First Aid- musculoskeletal, skin and ct drugs Flashcards Preview

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Flashcards in First Aid- musculoskeletal, skin and ct drugs Deck (60):
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lipoxygenase pathway yields

2

LTB4 functions as a

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function of PGI2

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function of LTC4, D4, and E4 

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MOA of aspirin

-irreverisbly inhibits COX 1 and 2 by acetylation --> decreases synthesis of both TXA2 and PGs

-increases BT but no effect on PT, PTT

-type of NSAID

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-irreverisbly inhibits COX 1 and 2 by acetylation --> decreases synthesis of both TXA2 and PGs

-increases BT but no effect on PT, PTT

-type of NSAID

MOA of aspirin

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Use of Aspirin

  • Low dose (< 300 mg/day): decreases platelet aggregation.
  • Intermediate dose (300–2400 mg/day): antipyretic and analgesic.
  • High dose (2400–4000 mg/day): anti-inflammatory. 

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  • Low dose (< 300 mg/day): decreases platelet aggregation.
  • Intermediate dose (300–2400 mg/day): antipyretic and analgesic.
  • High dose (2400–4000 mg/day): anti-inflammatory. 

Use of Aspirin

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toxicity for aspirin

  • Gastric ulceration, tinnitus (CN VIII).
  • Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding.
  • Risk of Reye syndrome in children treated with aspirin for viral infection.
  • Also stimulates respiratory centers, causing hyperventilation and respiratory alkalosis. 

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  • Gastric ulceration, tinnitus (CN VIII).
  • Chronic use can lead to acute renal failure, interstitial nephritis, and upper GI bleeding.
  • Risk of Reye syndrome in children treated with aspirin for viral infection.
  • Also stimulates respiratory centers, causing hyperventilation and respiratory alkalosis. 

toxicity for aspirin

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examples of NSAIDs

Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac. 

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Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac. 

examples of NSAIDs

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MOA for NSAIDs

  • Reversibly inhibit COX-1 and COX-2. Block PG synthesis. 

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  • Reversibly inhibit COX-1 and COX-2. Block PG synthesis. 

MOA for NSAIDs

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Use of NSAIDs

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

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

Use of NSAIDs

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toxicity of NSAIDs

  •  

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COX 2 inhibitor example

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MOA of COX 2 inhibitors

  • Reversibly inhibit COX 2, 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 TXA2 production is dependent on COX-1. 

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  • Reversibly inhibit COX 2, 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 TXA2 production is dependent on COX-1. 

MOA of COX 2 inhibitors

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Use of cox-2 inhibitors

  • Rheumatoid arthritis and osteoarthritis; patients with gastritis or ulcers. 

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  • Rheumatoid arthritis and osteoarthritis; patients with gastritis or ulcers. 

Use of cox-2 inhibitors

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toxicity for cox2 inhibitors

  • increased risk of thrombosis
  • sulfa allergy

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  • increased risk of thrombosis
  • sulfa allergy

toxicity for cox2 inhibitors

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MOA of acetaminophen

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

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

MOA of acetaminophen

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use of acetaminophen

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

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

use of acetaminophen

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toxicity for acetaminophen

  • Overdose produces hepatic necrosis; acetaminophen metabolite (NAPQI) depletes glutathione and forms toxic tissue adducts in liver.
  • N-acetylcysteine is antidote—regenerates glutathione. 

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  • Overdose produces hepatic necrosis; acetaminophen metabolite (NAPQI) depletes glutathione and forms toxic tissue adducts in liver.
  • N-acetylcysteine is antidote—regenerates glutathione. 

toxicity for acetaminophen

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Examples of bisphosphonates

alendronate and other "dronates"

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MOA for Bisphosphonates

  • pyrophosphate analogs
  • bind hydroxyapatite in bone, inhibiting osteoclast activity

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  • pyrophosphate analogs
  • bind hydroxyapatite in bone, inhibiting osteoclast activity

MOA for Bisphosphonates

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Use for BPs

  • osteoporosis, hypercalcemia, Paget's disease of bone

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  • osteoporosis, hypercalcemia, Paget's disease of bone

Use for BPs

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Toxicity of BPs

  • corrosive esophagitis, osteonecrosis of the jaw

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  • corrosive esophagitis, osteonecrosis of the jaw

Toxicity of BPs

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2 drug classes used for ACUTE gout

  • NSAIDS --> Naproxen, indomethacin
  • Glucocorticoids --> oral or intra-articular

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  • NSAIDS --> Naproxen, indomethacin
  • Glucocorticoids --> oral or intra-articular

2 drug classes used for ACUTE gout

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4 drugs used in CHRONIC gout

  • allopurinol
  • febuxostat
  • probenecid
  • colchicine

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  • allopurinol
  • febuxostat
  • probenecid
  • colchicine

4 drugs used in CHRONIC gout

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MOA for allopurinol

  • Inhibits xanthine oxidase, decreases conversion of xanthine to uric acid.
  • Also used in lymphoma and leukemia to prevent tumor lysis– associated urate nephropathy. increases concentrations of azathioprine and 6-MP (both normally metabolized by xanthine oxidase). 
  • Do not give salicylates; all but the highest doses depress uric acid clearance. Even high doses (5–6 g/day) have only minor uricosuric activity. 

43

  • Inhibits xanthine oxidase, decreases conversion of xanthine to uric acid.
  • Also used in lymphoma and leukemia to prevent tumor lysis– associated urate nephropathy. increases concentrations of azathioprine and 6-MP (both normally metabolized by xanthine oxidase). 
  • Do not give salicylates; all but the highest doses depress uric acid clearance. Even high doses (5–6 g/day) have only minor uricosuric activity. 

MOA for allopurinol

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MOA of febuxostat

  • inhibits xanthine oxidase

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  • inhibits xanthine oxidase

MOA of febuxostat

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MOA for probenecid

  • inhibits reabsorption of uric acid in PCT (also inhibtis secretion of peicillin)

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  • inhibits reabsorption of uric acid in PCT (also inhibtis secretion of peicillin)

MOA for probenecid

48

MOA of colchicine

  • Binds and stabilizes tubulin to inhibit microtubule polymerization, impairing leukocyte chemotaxis and degranulation.

  • Acute and prophylactic value. GI side effects. 

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  • Binds and stabilizes tubulin to inhibit microtubule polymerization, impairing leukocyte chemotaxis and degranulation.

  • Acute and prophylactic value. GI side effects. 

MOA of colchicine

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ALL TNF-alpha inhibitors predispose to:

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

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3 TNF-alpha inhibitor drugs

  • etanercept
  • infliximab, adalimumab

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  • etanercept
  • infliximab, adalimumab

3 TNF-alpha inhibitor drugs

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MOA for etanercept

  • Fusion protein (receptor for TNF-α + IgG1 Fc), produced by recombinant DNA.

  • Etanercept is a TNF decoy receptor. 

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  • Fusion protein (receptor for TNF-α + IgG1 Fc), produced by recombinant DNA.

  • Etanercept is a TNF decoy receptor. 

MOA for etanercept

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Use of etanercept

  • RA, psoriasis, ankylosing spondylitis

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  • RA, psoriasis, ankylosing spondylitis

Use of etanercept

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MOA for infliximab and adalimumab

Anti-TNF alpha monoclonal Ab

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Anti-TNF alpha monoclonal Ab

MOA for infliximab and adalimumab

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Use of infliximab, adalimumab

  • Crohn's disease, RA, ankylosing spondylitis, psoriasis

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  • Crohn's disease, RA, ankylosing spondylitis, psoriasis

Use of infliximab, adalimumab