Gout Flashcards Preview

Pharmacology > Gout > Flashcards

Flashcards in Gout Deck (30)
Loading flashcards...
1
Q

Indomethacin, NSAIDs GOUT class

A

Acute attacks of gouty arthritis

Control pain

2
Q

Indomethacin, NSAIDS GOUT Mechanism

A

Suppress leukocyte recruitment and activation

3
Q

Indomethacin, NSAIDS GOUT description

A

DOC = indomethacin

Others NSAIDs are also useful

4
Q

Indomethacin, NSAIDs Contraindications

A

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

5
Q

Indomethacin, NSAIDs GOUT AE

A

Bleeding
Na+ and H2O retention
Renal insufficiency

6
Q

Colchicine GOUT class

A

Acute attacks of gouty arthritis

Control pain

7
Q

Colchicine GOUT mechanism

A

Suppress leukocyte recruitment and activation

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*
9
Q

Colchicine fun fact

GOUT

A

no longer used due to side effects

10
Q

Colchicine AE

GOUT

A

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

11
Q

Colchicine contraindications

GOUT

A

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

12
Q

Glucocorticoids GOUT class

A

Acute attacks of gouty arthritis

Control pain

13
Q

Glucocorticoids GOUT mechanism

A

Suppress leukocyte recruitment and activation

14
Q

Glucocorticoids description

GOUT

A

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

Anti-inflammatory and immunosuppressive effects

15
Q

Allopurinol class GOUT

A

Chronic gout treatment

Normal serum urate

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)