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16 Cards in this Set
- Front
- Back
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In high doses, ASA may cause "salicylism." What is "salicylism?"
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Tinnitus, decreased hearing &
vertigo. |
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How does ASA affect platelet aggregation?
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It decreases platelet activation by changing the ratio of prostacyclin to thromboxane -> modification of cyclic AMP and calcium levels.
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What is the anti-platelet dose of ASA and how is it beneficial?
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81mg po QD.
Prevention of MIs, TIAs, ischemic attacks, strokes, PEs after surgery,occlusion of CABGs & HD fistulas. |
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True or false.
NSAIDs negate the beneficial aspects of aspirin on platelets. |
True.
Although there is ongoing research on this subject, the general consensus is that it does negate the benefits. |
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How should doses of ASA & NSAIDs be spaced to avoid interaction?
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Take NSAID at least 30 min after immediate-release ASA or 8hrs before(so ASA has time to bind to active site).
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What are the properties of salicylates?
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They:
are weak organic acids; inhibit PGs & TXA synthesis; decrease free radicals production; decrease superoxide production; alter cellular cAMP concentration & do not affect the disease course. |
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To avoid CV complications, it is recommended that the lowest effective dose of Celebrex be used.
What are these guidelines? |
200 mg QD for OA
200-400 mg QD for RA 400 mg QD for pain |
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What are the possible adverse effects by prescription or OTC NSAIDs on the GI tract & on platelets?
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GI Tract - ulcers, perforations, bleeding, obstruction strictures & enteropathy.
Platelets - inhibition of aggregation leading to increased potential for bleeding. |
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How does NSAIDs affect the renal system?
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Causes renal vasoconstriction & decreased renal perfusion (PGI2);
increased water retention (PGE2); decreased K+ excretion (PGI2) & decreased Na excretion (PGE2) & ARF (PGI2). Effect can be produced by COX-1 or COX-2. |
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What are potential obstetrical complications of NSAIDs?
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Delayed delivery at term & chance of bleeding complications d/t inhibition of PG production - mainly a COX-2 issue.
COX-2 is also related to implantation of ovum & angiogenesis needed for establishment of placenta. |
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What is Reye's Syndrome?
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A potentially fatal disease that is characterized by hepatic & cerebral encephalopathy & liver steatosis. It is associated with ASA & non-ASA salicylate consumption by children with viral diseases such as chicken pox or the flu.
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Match the following:
1. NSAIDs 2. Opiod analgesics a. Better to txs dull throbbing pain accompanying injury or inflammation b. Better to tx severe sharp visceral pain (associated with acute abdominal pain, myocardial infarction, etc. |
1. a
2. b |
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How does NSAIDs decrease pain?
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They prevent PGs from potentiating endogenous mediators of peripheral nerve stimulation (e.g. bradykinin; histamine) when tissue is damaged thus decreasing PG-induced hyperalgesic response of lowering threshold of polymodal nociceptors of C fibers which results in sensitization of afferent nerve endings to mechanical and chemical stimulation.
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What is NSAID's antipyretic mechanism of action?
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They inhibit pyrogen & IL1-induced production of PGEs [by COX-2] in the hypothalamus (altering temp regulating center). When bacterial endotoxins are released from macrophages,
PGs increase -> resetting of thermoregulatory system in hypothalmus. NSAIDs -> vasodilation and increased heat loss via increased sweating -> decrease temp. |
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What are the most common adverse effects of NSAIDs?
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GI complications including PUD;
approx 1% incidence with 3-6 mths use; 2-4% when used for 1 yr; could be a 3-5-fold increase in risk of upper GI bleeding or perforation. |
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What is the mechanism by which NSAIDs cause GI complications?
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They cause mucosal irritation d/t decrease in PGs synthesis and thus the decrease in "cytoprotective" PG activity (mainly PGEs and PGI2)leading to increased gastric acid, decreased bicarb secretion,decreased mucus secretion and decreased thickness of mucus layer.
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