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15 Cards in this Set
- Front
- Back
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Diphenhydramine
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H1 blocker, 1st gen
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Chorpheniramine
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H1 blocker, 1st gen
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Dimenhydrinate
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H1 blocker, 1st gen
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Doxylamine
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H1 blocker, 1st gen
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Cetirizine
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H1 blocker, 2nd gen, Zyrtec
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Loratidiine
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H1 blocker, 2nd gen, Claritin
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Fexofenadine
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H1 blocker, 2nd gen, Allegra
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Cimetidine
Famotidine Ranitidine Nizatidine |
H2 blockers
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What do H2 blockers do?
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Inhibit gastric acid secretion (clinical uses: h. pylori, GERD, gastritis)
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What are some adverse effects of 1st gen H1 blockers?
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Cholinergic = blocking of muscarinic receptors results in Dry Mouth, urinary retention, constipation, etc. (the classic Hot as a Hare, Dry as a bone, Red as a beat, Blind as a Bat and Mad as Hatter mnemonic associated with atropine toxicity applies here, only the severity of symptoms is not nearly as bad). A-adrenergic results in hypotension, dizziness, and reflex tachycardia (similar to the effects seen non-selective (phenoxybenzamine) and a1-selective blockers (prazosin). Serotonin just know it increases appetite, serotonin receptors should be covered as part of the neuro course as well as psychiatric pharm (SSRIs, etc). H1 Receptor to re-emphasize, 1st gen H1 blockers cross the BBB and thus decrease transmission at histaminergic neurons, the result is a sedative effect with cognitive and psychomotor impairments, THIS IS WHY PEOPLE WORKING CONSTRUCTION, FLYING PLANES, ETC should not take these drugs.
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How do 1st gen and 2nd gen H1 blockers differ?
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2nd gen doesn't cross blood-brain barrier.
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Why are NSAIDs more potent Cox-1 inh than Cox-2 inh?
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Related to differences in enzyme active site conformation
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What are some adverse effects of NSAIDs?
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Gastrointestinal (upper GI bleeding), Renal, Hematologic (inc bleeding time), Dermal (rash), Hepatic (hepatotoxicity from acetaminophen), Cardiovascular (inc MI and stroke from COX-2 inh)
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Why does chronic use of NSAIDs cause acute renal insufficiency?
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COX-1 is expressed constitually on kidney (as well as brain and bone).
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What is the mechanism of NSAIDs?
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NSAIDs non-selectively block the function of COX-1 and COX-2 enzymes, the result is that prostanoids production is significantly decreased. In an inflammatory state such as infection or tissue injury this decreases inflammation by removing the PGE2 stimulation of arteriole smooth muscle relaxation and indirectly decreases edema (ANTIINFLAMMATORY), decreases pain by reducing PGE2 nerve ending sensitization (ANALGESIC) and lastly reduces the amount of PGE2 released in the anterior hypothalamus allowing the body to reset its internal thermostat back to normal levels (ANTIPYRETIC).
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