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Pharmacology > Gout > Flashcards

Gout Flashcards

1
Q

Indomethacin, NSAIDs GOUT class

A

Acute attacks of gouty arthritis

Control pain

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2
Q

Indomethacin, NSAIDS GOUT Mechanism

A

Suppress leukocyte recruitment and activation

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3
Q

Indomethacin, NSAIDS GOUT description

A

DOC = indomethacin

Others NSAIDs are also useful

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4
Q

Indomethacin, NSAIDs Contraindications

A

**Aspirin (low dose) ->competes with uric acid for secretion at the PT and causes hyperuricemia***

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5
Q

Indomethacin, NSAIDs GOUT AE

A

Bleeding
Na+ and H2O retention
Renal insufficiency

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6
Q

Colchicine GOUT class

A

Acute attacks of gouty arthritis

Control pain

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7
Q

Colchicine GOUT mechanism

A

Suppress leukocyte recruitment and activation

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8
Q

Colchicine GOUT description

A
  • Binds tubulin* -> decrease polymerization -> no microtubules -> decrease mobility of granulocytes
  • Disrupts mitotic spindle* blocking cell division
  • Inhibits synthesis/release of LT’s*
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9
Q

Colchicine fun fact

GOUT

A

no longer used due to side effects

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10
Q

Colchicine AE

GOUT

A

Abdominal pain
Nausea, vomiting
Diarrhea
Chronic -> myopathy, neutropenia, aplastic anemia, and alopecia

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11
Q

Colchicine contraindications

GOUT

A

Use with caution in patients with hepatic, renal or CV disease

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12
Q

Glucocorticoids GOUT class

A

Acute attacks of gouty arthritis

Control pain

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13
Q

Glucocorticoids GOUT mechanism

A

Suppress leukocyte recruitment and activation

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14
Q

Glucocorticoids description

GOUT

A

Direct injection into a single affected joint when refractory to NSAIDs or colchicine

Anti-inflammatory and immunosuppressive effects

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15
Q

Allopurinol class GOUT

A

Chronic gout treatment

Normal serum urate

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16
Q

Allopurinol mechanism

GOUT

A

Purine analog -> inhibits Xanthine oxidase facilitating dissolution of tophi

17
Q

Allopurinol description

GOUT

A

Decreases uric acid synthesis

Prevent renal damage during cancer chemotherapy

Initially may increase attacks due to mobilization of tissue stores of uric acid -> coadminister with NSAID or colchicine

18
Q

Allopurinol AE

GOUT

A

Hypersensitivity

Skin rash may progress to Steven-Johnson syndrome (toxic epidermal necrolysis)

19
Q

Allopurinol contraindications

GOUT

A

If cutaneous rash develops, discontinue use

Reduce doses of 6-MP and azathioprine -> also metabolized by xanthine oxidase

20
Q 
Probenecid, Sulfinpyrazone class
GOUT
A

Chronic gout treatment

Normal serum urate

21
Q

Probenecid, Sulfinpyrazone mechanism

GOUT

A

Competes with urate for a transporter blocking reabsorption in the kidney

22
Q

Probenecid, Sulfinpyrazone description

GOUT

A

Uricosuric agents -> enhances uric acid excretion

Coadminister with NSAIDs to prevent acute attack early in treatment

23
Q

Probenecid, Sulfinpyrazone AE

GOUT

A

Mild GI irritation
Hypersensitivity
Renal stones (increase fluids)

Sulfinpyrazone can also decrease hematopoiesis and inhibit warfarin metabolism

24
Q

Probenecid, Sulfinpyrazone Contraindications

GOUT

A

Gouty patients with nephrolithiasis or overproduction

Blood dyscrasia

25
Q 
Rasburicase class
GOUT
A

Chronic gout treatment

Normal serum urate

26
Q

Rasburicase mechanism

GOUT

A

Enzyme that oxidizes uric acid to allantoin which is soluble and easily excreted by the kidney

27
Q

Rasburicase description

GOUT

A

Enhances uric acid metabolism *

Prevent renal damage during cancer chemotherapy

Recombinant version of Aspergillus uricase

28
Q

Gout

A

High levels of uric acid in the blood -> deposition of sodium urate (end product purine metabolism) crystals in tissues -> inflammation

29
Q

Urate

A

Filtered, secreted and reabsorbed in the kidney; only 10% filtered urate is excreted -> reabsorption predominates

30
Q

Gout and chemotherapy

A

Cancer chemotherapy causes massive lysis of tumor cells -> significant release of nucleotides** -> hyperuricemia -> massive renal injury (part of tumor lysis syndrome)

Pharmacology (24 decks)

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