sodas

A

GLUT9

50
Q

“priming” of uric acid reabsorption is dependent on […] loading the PCT cells with anions

A

sodium

51
Q

gout is defined as both […] and […]

A

crystal formation and inflammation

52
Q

adenosine deaminase deficiency causes

A

SCID

53
Q

how does adenosine deaminase deficiency cause SCID?

A

prevents adenosine breakdown –> adenosine builds up, inhibiting RNR –> reduces dNTP pool –> immune cells are very mitotically active so they are very sensitive to this

54
Q

unbalanced dNTPs can lead to

A

ds breaks in DNA

55
Q

ribonucletotide reductase inhibitors

A

hydroxyurea, gemcitabine

56
Q

condition resulting from defective purine salvage

A

Lesch-Nyhan

57
Q

can be given prophylactically to help prevent tumor lysis syndrome caused by chemotherapy

A

allopurinol

57
Q

converts ribose to PRPP

A

PRPP synthetase

57
Q

how does tumor lysis syndrome cause hyperuricemia?

A

high levels of nucleotide catabolism

58
Q

gout is caused by the precipitation of [….] crystals in joints

A

monosodium urate

59
Q

needle shaped crystals under polarized light

A

gout

60
Q

treatment for ACUTE gout [3]

A

NSAIDs, glucocorticoids, colchicine

61
Q

preventative treatment for chronic gout [2]

A

allopurinol
febuxostat

62
Q

allopurinol and febuxostat competitively inhibit

A

xanthine oxidase

63
Q

allopurinol can be used concurrently with chemotherapy to prevent

A

tumor lysis associated urate nephropathy

64
Q

allopurinol can increase the concentrations of [2]

A

azathioprine
6-MP

65
Q

recombinant uricase catalyzing uric acid to allantion

A

pegloticase

66
Q

inhibits reabsorption of uric acid in PCT

A

probenecid

67
Q

probenecid can also inhibit the secretion of

A

penicillin

68
Q

can precipitate uric acid calculi or lead to sulfa allergies

A

probenecid

69
Q

binds and stabilizes tubulin to inhibit microtubule polymerization

A

colchicine

70
Q

colchicine inhibits [….], causing impaired neutrophil […] and […]

A

microtubule polymerization
chemotaxis
degranulation

71
Q

rate determining enzyme of the HMP shunt

A

G6PD

72
Q

rate limiting enzyme of de novo purine synthesis

A

PRPP

73
Q

inhibits ribonucleotide reductase

A

hydroxyurea

74
Q

inhibits dihydrofolate reductase in humans

A

methotrexate

75
Q

lesch-nyhan is caused by

A

defective purine salvage

76
Q

one of the major causes of autosomal recessive SCID

A

adenosine deaminase deficiency

77
Q

what enzyme is absent in Lesch-Nyhan?

A

HGPRT

78
Q

key enzyme in the purine salvage pathway

A

HGPRT

79
Q

which pathway operates at a higher rate in children with Lesch-Nyhan?

A

de novo purine synthesis

80
Q

leflunomide inhibits [….] synthesis

A

pyrimidine

81
Q

medication that inhibits dihydoorotate dehydrogenase

A

leflunomide

82
Q

leflunoamide is used to treat

A

rheumatoid arthritis

M&M Test 1 (15 decks)

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