MSK, Skin, Connective Tissue

Question 1

Aspirin (MOA)

Answer 1

Irreversibly inhibits cyclooxygenase (both COX-1 and COX-2) by covalent acetylation which decreases synthesis of both thromboxane A2 and prostaglandins. Increases bleeding time until new platelets are produced (~7 days). No effect on PT/PTT. A type of NSAID.

Question 2

Aspirin (CU)

Answer 2

Low dose: decreases platelet aggregation. Intermediate dose: antipyeritic (fever reducer) and analgesic. High dose: anti-inflammatory.

Question 3

Aspirin (T)

Answer 3

Gastric ulceration, tinnitus (CN VIII). Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding. Reye syndrome. Stimulates respiratory centers causing hyperventilation and respiratory alkalosis.

Question 4

NSAID’s (ibuprofen, naproxen, indomethacin, ketorolac, diclofenac) (MOA)

Answer 4

Reversibly inhibits COX 1 & 2. Block PG synthesis.

Question 5

NSAID’s (ibuprofen, naproxen, indomethacin, ketorolac, diclofenac) (CU)

Answer 5

Antipuretic, analgesic, anti-inflammatory. Naproxen and indomethacin can be used to treat acute gout. Indomethacin is used to close PDA.

Question 6

NSAID’s (ibuprofen, naproxen, indomethacin, ketorolac, diclofenac) (T)

Answer 6

Interstitial nephritis, gastric ulcer, renal ischemia, (PGs vasodilate afferent arterioles)

Question 7

Celecoxib (MOA)

Answer 7

Reversibly inhibits COX2 (found in inflammatory cells and vascular endothelium and mediates inflammation and pain) spares COX1 (which helps maintain GI function). Spares platelet function as TXA2 production is dependent on COX1.

Question 8

Celecoxib (CU)

Answer 8

Rheumatoid arthritis and osteoarthritis pts with gastritis and ulcers

Question 9

Celecoxib (T)

Answer 9

increased risk of thrombosis. sulfa allergy

Question 10

Acetaminophen (MOA)

Answer 10

Reversibly inhibits COX, mostly in the CNS. Peripherally inactivated.

Question 11

Acetaminophen (CU)

Answer 11

Antipyretic, analgesic, non-inflammatory. Used instead of aspirin in children with viral illness.

Question 12

Acetaminophen (T)

Answer 12

Overdose produces hepatic necrosis; acetaminophen metabolite NAPQ1 depletes glutathione and forms toxic tissue adduct in liver, N-acetlycycteine is antidote-regenerates glutathione.

Question 13

Alendronate, other -dronates (MOA)

Answer 13

Bisphosphonate. Pyrophosphate analogs; bind hydroxyapatite in bone, inhibiting osteoclast activity

Question 14

Alendronate, other -dronates (CU)

Answer 14

Osteoporosis, hypercalcemia, paget ds of bone

Question 15

Alendronate, other -dronates (T)

Answer 15

Corrosive esophagitis, osteonecrosis of the jaw

Question 16

Allopurinol (MOA)

Answer 16

Inhibits xanthine oxidase. Decreases conversion of xanthine to uric acid.

Question 17

Allopurinol (CU)

Answer 17

Hyperuricemia. Chronic gout (preventative). Also used in lymphoma and leukemia to prevent tumor lysis-associated rate nephropathy.

Question 18

Allopurinol (T)

Answer 18

Increases concentration of Azathioprine and 6-MP (both normally metabolized by xanthine oxiadase). Do not give salicylates; all but the highest doses depress uric acid clearance. Even high doses have only minor uricosuric activity.

Question 19

Febuxostat

Answer 19

Inhibits xanthine oxidase. Chronic gout (preventative). Less side effects.

Question 20

Probenecid

Answer 20

Inhibits resorption of uric acid in PCT (also inhibits secretion of penicillin). Chronic gout (preventative)

Question 21

Colchicine

Answer 21

Binds and stabilizes tubulin to inhibit microtubule polymerization, impairing leukocyte chemotaxis and degranulation. Acute and prophylactic value for gout. GI side effects.

Question 22

Etanercept

Answer 22

Fusion protein (receptor for TNF-a) produced by recombinant DNA. Decoy receptor. RA, psoriasis, ankylosing spondy. Reactivation TB.