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Pharmacology > Gout > Flashcards

Flashcards in Gout Deck (30):
1

Indomethacin, NSAIDs GOUT class

Acute attacks of gouty arthritis
Control pain

2

Indomethacin, NSAIDS GOUT Mechanism

Suppress leukocyte recruitment and activation

3

Indomethacin, NSAIDS GOUT description

DOC = indomethacin

Others NSAIDs are also useful

4

Indomethacin, NSAIDs Contraindications

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

5

Indomethacin, NSAIDs GOUT AE

Bleeding
Na+ and H2O retention
Renal insufficiency

6

Colchicine GOUT class

Acute attacks of gouty arthritis

Control pain

7

Colchicine GOUT mechanism

Suppress leukocyte recruitment and activation

8

Colchicine GOUT description

*Binds tubulin* -> decrease polymerization -> no microtubules -> decrease mobility of granulocytes

*Disrupts mitotic spindle* blocking cell division

*Inhibits synthesis/release of LT's*

9

Colchicine fun fact
GOUT

no longer used due to side effects

10

Colchicine AE
GOUT

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

11

Colchicine contraindications
GOUT

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

12

Glucocorticoids GOUT class

Acute attacks of gouty arthritis

Control pain

13

Glucocorticoids GOUT mechanism

Suppress leukocyte recruitment and activation

14

Glucocorticoids description
GOUT

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

Anti-inflammatory and immunosuppressive effects

15

Allopurinol class GOUT

Chronic gout treatment

Normal serum urate

16

Allopurinol mechanism
GOUT

Purine analog -> inhibits *Xanthine oxidase* facilitating dissolution of tophi

17

Allopurinol description
GOUT

*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

Allopurinol AE
GOUT

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

19

Allopurinol contraindications
GOUT

If cutaneous rash develops, discontinue use

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

20

Probenecid, Sulfinpyrazone class
GOUT

Chronic gout treatment

Normal serum urate

21

Probenecid, Sulfinpyrazone mechanism
GOUT

Competes with urate for a transporter *blocking reabsorption* in the kidney

22

Probenecid, Sulfinpyrazone description
GOUT

*Uricosuric agents* -> enhances uric acid excretion

Coadminister with NSAIDs to prevent acute attack early in treatment

23

Probenecid, Sulfinpyrazone AE
GOUT

Mild GI irritation
Hypersensitivity
**Renal stones (increase fluids)**

**Sulfinpyrazone can also decrease hematopoiesis** and inhibit warfarin metabolism

24

Probenecid, Sulfinpyrazone Contraindications
GOUT

Gouty patients with nephrolithiasis or overproduction

Blood dyscrasia

25

Rasburicase class
GOUT

Chronic gout treatment

Normal serum urate

26

Rasburicase mechanism
GOUT

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

27

Rasburicase description
GOUT

Enhances uric acid metabolism *

Prevent renal damage during cancer chemotherapy

Recombinant version of Aspergillus uricase

28

Gout

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

29

Urate

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

30

Gout and chemotherapy

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