Pharm - Gout Flashcards

1
Q

describe the pathway from purines to uric acid

A

GMP –> guanosine –> guanine –> xanthine –> uric acid

AMP –> IMP –> inosine –> hypoxanthine –> xanthine –> uric acid

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2
Q

what enzyme do other animal species have that prevents them from getting gout

A

uricase (breaks down uric acid into allantoin)

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3
Q

what enzyme converts free adenine to AMP

A

adenine phosphoribosyl transferase (APRT)

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4
Q

what enzyme converts hypoxanthine to AMP and guanine to GMP (in the salvage pathway)

A

hypoxanthine-guanine phosphoribosyl transferase (HGPRT)

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5
Q

absence or deficiency in HGPRT results in

A

lesch-nyhan syndrome

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6
Q

what can cause urate overproduction in secondary hyperuricemia

A
  • excessive purine intake

- tumor lysis syndrome

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7
Q

what are the recommended NSAIDs for acute gout

A
  • naproxen
  • indomethacin
  • celecoxib
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8
Q

in acute gout, when do you give glucocorticoids

A

if only a few joints or NSAIDs and colchicine are contraindicated

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9
Q

MOA and effects of colchicine

A

blocks formation of microtubules

leads to inhibition of leukocyte migration and phagocytosis

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10
Q

indications colchicine

A

used in acute gout pts with NSAID intolerance or absolute contraindications to NSAIDs

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11
Q

administration, half life, and metabolism of colchicine

A

administration: oral

half life: 27-31 hours

metabolism: CYP3A4 and excreted by kidneys

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12
Q

colchicine is contraindicated in pts with _____

A

renal or hepatic impairment

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13
Q

adverse effects colchicine

A

GI distress (N/V/D)

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14
Q

MOA and effects of allopurinol

A

competitively inhibits xanthine oxidase

hypoxanthine and xanthine are both excreted

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15
Q

indications allopurinol

A

recurrent gout

cancer-chemo induced hyperuricemia (tumor lysis syndrome)

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16
Q

administration, half life, and metabolism of allopurinol

A

administration: oral

half life: 15 hours

metabolism: eliminated by kidneys

17
Q

lower doses of allopurinol need to be given in patients with _____

A

renal impairment

18
Q

adverse effects allopurinol

A
  • skin rash
  • can trigger acute gout attack
  • N/V
  • increased liver enzymes
  • Stevens-johnson syndrome
19
Q

MOA and effect febuxostat

A

non-competitive inhibitor of xanthine oxidase

hypoxathine and xanthine are both excreted

20
Q

indications febuxostat

A

recurrent gout in patients who cannot tolerate allopurinol

also cancer-chemo induced hyperuricemia (tumor lysis syndrome)

21
Q

administration and half life of febuxostat

A

administration: oral

half life: 5-8 hours

22
Q

downsides of febuxostat

A

VERY expensive

23
Q

MOA and effects of pegloticase

A

recombinant mammalian uricase –> covalently attaches to methoxy polyethylene glycol

converts uric acid to the far more soluble allantoin

24
Q

indications pegloticase

A

treatment of chronic gout in those unable to receive conventional therapy

25
administration of pegloticase
IV every 2 weeks
26
adverse reactions pegloticase
infusion reactions (fever, chills, rash, angioedema, bronchospasm, hypotension)
27
MOA rasburicase
nonpegylated recombinant uricase
28
indications rasburicase
prevention of acute uric acid nephropathy due to tumor lysis syndrome in pts with high risk lymphoma or leukemia
29
MOA and effects of probenecid
blocks urate reabsorption more than urate secretion increases fractional excretion of urate and decreases plasma urate concentration
30
indications probenecid
reduces urate levels in underexcreters with GFR > 60
31
administration and half life probenecid
administration: oral half life: 6-12 hours
32
adverse effects probenecid
increases risk of kidney stones may cause gouty arthritis flare