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Pharm collaboration: Musculoskeletal/Rheumatology > Drugs for Gout > Flashcards

Drugs for Gout Flashcards

1
Q

What is the definition of hyperuricemia?

A

Hyperuricemia is defined as the condition in which the concentration of uric acid in the plasma is > 7 mg/dL

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2
Q

What are the two broad categories of causes of hyperuricemia?

A

Metabolic (10%)

Renal (90%)

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3
Q

What are the metabolic causes of hyperuricemia?

A

Primary:
Specific enzyme abnormalities

Secondary:
Increased purine biosynthesis, Certain blood disorders, chemotherapy, or radiation therapy

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4
Q

What are the renal causes of hyperuricemia?

A

Primary:
Kidney disease

Secondary: (the majority)
Long-term diuretic therapy
Toxemia of pregnancy

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5
Q

What are the drugs used to treat gout?

A 
Colchicine
Indomethacin
Allopurinol
probenicid 
Febuxostat
Pegloticase
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6
Q

What are the therapeutic applications for gout?

A

Colchicine is only effective against gout.
It is used as a prophylactic agent against attacks of gout, or to terminate acute attacks. It can also be used in familial mediteranean fever

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7
Q

What is the MOA of colchicine?

A

Colchicine depolimerizes microtubules

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8
Q

What are some important side effects of Colchicine?

A 
G.I. disturbances (acute)
Blood dyscrasias (chronic)
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9
Q

What is the MOA of Indomethacin?

A

Indomethacin is a cyclooxygenase inhibitor that functions as an analgesic, antipyretic, and inhibitor of leukocyte motility.

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10
Q

Is indomethacin better for acute attacks or chronic management of gout?

A

Indomethacin is better for treatment of acute attacks of gout.

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11
Q

What should be taken with Indomethacin to improve its absorption?

A

antacids

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12
Q

What ADEs are associated with Indomethacin?

A

GI: N/V , ulcers
CNS: severe frontal headache
Hematopoietic disorders
Antagonizes Furosemide and HCTZ

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13
Q

What is the MOA of Allopurinol?

A

Competitive inhibitor of Xanthine oxidase

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14
Q

What is Allopurinol metabolized to?

A

Oxypurinol (a non-competitive inhibitor of xanthine oxidase)

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15
Q

What are the therapeutic effects of allopurinol?

A
  1. Reduces plasma levels and urinary excretion of Uric acid
  2. Increases Xanthine and oxyxanthine excretion
  3. facilitates dissolution of uric acid crystals in the joints
  4. prevents formation of kidney stones
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16
Q

In what clinical situations should allopurinol be prescribed?

A

Should be used for the prophylactic treatment of primary hyperuricemia due to enzyme abnormalities or Secondary hyperuricemia due to hematologic disorders and chemotherapy.

17
Q

What are some adverse effects associated with allopurinol?

A
  1. increased acute gout
  2. Hypersensitivity (dermatitis)
  3. Liver toxicity
  4. contraindicated with 6-MP, ampicillin, and related antibioltics.
18
Q

What is the MOA of febuxostat?

A

potent inhibitor of both the oxidized and reduced forms of xanthine oxidase that is not structurally related to allopurinol

19
Q

Which is better allopurinol or febuxostat?

A

Febuxostat is more potent than allopurinol and has less adverse effects.

20
Q

What medical conditions might limit the use of allopurinol but not febuxostat?

A

Renal impairment

21
Q

What are the ADEs associated with febusostat?

A

Transaminase elevation

22
Q

How does the kidney handle uric acid?

A
  1. Filtration then reabsorption in PCT

2. Secreted then partially reabsorbed

23
Q

What is the MOA of probenacid?

A

Probenacid inhibits the transport of organic anions across epithelial barriers (especially the PCT brush border). Prevents the renal reabsorption of uric acid leading to lower UA levels in the the blood and the dissolution of uric acid crystals in the joints.

24
Q

What ADEs are associated with probenacid?

A

Salicylates inhibit uricosuric action of probenacid.

25
Q

What is the MOA of Pegloticase?

A

Pegloticase is a recombinanat urate oxidase which converts urate into allantoin. Humans do not have this enzyme but other mammals do. Reduces both urate crystals and urinary excretion of uric acid. Will also dissolve tophi.

26
Q

When is good time to clinically use pegloticase?

A

When other gout treatments have failed to control severe gout.

27
Q

What is a potentially hazardous side effect of the dissolution of tophi?

A

The dissolution of tophi may cause flare ups of gout as the urate from the tophi is released.

28
Q

What are some potential limitations to the use of pegloticase?

A

89% of the people taking pegloticase develop antibodies against the drug

it costs over $30,000 a year

29
Q

What is the rate limiting step in the biosynthesis of uric acid?

A

Ribose-5-P –> PRPP

via the enzyme phosphoribosyl pyrophosphate synthetase synthetase

30
Q

What enzyme deficiencies will lead to hyperuricemia?

A

PRPP synthetase

HGPRT

Pharm collaboration: Musculoskeletal/Rheumatology (5 decks)

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