Duan: Gout Drugs

Question 1

caused by deposition of uric acid crystals in the joint space as a result of long-standing hyperuricemia (increased production or decreased excretion of uric acid), causing an inflammatory reaction.

Answer 1

gout

Question 2

What is happening in the inflammatory process in gout?

Answer 2

deposition of uric acid crystals causes phagocytic cells to infiltrate and attempt to phagocytize the urate crystals;
lactate production is high in synovial joints and this low pH environment causes further deposition of uric acid

Question 3

Urate is also deposited in the interstitial tissues of the kidney. What problem can this lead to?

Answer 3

kidney stones

Question 4

What are some conditions that increase uric acid?

Answer 4

height
body weight
blood pressure
warm climate
diabetes
hyperlipidemia
alcohol
social status
intelligence

Question 5

At what age is gout most likely to occur in males and females?

Answer 5

70’s for men

80+ for females

Question 6

Uric acid (which is converted to urate) is a product of (blank) metabolism

Answer 6

purine

Question 7

Deficiency in this enzyme can cause primary gout

Answer 7

HPRT (hypoxanthine-guanine phosphoribosyl transferase)

**Lesch-Nyhan disease

Question 8

Overproduction of urate secondary to increased breakdown of blood cells as in leukemia.

Chemotherapy or radiation.

Decreased excretion of urate due to use of alcohol, thiazide diuretics or low doses of aspirin.

Answer 8

secondary gout

Question 9

Describe the disease progression of gout

Answer 9

asymptomatic with high levels of serum urate
acute gout: very painful monoarticular arthritis, usu in a big toe initially
intercritical period: remission
chronic tophaceous gout: gouty arthritis with crystals in synovium and some degree of bone erosion
uric acid kidney stones can form

Question 10

Chronic gout leads to deposition of urates into a chalky mass known as a (blank). This mass can destroy the joint and adjacent bone

Answer 10

tophus

Question 11

Pale areas seen in histology of gout, aggregates of urate crystals surrounded by infiltrated of immune mediating cells

Answer 11

tophi

Question 12

Synovial fluid is aspirated from a patient with gout and examined for the presence of (blank)

Answer 12

sodium urate crystals

Question 13

In this disease, there is formation of rhomboid or coffin-shaped calcium pyrophosphate crystals

Answer 13

pseudogout

Question 14

A unique antiinflammatory agent in that it is effective only against gouty arthritis. It provides dramatic relief of inflammation and pain in acute gouty arthritis, and is an effective prophylactic agent against such attacks.
Drug of choice for acute attacks.
Reduction of inflammation and relief from pain occur 12—24 hours after oral administration.

Answer 14

colchicine

Question 15

What is the MOA of colchicine? Does it effects the concentration of uric acid in the blood or its renal excretion?

Answer 15

may inhibit granulocytes from infiltrating into inflamed area, inhibits release of histamine from mast cells; no it does not influence renal excretion of blood concentration of uric acid

Question 16

How long after admin of colchicine will there be relief from inflammation and pain?

Answer 16

12-24 hours

Question 17

Adverse effects of colchicine?

Orally?
IV?
High dose?

Answer 17

orally: nausea, vomiting, abdominal pain, diarrhea

IV: sloughing skin and subcutaneous tissue

high dose can result in liver damage and blood dyscrasias

Question 18

useful in the treatment of gout because they increase the excretion of uric acid by blocking its reabsorption for the urine.

Answer 18

uricosuric agents

Question 19

These two uricosuric agents reduce urate levels by preventing reabsorption of uric acid in renal tubules; used for chronic gout in combo with colchicine

Answer 19

probenecid

sulfinpyrazone (also an NSAID)

Question 20

What can uricosuric agents do to the urine?

Answer 20

increased urinary concentration of uric acid may result in urolithiasis or urate stones

Question 21

Inhibits the synthesis of uric acid by inhibiting xanthine oxidase, an enzyme that converts hypoxanthine to xanthine and xanthine to uric acid, the terminal steps in uric acid biosynthesis

Answer 21

allopurinol

Question 22

What enzyme does allopurinol block?

Answer 22

xanthine oxidase

Question 23

What are these?

indomethacin
naproxen
sulindac

Answer 23

NSAIDs that are FDA approved for ACUTE gout

**faster onset
less toxic
cost effective

Question 24

Can be injected into joint to relieve pain locally; have less utility in ACUTE gout bc they do not work as well as NSAIDs or colchicine

Answer 24

corticosteroids

Question 25

Acute gout is treated with (blank) (indomethacin, naproxen, and sulindac). These NSAIDs are preferred to colchicine because of the (blank) associated with he use of colchicine.

Answer 25

NSAIDs; diarrhea

Question 26

Chronic gout is treated with (blank) to increase the elimination of uric acid (probenecid, sulfinpyrazone) and allopurinol to inhibit uric acid production

Answer 26

uricosuric agents

Question 27

3 maintenance drugs for gout

Answer 27

allopurinol probenecid sulfinpyrazone