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32 Cards in this Set
- Front
- Back
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What enzyme is needed to make leukotrieenes?
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lipoxygenase
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What enzyme is needed to make thromboxane?
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cyclooxygenase
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What does LTB4 do?
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Neutrophil chemotactic agent
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What do LTC4, D4, and E4 do?
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bronchoconstriction, vasoconstriction, contraction of smooth muscles, and increased vascular permeability
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What does PGI2 do?
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Inhibits platelet aggregation and promotes vasodilation
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MOA of aspirin?
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Irreversible COX 1 and 2 inhibitor
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Describe the difference in effect of low dose, medium dose, and high dose aspirin.
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Low dose- decreases platelet aggregation
Medium dose- antipyretic/painkiller High dose- anti-inflammatory |
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What are the side effects of aspirin?
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Gastric upset, renal, Reye's syndrome in children with viral illness
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What is the MOA of NSAIDs?
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Reversibly inhibit cox 1 and cox 2
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Side effects of NSAIDs (5)?
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GI, renal (decrease renal blood flow by dec. prostaglandins), fluid retention, ulcers, aplastic anemia
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Which NSAID is used to close a PDA?
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Indomethacin
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What happens when you OD on salicylates?
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1) respiratory alkalosis (centrally mediated)- hyperventilation
2) anion gap metabolic acidosis because the drug interferes with the krebs cycle so you get anaerobic glycolysis & lactic acidosis |
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thromboxane is produced by?
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platelets
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PGI2 is produced by?
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endothelial cells
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What does dipyramidol do?
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selectively blocks the synthesis of thromboxane
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What reaction do corticosteroids block?
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Membrane lipid (like phosphatidylinositol) --> arachidonic acid
Enzyme? phosphalipase A2 |
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What is the positive and negative result of selective COx 2 inhibitors?
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Negative- increased risk of clotting/thrombosis
Positive- less GI toxicity |
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What is the MOA of acetaminophen?
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reversibly inhibits cyclooxygenase, mostly in the CNS
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What is different between NSAIDs and acetaminophen?
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NSAIDs are anti-inflammatory, acetaminophen is ONLY anti-pyretic and anti-pain bc it works mostly in the CNS
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Acetaminophen OD causes?
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Hepatic necrosis
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How do you treat acetaminophen OD and why does it work?
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Treat with N-acetylcysteine
It works because an acetominophen metabolite depletes glutathione and the N-acetylcysteine helps regenerate it |
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What is the mechanism of action of bisophosphanates?
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inhibit osteoclastic activity
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What are the possible side effects of bisophosphanates?
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corrosive esophagitis, nausea, diarrhea, osteonecrosis of the jaw
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Which bisphosphanate does NOT have the risk of corrosive esophagitis?
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Zalendronate
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What is the DOC for acute gout for step 1?
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NSAIDs
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What is the MOA of colchicine?
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binds and stabilizes tubulin to inhibit polymerization, impairing leukocyte chemotaxis and degranulation (basically anti-inflammatory, it seems)
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What are the side effects of colchicine?
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GI
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What is the mechanism of action of probenecid?
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It inhibits the reabsorption of uric acid in the proximal convoluted tubule --> more uric acid excretion
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What drug does probenecid inhibit the excretion of?
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penicillin
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What is the MOA of allopurinol?
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Inhibits xanthine oxidase which is enzyme needed to break down purines into uric acid
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What drugs does allopurinal increase the concentration of?
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azathioprine and 6MP because they are normally metabolized BY XO
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Why don't you give salicylates to someone with gout?
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because all but the highest doses INHIBIT uric acid clearance (I think this is the whole competing for the same receptor to get cleared thing)
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