MSK and Derm pharmacology

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jknell
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MSK and Derm pharmacology
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2013-04-02 17:41:44
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MSK and Derm pharmacology
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    • Aracidoni acid →
    • 1. Lipoxygenase pathway
    •  - Leukotrienes

    • 2. Cyclooxygnase pathway
    •  - Prostacyclin
    •  - Prostaglandins
    •  - Thromboxane
  1. Arachadonic acid products
    Lipoxygenase pathway
    • Lypoxygenase → Leukotrienes
    • LTB4 → neutrophils (*"Neutrophils arrive B4 others")
    • LTC4, D4, E4 functions: bronchoconstriction, vasoconstriction, contraction of smooth muscle, ↑ vascular permeability
  2. Arachadonic acid products
    Cyclooxygenase pathway: PGI2
    • PGI2 inhibits platelet aggregation and promotes vasodilation
    • *Platelet-Gathering Inhibitor
  3. Aspirin
    • MechanismIrreversibly inhibits cyclooxygenase (both COX-1 and COX-2) by acetylation
    • -↓ synthesis of TXA2 and prostaglandins

    • -↑ bleeding time
    • -No effect on PT, PTT

    • Clinical use:
    • -Low dose (<300mg/day): ↓ platelet aggregation
    • -Intermediate dose (300-2400mg/day): antipyretic and analgesic
    • -High dose (2400-4000mg/day): anti-inflammatory

    • Toxicity:
    • -Gastric ulceration
    • -tinnitus
    • -Chronic use → renal failure, interstitial nephritis, upper GI bleeding
    • -Reye's syndrome in children (when treated with ASA for viral infection)
    • -Stimulates respiratory centers → hyperventilation, respiratory alkalosis
  4. NSAIDs
    Ibuprofen, naproxen, indomethacin, ketorolac, diclofenac

    • Mechanism:
    • -Reversibly inhibit cyclooxygenase (COX-1, COX-2)
    • -Block prostaglandin synthesis

    • Clinical use:
    • -Antipyretic
    • -Analgesic
    • -Anti-inflammatory
    • -*Indomethacin is used to close a PDA

    • Toxicity:
    • -Interstitial nephritis
    • -Gastric ulcers (PGs protect gastric mucosa)
    • -Renal ischemia (PGs vasodilate afferent arteriole)
  5. COX-2 inhibitor
    Celecoxib
    • Mechanism: Reversibly inhibits COX-2
    • -isoform found in inflammatory cells and vascular endothelium; mediates inflammation and pain
    • -Spares COX-1; decrease GI effects
    • -Spares platelet function (TXA2)

    • Clinical use:
    • -RA
    • -Osteoarthritis
    • -Pts with gastritis or ulcers

    • Toxicity:
    • -Increase risk of thrombosis
    • -Sulfa allergy
  6. Acetaminophen
    • Mechanism:
    • -Reversibly inhibits cyclooxygenase, mostly in CNS (inactivated peripherally)

    • Clinical use:
    • -Antipyretic
    • -Analgesic
    • -NOT anti-inflammatory
    • -Used to avoid Reye's syndrome in children with viral infection

    • Toxicity:
    • -OD produces hepatic necrosis
    • -metabolites deplete glutathione and form toxic tissue adducts in liver
    • -N-acetylcysteine is antidote (regenerates glutathione)
  7. Bisphosphonates
    Alendronate, "-dronates"

    • Mechanism:
    • -Pyrophosphate analog
    • -bind hydroxyapatite in bone, inhibits osteoclast activity

    • Clinical use:
    • -Osteoporosis
    • -Hypercalcemia
    • -Paget's disease of bone

    • Toxicity:
    • -Corrosive esophagitis
    • -Osteonecrosis of the jaw
  8. Purine → Hypoxanthine → Xanthine → Uric acid
  9. Chronic gout drugs
    • Allopurinol
    • Febuxostat
    • Probenecid
    • Colchicine
  10. Acute gout drugs
    • NSAIDs: Naproxen, indomethacin
    • Glucocorticoids: oral or intraarticular
  11. Allopurinol
    • Inhibits xanthine oxidase
    • ↓ conversion of xanthine to uric acid
    • Other uses: lymphoma, leukemia (to prevent tumor lysis-associated urate nephropathy)
    • **Increases concentration of azathioprine and 6-MP (both normally metabolized by XO)
  12. Febuxostat
    Inhibits Xanthine oxidase
  13. Probenecid
    • Inhibits reabsorption of uric acid in PCT
    • also inhibits secretion of penicillin
  14. Colchicine
    • Binds and stabalizes tubulin to inhibit polymerization
    • Impairs leukocyte chemotaxis and degranulation
    • Side effects: GI (oral)
  15. TNF-α inhibitors
    Etanercept, infliximab, adalimumab
    • All TNF-α inhibitors predispose pts to infection (including reactivation of latent TB)
    • TNF blockade prevents activation of macrophages and destruction of phagocytosed microbes
  16. Etanercept
    • Mechanism:
    • -Fusion protein (receptor for TNF-α + IgG1 Fc), produced by recombinant DNA
    • -*Etanercept is a TNF decoy receptor

    • Clinical use:
    • -Rheumatoid arthritis
    • -Psoriasis
    • -Ankylosing spondylitis
  17. Infliximab, adalimumab
    • Mechanism:
    • -Anti-TNF-α monoclonal antibody

    • Clinical use:
    • -Crohn's disease
    • -Rheumatoid arthritis
    • -Ankylosing spondylitis
    • -Psoriasis

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