Musculoskeletal, Skin, and CT Pharm Flashcards

1
Q

NSAIDs Examples

A

Ibuprophen, naproxen, indomethacin, ketorolac, diclofenac

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2
Q

NSAIDs MOA

A

Reversibly inhibit COX 1 and 2. Block PG synthesis.

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3
Q

NSAIDs Clinical Use

A

Antipyretic, analgesic, anti-inflammatory. Indomethacin is used to close a PDA.

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4
Q

NSAIDs Toxicity

A

Interstitial nephritis, gastric ulcer (PGs protect gastric mucosa), renal ischemia (PGs vasodilate afferent arteriole)

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5
Q

COX-2 Inhibitors (celeCOXib) MOA

A
  • Reversibly inhibit specifically the COX-2 isoform, which is found in inflammatory cells and vascular endothelium and mediates inflammation and pain.
  • Spares COX-1, which helps maintain the gastric mucosa. Thus, should not have the corrosive effects of other NSAIDs on the GI lining.
  • Spares platelet function as TXAs production is dependent on COX-1.
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6
Q

COX-2 Inhibitors (celeCOXib) Clinical Use

A

Rheumatoid arthritis and osteoarthritis; patients with gastritis or ulcers.

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7
Q

COX-2 Inhibitors Toxicity

A

Increased risk of thrombosis. Sulfa allergy.

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8
Q

Acetaminophen (Tylenol) MOA

A

Reversibly inhibits cyclooxygenase, mostly in the CNS. Inactivated peripherally.

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9
Q

Acetaminophen Clinical Use

A

Antipyretic, analgesic, but NOT anti-inflammatory. Used instead of aspirin to avoid Reye’s syndrome in children with viral infection.

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10
Q

Acetaminophen Toxicity

A

Overdose produces hepatic necrosis; acetaminophen metabolite depletes glutathione and forms toxic tissue adducts in liver
Antidote? N-acetylcysteine which regenerates glutathione

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11
Q

Bisphosphonates (Alendronate and other -dronates) MOA

A

Pyrophosphate analogs; bind hydroxyapatite in bone inhibiting osteoclast activity–> less bone resorption

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12
Q

Bisphosphonates (Alendronate and other -dronates) Clinical Use

A

Osteoporosis, hypercalcemia, Paget’s disease of bone

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13
Q

Bisphosphonates (Alendronate and other -dronates) Toxicity

A

Corrosive esophagitis, osteonecrosis of the jaw

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14
Q

Chronic Gout Drugs

A

Allopurinol, Febuxostat, Probenecid, Colchicine

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15
Q

Acute Gout Drugs

A

NSAIDs (naproxen and indomethacin)

Glucocorticoids (oral or intra-articular)

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16
Q

Allopurinol

A
  • Inhibits xanthine oxidase, decreases conversion of xanthine to uric acid.
  • Also used in lymphoma and leukemia to prevent tumor lysis- associated urate nephropathy.
  • Increased concentrations of azathioprine and 6-MP (both normally metabolized by xanthine oxidase).
17
Q

What should you not give with allopurinol?

A

Do not give salicylates (aspirin).
All but the highest doses depress uric acid clearance.
Even high doses (5-6g/day) have only minor uricosuric activity.

18
Q

Febuxostat MOA

A

Inhibits xanthine oxidase

19
Q

Probenecid MOA

A

Inhibits reabsorption of uric acid in PCT (also inhibits secretion of penicillin)

20
Q

Colchicine MOA

A

Binds and stabilizes tubulin to inhibit polymerization (disrupts the cytoskeleton), impairing leukocyte chemotaxis and degranulation.

21
Q

TNF-alpha Inhibitors Examples

A

AEI (vowels)

  • Adalimumab
  • Etanercept
  • Infliximab
22
Q

Side Effect of TNF-alpha Inhibitors

A

All TNF-alpha inhibitors predispose to infection including reactivation of latent TB since TNF blockade prevents activation of macrophages and destruction of phagocytosed microbes.

23
Q

Etanercept MOA

A
Fusion protein (receptor for TNF-alpha + IgG Fc) produced by recombinant DNA.
EtanerCEPT is a TNF decoy reCEPTor.
24
Q

Etanercept Clinical Use

A

RA, psoriasis, ankylosing spondylitis

25
Q

Infliximab, Adalimumab MOA

A

Anti-TNF alpha monoclonal antibody

26
Q

Infliximab, Adalimumab Clinical Use

A

Crohn’s disease, RA, psoriasis, ankylosing spondylitis

27
Q

Contraindication of chronic gout drugs?

A

Allopurinol, febuxostat, and probenecid are CI’ed in acute gouty arthritis and may actually precipitate acute attacks.
–> as uric acid is being eliminated, the body starts to release stored uric acid