Pharm -6- NSAIDS
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| T/F NSAID's provide analgesia by acting on central receptors | F they inhibit prostaglandin production, reduce nociceptors sensitization and increase pain threshold in the periphery not centrally
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| How do NSAIDS have antipyretic effects | inhibit prostaglandin production in the hypothalamus and reset the hypothalamic thermostat
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| How do NSAIDS have anti-inflammatory effects | inhibit prostaglandin production at site of inflammation, inhibit inflammatory mediator cascade, reduce edema, inhibit chemotaxis and stabilize lysosomal enzymes
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| Which cyclooxygenase Isoform is Proinflammatory | cox-2
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| What are the clinical signs of inflammation | Erythema-due to vasodilation of capillaries (rubor), Edema- fluid accumulation in intercellular spaces (tumor), tenderness/hyperalgesia (dolor) and Pain (dolor)
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| What do the following have in common- prostaglandins, leukotrienes, interleukins, tumor necrosis factor, colony stimulating factors, histamine, bradykinin, serotonin, proteases, collagenases, Elastase | inflammatory mediators
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| What are the three phases of inflammatory response | acute/transient phase, delays/subacute phase and chronic/proliferative phase
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| Which phase of the inflammatory response is marked by local vasodilation, and increased capillary permeability | acute/transient phase
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| What phase of the inflammatory response is marked by infiltration of leukocytes, and Phagocytosis | delayed/subacute phase
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| What phase of the inflammatory response is marked by tissue degeneration and fibrosis | chronic/proliferative phase
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| what is the function of Cox-1 | physiologic protection of the stomach, regulation of platelet aggregation TXA2, peripheral vascular resistance (PGI2) renal blood flow distribution (PGI2 and PGE2) and sodium excretion (PGE2)
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| What is the function of COx-2 | Proinflammatory prostanoid in fibroblasts, and macrophages and other cells
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| T/F aspirin is more selective for COX-2 than COX-1 | F favors COX-1
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| What NSAID favors COX-2 the most | Rofecoxib
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| How does aspirin prevent platelet aggregation at low doses | It inhibits COX which plays an important role in platelet aggregation.
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| What signal is produced by platelets that is a potent vasoconstrictor and inducer of platelet aggregation | TXA2 synthesized by Thromboxane synthase
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| What substance do endothelial cells produce to inhibit platelet aggregation and is a vasodilator | prostacyclin (PGI2)
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| What type of drug are the following, Aspirin, Ibuprofen, Indomethacin, Ketorolac, Naproxen, Piroxicam, Sulindac, Diclofenac, Diflunisal | NSAIDS cyclooxygenase inhibitors
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| What type of drug is celecoxib | COX-2 specific inhibitor reduces incidence of GI side effects
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| Place the following in order of longest Half Life to shortest- Ibuprofen, Naproxen, Piroxicam | Piroxicam>Naproxen>Ibuprofen
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| T/F most NSAIDS are rapidly absorbed by passive diffusion and are free in the plasma | F they are absorbed by passive diffusion and are bound to protein in the plasma
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| Where are the majority of NSAIDS metabolized | Most metabolized in the liver to conjugated metabolites
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| T/F aspirin irreversibly inhibits the COX isoenzyme both 1 and 2 | T
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| T/F aspirin aids granulocytes adhering to damaged vasculature and destabilized lysosomes to aid in healing | F just inhibits adherence of granulocytes to damaged vasculature and stabilized lysosomes
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| T/F Aspirin inhibits chemotaxis of polymorphonuclear leukocytes and macrophages | T
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| What can you prescribe in low doses for coronary artery disease, deep vein thrombosis, unstable angina, and as prophylaxis for MI and stroke | Aspirin
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| What formulation of aspirin can be taken to minimize GI irritation | enteric coated aspirin
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| At ____ doses of aspirin uric acid secretion is decreased and net uric acid excretion is decreased and at _____ doses net uric acid excretion is increased | At _LOW_ doses of aspirin uric acid secretion is decreased and net uric acid excretion is decreased and at _HIGH_ doses net uric acid excretion is increased
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| This is a potentially fatal toxicity from aspirin use in children with viral infections | Reye's syndrome causes liver dysfunction and encephalopathy
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| Aspirin Toxicity may lead to salicylism which prevents with what signs | tinnitus and vertigo
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| What are the toxicities that can occur from aspirin use | GI distress/bleeding, Hypersensitivity, Salicylism, bronchoconstriction, renal dysfunction
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| T/F acetaminophen is recommended for tx of inflammation and fever | F in has NO anti inflammatory actions
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| What is the drug of choice in antipyretic of children | Acetaminophen
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| Your pt is concerned about a possible allergy to aspirin and don't want to take it for prophylaxis of an MI you tell the not to worry just take acetaminophen because it also can prevent the platelets from aggregating did you give them good or bad info | Bad info Acetaminophen has not antiplatelet activity it also has no anti inflammatory action but it also has no significant GI side effects
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| T/F Ibuprofen and Naproxen are highly effective anti-inflammatory and analgesic agents and are effective for symptomatic tx of gout, RA and osteoarthritis | T
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| This drug is effective for osteoarthritis and musculoskeletal sprains. It has both peripheral and central mechanism to block the pain, irreversibly inhibits Thromboxane and has 4x potency of aspirin | Diflunisal (Dolobid)
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| What NSAID is highly indicated in tx of RA, acute gouty arthritis, osteoarthritis and indicated for closure of patent ductus arteriosus | Indomethacin
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| What properties of Sulindac (Clinoril) would influence you to possibly choose it over other NSAIDS | it is a prodrug metabolized in the liver highly potent Cox inhibitor used for long term treatment of osteoarthritis, RA, bursitis, and acute gouty arthritis
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| What benefits do piroxicam and meloxicam have as NSAIDS | they have long half life and permit once daily dosing for tx of RA, Osteoarthritis, and acute gout
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| What NSAID is has potent analgesic action and is an alternative to opioids for short term tx of moderate pain | ketorolac
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| This is a highly selective COX-2 inhibitor that is indicated in long term tx of osteoarthritis, ankylosing spondylitis (accumulates in synovial fluid) and short term tx of acute musculoskeletal and post operative pain | Diclofenac (Voltaren)
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| What benefit does Celecoxib have that may influence you to prescribe it | selective COX-2 inhibitor less incidence of GI ulcers, less effect of platelets and bleeding time approved for dysmenorrhea, osteoarthritis, and RA and acute post operative pain
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| Place the following in order from most to least in analgesic strength- Ketorolac, Aspirin, Ibuprofen and Naproxen | Ketorolac>Naproxen>Ibuprofen>Aspirin
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| T/F NSAIDS not only tx pain associated with RA but can also help prevent disease progression | F great for symptomatic tx of pain but don't halt progression
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| What is the common toxic side effect shared by all NSAIDS | GI toxicity, dyspepsia, abd pain, diarrhea, induction of gastric and intestinal ulcers, exacerbation of peptic ulcers, High concentrations may damage gastric mucosa, inhibition of prostaglandin synthesis by gastric mucosa leads to increased acid secretion
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| Pt has suffered from recurrent GI ulcers what NSAID would be best for them and what other things can you do to help them out | Lowest effective dose and use a COX-2 specific inhibitor and give co-therapy of misoprostol, high dose H2 receptor antagonist, PPI, avoid concomitant anticoag or corticosteroid use
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| What are the potential s/e of COX-2 selective inhibitors | Increased risk of stroke and MI by increasing risk of thrombosis
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| What concern should you have with NSAIDS and pt with renal compromise | it can induce nephrotoxicity and cause acute renal failure
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| Why are NSAIDS contraindicated in pregnancy and when are they contraindicated | contraindicated in the third trimester due to risk of post-partum hemorrhage and delayed labor
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| Why do NSAIDS cause drug interactions with anticoags, Phenytoin, sulfonamides and sulfonylureas | they are highly bound to plasma protein and displace those drugs increasing their bio availability
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| What is the cause of gout | Monosodium urate crystals getting deposited in the joint leading to inflammatory rxn
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| What are the initial drugs of choice in an acute gouty attack | Indomethacin and Ibuprofen
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| What drugs can be considered in acute gouty arthritis after indomethacin and ibuprofen | Naproxen and Diclofenac
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| What is the MOA of colchicine | bind tubulin in mitotic spindles and other microtubule structures stopping cell division, cell motility and release of Chemotactic factors. Inhibits migration of leukocytes and granulocytes into inflamed area and decreases phago activity and degranulation
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| What are the s/e of giving colchicine | Diarrhea, N/V and high toxicity limits duration of therapy
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| If pt doesn't respond to NSAIDS or colchicine for their acute gout attack what can you give to treat them | Corticosteroids also used for pts with polyarticular involvement
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| What drug is a competitive inhibitor of Xanthine oxidase the enzyme that catalyzes the final steps in uric acid formation and reduces plasma uric acid levels and is well tolerated | Allopurinol
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| T/F allopurinol is the drug of choice in an acute gout attack | F should not be given during an acute attack of gouty arthritis
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| How is allopurinol metabolized | metabolized in liver to oxypurinol slowly excreted in urine use caution in pts with hepatic and renal impairment
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| What is the MOA of Probenecid for tx of gout | blocks proximal tubular reabsorption of uric acid and is used to lower serum levels of uric acid in chronic gout
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