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Pharm - MSK/Derm
MSK/Derm Pharmacology from First Aid 2013
Question | Answer |
---|---|
What is the first step in the arachadonic acid pathway? What inhibits it? | Phospholipase A2 turns phosphatidylinositol into arachadonic acid. Inhibited by corticosteroids. |
What are the next two options in the AA pathway? What inhibits them? | Lipooxygenase (LOX) - Zileuton Cyclooxygenase (COX-1, COX-2) - NSAIDS, et al. |
What does the LOX pathway produce? What inhibits them? | Leukotrienes: LTB4 - neutrophil chemotaxis, arrive B4 others LTC, LTD - inc bronchial tone (montelukast) |
What does the COX pathway produce? | Prostacyclin (PGI2) Prostaglandins (PGE2, PGF2) Thromboxane A2 (TXA2) |
What does prostacyclin (PGI2) do? Where is it produced? | Endothelial cells: vasodilation, decreased platelet aggregation, decreased bonchial tone, decreased uterine tone |
What does prostaglandin (PGE2) do? | Keeps the PDA open, decreased vascular tone, decreased bronchial tone, INCREASED uterine tone, protects the gastric mucosa, vasodilates the afferent artery of the kidney (reason why NSAIDs are nephrotoxic) |
What does TXA2 do? | Increase vascular tone, constrict bronchioles, increase platelet aggregation |
Omega-3 fatty acid has what effect on platelets? | Decreases platelet aggregation. |
What does dipyrimadole inhibit? | TXA2 |
NSAIDs: examples, MOA, Use | Ibuprofen, naproxen, indomethacin MOA: reversible COX-1,2 inhibitors Use: antipyretic, anti-inflammatory analgesic Indomethacin maintains a PDA. |
What are some NSAID toxicities? | Gastric ulcer (PGE protects mucosa) Renal ischemia (PGE dilates aff. arteriole) Interstitial nephritis |
Selective COX-2 inhibitor: name, MOA, Use, Tox | Nom: Celecoxib MOA: COX2 found only in endothelium and inflammatory cells, spares COX1 in gastric mucosa Use: arthritis, patients with ulcers Tox: thrombosis |
Acetaminophen: MOA, Use | Reversible inhibit COX in CNS, less so peripherally (inactivated). Use: antipyretic and analgesic, NOT anti-inflammatory. Use in kids to avoid Reye's syndrome. |
Acetaminophen toxicity mechanism and treatment? Why does alcohol or isoniazid make it worse? | CYP2E1 metabolizes acetaminophen into NAPQI, which depletes the liver's supply of glutathione. --> free radicals Give N-acetylcysteine (mercaptan) to regenerate glutathione and activated charcoal to absorb the XS drugs. |
Bisphosphonates: naming, MOA, Use, Tox | Nom: Alendronate, "-dronate" MOA: bind HA in bone, inhibiting OC's Use: Osteoporosis, Pagets, hyperCa Tox: esophagitis, necrosis of jawbone |
What are all of the effects of corticosteroids vis-a-vis inflammation? | Inhibit PLA2 in AA pathway. Decrease adhesion molecules -> neutrophilia. Inhibit eosinophils. Induce lymphocyte apoptosis. |
Name two chronic gout drugs that treat overproduction? What is its MOA? Uses? | Allopurinol, febuxostat - xanthine oxidase inhibitors Gout and TLS. |
What treats gout under-secretion? What other use does it have? | Prohibits reabsorption of uric acid in PCT. Also increases half-life of penicillin. |
What is colchicine's Use, MOA, Tox? | Use: Acute gout! MOA: Inhibits neutrophil MT's. Tox: GI sfx. |
How do you treat acute gout? | NSAIDS, glucocorticoids, colchicine |
Name two TNFa inhibitors? What conditions are they used for? | Etanercept - TNF decoy receptor Infliximab - TNF antibody Psoriasis, ankylosing spondylitis, RA, Crohn's (infliximab) |