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Drugs for Inflamm
Pharmacology 445
| Question | Answer |
|---|---|
| What is the primary injury? | intial injury to area, causing primary blood flow |
| What is the cause of the secondary injury? | originally healthy cells die from hypoxic nature of ischemic blood flow |
| What chemical mediators are released withing the first 24hrs? | histamine, seretonin, bradykinin, luekotrienes, prostaglandins, TNF, |
| Histamine causes: | vasodilation by increasing space between cells |
| Seretonin increases: | cell permeability |
| Bradykinin causes: | vasodilation and pain |
| Leukotrienes are: | an eicosanoid that promotes chemotaxis |
| Prostaglandins: | are an eicosanoid that cause vasodilation and pain, supresses excessive inflammatory repsonse |
| TNF is: | tumor necrosis factor, stimulates enzymes to produce eicosanoids |
| What events occur in the clotting effects? | Margination leading to temporary platelet plug, enzyme X causes Prothrombin to convert to Thrombin, Thrombin stimulates fibrongen which in turn converts Fibrin. Fibrin replaces platelet plug as connective tissue. |
| what occurs during phagocytosis? | Neutrophils arrive first, macrophages arrive later, stay longer, digest waste from dead cells |
| What events occur during the proliferation phase? (72hrs to 3wks) | Debris is removed, tissue reconstruction/regeneration, type 3 collagen is laid down. |
| Maturation phase includes what events? | Type 3 collagen is replaced by type 1, tissue strengthens (SAID principle) |
| The drug Singular affects what eiosanoid pathway? | affects senthesis of leukotrienes |
| COX pathway leads to what synthesis? | prostaglandin (causing swelling and pain) |
| Glucosteroids block what bening released? | Phospholipids from cell membrane |
| Name a few NSAIDs | Asprin (acetylsalicylic acid), Motrin, Aleve (naproxem) Indocin (Indomethacin) Vioxx, Taradol |
| How are NSAIDs effective? | block COX pathway, inhibits chemotaxis |
| Dosage and actions of Asprin: | 3000-6000mg/day; blocks COX pathway, anti-inlfamatory and reduces edema, analgesia |
| Adverse effects of Asprin: | reduces platelet action (increased bleeding), GI upset, tinnitus and nasal irritation |
| Ibuprofen dosage and actions: | 2400-3200mg daily; quick onset (15min) blocks COX and is anti-inflamm, less inhibition of platelets |
| Naproxen dosage and actions: | 750-1000mg/ 2x daily; blocks COX pathway, used to treat migranes and joint inflammation (TMJ) |
| Adverse effects of Naproxen: | increased GI bleed over Ibuprofen, caution with patients who have compromised kidneys |
| Indomethacin is used to treat: | rhematoid arthritis, gout, supress uterine contractions in preterm labor |
| drug-drug interaction of NSAIDs: | BP meds/antibiotics cause kidney damage, anticoagulant scause increased GI bleed, anti-epileptic cause decreased effectiveness of AED |
| Drugs classified as Glucosteroids: | cortisone, hydrocortisone, dexamethasone, prednisone |
| Glucosteroids: | are naturally made by adrenal glands, inhbit; phospholipase, COX-2 pathway, TNF, Chemotaxis and protien synthesis |
| Intal is a ____ stabilizer: | mast cell stabilizer, too many mast cells cause increased chemical mediators |
| Glucosteroids can be administered in what forms? | oral , inhalant, IV, IM, IA, ionto and phonophoresis |
| Adverse effects of Glucosteroids inglude: | decreased elasticity of tendons and ligaments, vasovagal sympathy, avascular necrosis of cartilage |
| Nuetrophils are presents when? | first 6 hours |
| Lymphacystes release what? | antibodies |
| macrophages arrive after the first___? | 24 hours |
| Injury process: | initial trauma (Phospholipids are released freeing acrhadonic acid), COX or lipoxygenase pathway, acute clotting mechanism, phagocytic cell accumulation, proliferation, maturation |
| What two chemicals cause pain? | prostglandins and bradykinins |
| SAID principle: | Specific adaptations to implied demands |
| 5 signs of inflammation | redness, swelling, pain, L.O.F., and increased temp |
Created by:
cwc2447
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