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32 Cards in this Set

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What enzyme is needed to make leukotrieenes?
lipoxygenase
What enzyme is needed to make thromboxane?
cyclooxygenase
What does LTB4 do?
Neutrophil chemotactic agent
What do LTC4, D4, and E4 do?
bronchoconstriction, vasoconstriction, contraction of smooth muscles, and increased vascular permeability
What does PGI2 do?
Inhibits platelet aggregation and promotes vasodilation
MOA of aspirin?
Irreversible COX 1 and 2 inhibitor
Describe the difference in effect of low dose, medium dose, and high dose aspirin.
Low dose- decreases platelet aggregation
Medium dose- antipyretic/painkiller
High dose- anti-inflammatory
What are the side effects of aspirin?
Gastric upset, renal, Reye's syndrome in children with viral illness
What is the MOA of NSAIDs?
Reversibly inhibit cox 1 and cox 2
Side effects of NSAIDs (5)?
GI, renal (decrease renal blood flow by dec. prostaglandins), fluid retention, ulcers, aplastic anemia
Which NSAID is used to close a PDA?
Indomethacin
What happens when you OD on salicylates?
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
thromboxane is produced by?
platelets
PGI2 is produced by?
endothelial cells
What does dipyramidol do?
selectively blocks the synthesis of thromboxane
What reaction do corticosteroids block?
Membrane lipid (like phosphatidylinositol) --> arachidonic acid
Enzyme? phosphalipase A2
What is the positive and negative result of selective COx 2 inhibitors?
Negative- increased risk of clotting/thrombosis

Positive- less GI toxicity
What is the MOA of acetaminophen?
reversibly inhibits cyclooxygenase, mostly in the CNS
What is different between NSAIDs and acetaminophen?
NSAIDs are anti-inflammatory, acetaminophen is ONLY anti-pyretic and anti-pain bc it works mostly in the CNS
Acetaminophen OD causes?
Hepatic necrosis
How do you treat acetaminophen OD and why does it work?
Treat with N-acetylcysteine

It works because an acetominophen metabolite depletes glutathione and the N-acetylcysteine helps regenerate it
What is the mechanism of action of bisophosphanates?
inhibit osteoclastic activity
What are the possible side effects of bisophosphanates?
corrosive esophagitis, nausea, diarrhea, osteonecrosis of the jaw
Which bisphosphanate does NOT have the risk of corrosive esophagitis?
Zalendronate
What is the DOC for acute gout for step 1?
NSAIDs
What is the MOA of colchicine?
binds and stabilizes tubulin to inhibit polymerization, impairing leukocyte chemotaxis and degranulation (basically anti-inflammatory, it seems)
What are the side effects of colchicine?
GI
What is the mechanism of action of probenecid?
It inhibits the reabsorption of uric acid in the proximal convoluted tubule --> more uric acid excretion
What drug does probenecid inhibit the excretion of?
penicillin
What is the MOA of allopurinol?
Inhibits xanthine oxidase which is enzyme needed to break down purines into uric acid
What drugs does allopurinal increase the concentration of?
azathioprine and 6MP because they are normally metabolized BY XO
Why don't you give salicylates to someone with gout?
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)