AntiGout Flashcards

1
Q

a metabolic disease characterized by recurrent episodes of acute arthritis due to deposits of monosodium
urate in joints and cartilage

A

Gout

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2
Q

Gout is a metabolic disease characterized by recurrent episodes of _____________ due to deposits of monosodium
urate in joints and cartilage

A

acute athritis; monosodium
urate

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3
Q

a systemic disease caused by the buildup of uric acid in the joints, causes inflammation, swelling and pain

A

Gout

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4
Q

urate level > 8mg/dL in men and 7 mg/dL in women

A

Hyperuricemia

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5
Q

ost common first symptom of gout

A

Pain in one joint of the lower extremity

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6
Q

end product of purine metabolism

A

Uric acid

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7
Q

rate limiting step in the formation of the uric
acids

A

Xanthine oxidase

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8
Q

serves no known biological functions, but the body has
content of 1.0-.2g

A

Uric acid

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9
Q

Approximately ________ of Uric acid is excreted via the ________

A

70-80%; kidneys

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10
Q

result of an innate defect in purine metabolism of uric acid excretion

A

Primary gout

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11
Q

Causes of primary gout

A

Uric acid overproduction (overproducers)
Impaired renal clearance of uric acid (underexcreters)
Combination of both

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12
Q

causes of Secondary gout

A
  • Hematologic disorders
  • Drug induced – salicylates,diuretics (thiazide), ethambutol, pyrazinamide, nicotinic acid, ethanol, niacin and cyclosporine
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13
Q

Treatment Goals for gout

A
  • Relieve pain and inflammation
  • Reduce serum uric acid concentration (urate lithiasis)
  • Prevent recurrent gout attacks
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14
Q

Treatment for acute gouty athritis attack

A
  • Colchicine
  • NSAIDs
  • Corticosteroids
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15
Q

Antimitotic drug that is highly effective in relieving acute gout attack

A

Colchicine

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16
Q

Has low –benefit to toxicity ratio, thus it is used less often than NSAIDs

A

Colchicine

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17
Q

Colchicine is most effective when initiated within ____________ of the attack

A

12-36 hours

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18
Q

T/F: Colchicine’s likelihood of success increase substantially if treatment is delayed longer than 48 hours after symptom onset.

A

false: decrease

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19
Q

type of colchicine that causes dose-dependent GI adverse effect (nausea, vomiting, bloating, emesis and diarrhea) that occur in up to 80% of patients

A

oral colchicine

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20
Q

first-line drugs for acute gout

A

NSAIDs, corticosteroids, or

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21
Q

was the primary treatment for many years due to its efficacy in treating and preventing acute gout flares

A

colchicine

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22
Q

Colchicine can be taken with or without food and is sometimes given in combination with
NSAIDs

A

True

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23
Q

Colchicine is an alkaloid isolated from the autumn crocus, ______________

A

Colchicum autumnale

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24
Q

relieves the pain and inflammation of gouty arthritis in 12–24 hours without altering urate metabolism or excretion and without other analgesic effects

A

Colchicine

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25
Q

Colchicine relieves the pain and inflammation of gouty arthritis in ________ without altering ___________ and without other analgesic effects

A

12–24 hours; urate metabolism or excretion

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26
Q

Colchicine relieves the pain and inflammation of gouty arthritis in 12–24 hours _________ (with/without) altering urate metabolism or excretion and without other analgesic effects

A

without

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27
Q

mainstay of therapy because of their excellent efficacy and minimal
toxicity with short-term use.

A

NSAIDs

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28
Q

NSAIDs Therapy should be initiated with ____________ (maximum/minimum) recommended dose for gout at the onset of symptoms and continued for ______- after resolution of an acute attack, then tapered quickly over _____

A

maximum; 24 hours; 2-3 days

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29
Q

NSAID most common adverse effects involve _____

A

GI system

30
Q

most extensively studied NSAID in the treatment of an acute gouty arthritis attack

A

Indomethacin

31
Q

In addition to inhibiting prostaglandin synthase, __________ inhibit urate crystal phagocytosis and reduce inflammation and pain in acute gout flare

A

NSAIDs

32
Q

NSAIDs inhibit

A

-prostaglandin synthase
-urate crystal phagocytosis

33
Q

Why is Aspirin not used in Gout treatment?

A

because it causes renal retention of uric acid at lower doses (≤2.6 g/d); it is uricosuric at doses >3.6 g/d.

34
Q

T/F: All NSAIDs except aspirin, salicylates, and tolmetin have been successfully used to treat acute gouty episodes

A

true

35
Q

lowers serum uric acid, is theoretically a good choice and all NSAIDs appear to be as effective and safe as the older drugs like indomethacin

A

Oxaprozin

36
Q

equivalent to NSAIDs for treatment of acute gout flares

A

Corticosteroids

37
Q

Corticosteroids are effective when given _________

A

intra-articulary, IV or orally.

38
Q

Oral Corticosteroid

A

Prednisone

39
Q

long acting corticosteroid, IM, ntra-articular (can be given if the patient is unable to take oral medications)

A

Triamcinolone acetonide or methlyprednisolone

40
Q

decrease activation, proliferation, and survival of various inflammatory cells

A

corticosteroids

41
Q

decrease the migration of neutrophils, and they inhibit prostaglandins and proinflammatory cytokines such as IL-1β.

A

corticosteroids

42
Q

a good alternative for patients in whom NSAIDs or colchicine are contraindicated and in those with renal impairment or chronic kidney disease.

A

Corticosteroids

43
Q

sometimes used in the treatment of severe symptomatic gout, by oral, intra-articular, systemic, or subcutaneous routes.

A

Corticosteroids

44
Q

The goal of _____________ is to achieve and maintain a serum uric acid concentration < 6mg/dL and preferably < 5mg/dL

A

urate lowering therapy

45
Q

Reduction of the serum urate concentration un Uric Acid Lowering Therapy can be accomplished b

A
  • decreasing uric acid synthesis (xanthine oxidase inhibitor)
  • Increasing the renal excretion of the uric acid (uricosurics)
46
Q

Uric Acid Lowering therapy are not be used during as ______

A

acute gouty arthritis attack

47
Q

Allopurinol, Febuxostat

A

Xanthine Oxidase Inhibitors

48
Q

reduce uric acids by impairing the conversion of hypoxanthine to xanthine and xanthine to uric acid.

A

Xanthine Oxidase Inhibitors

49
Q

effective in both overproducers and underexcretion of uric acids

A

Xanthine Oxidase Inhibitors

50
Q

most widely prescribed agents for long-term prevention of recurrent gout attacks

A

Xanthine Oxidase Inhibitors

51
Q

responsible for the conversion of xanthine and hypoxanthine to uric acid

A

Xanthine oxidase

52
Q

a purine analogue that inhibits this enzyme, resulting in a fall in the plasma urate level and a decrease in the overall urate burden.

A

Allopurinol

53
Q

Allopurinol is a _________ analogue that inhibits this enzyme, resulting in a fall in the _________ and a decrease in the _____

A

purine; plasma urate level; overall urate burden

54
Q

The result of xanthine oxidase inhibition is

A

build-up of its substrates, the more soluble xanthine and hypoxanthine

55
Q

The result of xanthine oxidase inhibition is a build-up of its substrates, the _______ (more/less) soluble xanthine and hypoxanthine.

A

more

56
Q

is often the first-line agent for the treatment of chronic gout in the period between attacks, and it tends to prolong the intercritical period

A

Allopurinol

57
Q

Allopurinol is often the first-line agent for the treatment of chronic gout in the period between attacks, and it tends to prolong the ________

A

intercritical period

58
Q

T/F: Allopurinol Therapy is continued for years if not for life.

A

true

59
Q

a potent and selective non-purine inhibitor of xanthine oxidase thereby reducing the formation of xanthine and uric acid without affecting other enzymes in the purine or pyrimidine metabolic pathway

A

Febuxostat

60
Q

Febuxostat is a potent and ___________ non-purine inhibitor of xanthine oxidase thereby reducing the formation of _______ without affecting other enzymes in the ________

A

selective; xanthine and uric acid; purine or pyrimidine metabolic pathway

61
Q

Febuxostat is a potent and selective __________ inhibitor of xanthine oxidase thereby reducing the formation of xanthine and uric acid ________ (with/without) affecting other enzymes in the purine or pyrimidine metabolic pathway

A

non-purine; without

62
Q

uricosuric agent have been discontinued in the USA

A

Sulfinpyrazone and Lesinurad

63
Q

Probenecid

A

Uricosuric Drug

64
Q

They increase the renal clearance of uric acid by inhibiting the postsecretory renal proximal tubular reabsorption of uric acid.

A

Uricosuric Drugs

65
Q

should be initiated in gouty patients with underexcretion of uric acid when allopurinol or febuxostat is contraindicated

A

Uricosuric therapy (Probenecid)

66
Q

Uricosuric therapy (Probenecid) should be initiated in gouty patients with underexcretion of uric acid when ________ or _________ is contraindicated

A

allopurinol; febuxostat

67
Q

T/F: Probenecid can be used as monotherapy or in combination with a xanthine oxidase inhibitor

A

True

68
Q

Canakinumab, Anakinra,
and Rilonacept

A

INTERLEUKIN 1 INHIBITORS IN GOUT

69
Q

inhibit the IL-1 receptor pathway

A

INTERLEUKIN 1 INHIBITORS IN GOUT

70
Q

main proinflammatory cytokine responsible for the crystal-induced inflammation of gout.

A

IL-1β

71
Q

T/F: Canakinumab, Anakinra,
and Rilonacept are not yet FDA-approved for the treatment of gout.

A

True

72
Q

All three IL-1 inhibitors are administered

A

subcutaneously