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29 Cards in this Set
- Front
- Back
Lipoxygenase
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Converts arachidonic acid to leukotrienes
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LTB4
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Neutrophil chemotactic agent
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LTC4, LTD4, LTE4
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Bronchoconstriction
Vasoconstriction Contraction of smooth muscle Increased vascular permeability |
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PGI2
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Prostacyclin
Inhibits aggregation of platelets Decreases uterine tone Vasodilates "Platelet Gathering Inhibitor" |
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Phospholipase A2
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Converts membrane lipids to arachidonic acid
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COX-1, COX-2
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Convert arachidonic acid to TxA2, prostacyclin (PGI2) and prostaglandin (PGE2)
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PGE2
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Prostaglandin
Increases: pain, temp, uterine tone Vasodilates |
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TxA2
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Platelet aggregation
Vasoconstriction |
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Zileuton
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Lipoxygenase inhibitor. Prevents formation of Leukotrienes.
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Montelukast/Zafirlukast
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Leukotriene receptor inhibitor
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COX-1 acts mainly on
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gastric mucosa
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COX-2 acts mainly on
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inflammatory cells
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Corticosteroid: mechanism for anti-inflammatory action
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Inhibit Phospholipase A2
Inhibit protein synthesis required for COX-1, COX-2 production |
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NSAIDs
Acetaminophen Aspirin MOA |
Inhibit COX-1, COX-2 formation of prostaglandins (PGE2)
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Aspirin
1. MOA 2. Use and dosage 3. Toxicity |
1. Irreversibly and covalently binds COX, decreasing synthesis of both PGE2 and TxA2
2. Low dose: anti-platelet Intermediate dose: anti-pyretic and analgesic High-dose: anti-inflammatory 3. Gastric upset. Renal failure, interstitial nephritis, upper GI bleed. Reye's syndrome in kids after viral illness. |
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Reye's syndrome
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Fatty liver and extreme encephalopathy, among other symptoms.
Caused by aspirin use in children post viral illness. |
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NSAIDs
1. MOA 2. Use 3. Toxicity |
Ibuprofen, naproxen, indomethacin, ketorolac
1. Reversibly inhibits COX-1, COX-2, blocking PGE2 synthesis. 2. Anti-pyretic, analgesic, anti-inflammatory 3. Renal damage, aplastic anemia, GI distress, ulcers |
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COX-2 inhibitors
1. aka ____ 2. MOA 3. Use 4. Toxicity |
1. Celecoxib
2. Reversibly inhibits COX-2, found on inflammatory cells, vascular endothelium, mediating inflammation and pain. Helps maintain gastric mucosa, no corrosive effects. 3. RA and OA 4. Increased risk of thrombosis. Sulfa drug allergy. Less toxicity to GI mucosa |
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Acetamenophen
1. MOA 2. Use 3. Toxicity |
1. Reversibly inhibits COX in CNS. Inactivated peripherally.
2. Anti-pyretic, analgesic. NO ANTI-INFLAMMATORY properties. Used instead of aspirin in kids to avoid Reye's syndrome. 3. Hepatic necrosis after overdose. |
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Bisphosphonates
1. MOA 2. Use 3. Toxicity |
1. Inhibit osteoclastic activity.
2. Malignancy-associated hypercalcemia, Paget Disease of the bone, post-menopausal osteoporosis. 3. Corrosive esophagitis, nausea, diarrhea |
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What is used to Tx:
Acute gout? Chronic gout? |
1. Colchicine
2. Probenecid and/or Allopurinol |
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Colchicine
1. MOA 2. Use 3. Toxicity |
1. Stabilizes tubulin to inhibit polymerization, impairing leukocyte chemotaxis and degranulation.
2. Acute gout 3. GI toxicity |
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Probenecid
1. MOA 2. Use 3. Toxicity |
1. Inhibit reabsorption of uric acid in PCT
2. Chronic Gout 3. inhibits secretion of penicillin |
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Allopurinol
1. MOA 2. Use 3. Toxicity |
1. Inhibits Xanthine Oxidase, preventing conversion of xanthine to uric acid.
2. Chronic gout, lymphoma and leukemia to prevent tumor-lysis associated urate nephropathy. 3. Increases concentrations of azothioprine and 6-MP (metabolized by XO) |
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What drug should not be given in a patient with gout?
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Salicylates and certain diuretics.
Salicylates decrease uric acid clearance. |
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TNF-a inhibitors (3)
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Etanercept
Infliximab Adalimumab |
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Etanercept
1. MOA 2. Use |
1. TNF-a receptor decoy --> inhibits TNF-a
2. RA, psoriasis, ankylosing spondylitis |
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Infliximab
1. MOA 2. Use 3. Toxicity |
1. anti-TNF-a Ab
2. Chron's, RA, ankylosing spondylitis 3. Predisposes to infxns (i.e. reactivation of latent TB) |
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Adalimumab
1. MOA 2. Use |
1. anti-TNF-a Ab
2. RA, psoriasis, ankylosing spondylitis |