Pharm - OA

Question 1

What is the place in therapy for topical NSAIDs in mild OA?

Answer 1

Considered over PO in patients with mild OA

Question 2

What are the advantages of topical NSAIDs vs. PO NSAIDs?

Answer 2

• useful for pain relief while avoiding serious system side effects
• 60% receive 50% improvement in pain when compared to oral

Question 3

What are the ADRs of topical NSAIDs?

Answer 3

• prutitis
• burning
• pain
• rash at application site

Question 4

Name the topical NSAIDs

Answer 4

• diclofenac (cream, gel, patch, solution)

- ketoprofen (cream, gel)

Question 5

State the place in therapy for topical capsaicin

Answer 5

used when other products are ineffective or contraindicated

Question 6

MOA for topical capsaicin

Answer 6

Alleviates pain through down-regulation of the TRPV1 receptor activity of nociceptive sensory neurons and maybe through depletion of substance P

Question 7

Name the drugs that are topical capsaicins.

Answer 7

• Capzasin

- Zostrix

Question 8

ADRs of topical capsaicins

Answer 8

Burning, stinging, erythema at application site (usually gets better with repeat use)

**warn pt not to get it in their eyes/mouth and to wash hands after application

Question 9

What is the appropriate dosing regimen for topical capsaicin?

Answer 9

• must be used regularly, takes 2 weeks to take effect: gives preparation time to deplete substance P in nerve fibers supplying painful joints
• application can be 2-4 times a day to affected joints (don’t have long term effects)

Question 10

What is the place in therapy for PO NSAIDs in mod-severe OA?

Answer 10

consider on as-needed basis in patients who have insufficient relief with topical NSAIDs or have symptomatic OA in multiple joints (ex: spine and hip)

Question 11

What GI toxicity is related to PO NSAID use?

Answer 11

• minor: dyspepsia, anorexia, diarrhea (in 10-60%)

- major: GI bleeding and gastric mucosal injury - gastric/duodenal ulcers (in 7-13%)

Question 12

What should you add to PO NSAID therapy to decrease GI toxicity?

Answer 12

**PPI

Use PPI with NSAIDs OR use celecoxib (COX-2) - can use Celecoxib and PPI in highest risk

Question 13

What are the risk factors for GI toxicity in NSAID use?

Answer 13

• increased age, hypertension, concomitant aspirin/corticosteroid use
• H/o complicated ulcer, anticoagulant use, use of multiple NSAIDs over time

Question 14

Cardiovascular toxicity related to PO NSAID use

Answer 14

• CV thrombotic events
• MI
• Stroke
• *risk increases with duration of use

Question 15

Which patients are most appropriate to use COX-2 NSAID?

Answer 15

• use with PPI for patients with increased GI risk (>70 y/o) without increased CV risk
• if high risk to CV risk without as much GI risk: use naproxen + PPI

Question 16

What are the risk factors for nephrotoxicity secondary to NSAID?

Answer 16

• those with conditions associated with decreased renal blood flow: chronic renal insufficiency, CHF, severe hepatic disease, nephrotic syndrome)
• those taking certain meds: diuretics, ACE inhibitors, cyclosporine, aminoglycosides
• those of advanced age

Question 17

What are the clinical features of renal toxicity secondary to NSAID use?

Answer 17

• increased serum creatinine and BUN
• hyperkalemia
• elevated BP
• peripheral edema
• weight gain

Question 18

Which patient allergy should cause you to avoid Celecoxib?

Answer 18

Contraindicated in patients with sulfa allergy

Question 19

What is the impact of nonselective NSAIDs on platelet function?

Answer 19

***ALL nonselective NSAIDs increase bleeding risk

• aspirin inhibitors platelet aggregation irreversibly - bleeding time needs 5-7 days to normalize after stopping therapy
• others inhibit platelet function reversibly with normalization 1-3 days after stopping
• COX-2 selective NSAIDs have no bleeding risk but can increase CV events with increased thrombotic events

Question 20

What is the place in therapy for duloxetine in mod-severe OA?

Answer 20

• for patients with OA in multiple joints and concomitant comorbidities that contraindicate NSAIDs
• those who have not responded satisfactorily to NSAIDs

Question 21

What is the place in therapy for intra-articular glucocorticoids in mod-severe OA?

Answer 21

Can provide excellent pain relief, particularly when a joint effusion is present

Question 22

Which glucocorticoids are used for intra-articular injection?

Answer 22

• Triamcinolone hexacetonide

- methylprednisolone acetate

Question 23

What are the systemic adverse effects secondary to intra-articular glucocorticoids?

Answer 23

• hyperglycemia
• edema
• elevated BP
• dyspepsia
• rarely adrenal suppression

Blood glucose will rise within 24 hours to peak and then decline in next 3-5 days