Term
| Arachidonic acid pathway? |
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Definition
| Starts in cell membrane (phospholipid bilayer) -> oxidized by phospholipase A2 -> further metabolism by cytochrome P450, lipooxygenase (into leukotrienes), or COX (into prostaglandins and thromboxanes) |
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|
Term
| Which cyclooxygenase performs "housekeeping" functions & protects gastric epithelium? |
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Definition
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Term
| What factors upregulate COX-2 immediate response? |
|
Definition
| Sheer stress, growth factors, tumor promoters, cytokines |
|
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Term
| What are the effects of thromboxane A2? |
|
Definition
| Amplifies fx of platelet agonists like thrombin; vasoconstriction -> hypertension + decline in renal function |
|
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Term
| Effect of COX-1 in the kidneys? |
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Definition
|
|
Term
| Effect of COX-2 in renal medullary cells? |
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Definition
|
|
Term
| Which molecules raise body temperature, causing fever? |
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Definition
|
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Term
| In what form are most NSAIds present in our blood? |
|
Definition
| Bound to protein (albumin) |
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|
Term
| Which COX-2 selective inhibitor carries a black box warning for CV risk? |
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Definition
|
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Term
| What are the main differences b/w non-selective NSAIDs and COX-2 selective? |
|
Definition
| COX-2 doesn't affect platelets or GI, but carries higher risk of edema, MI, HTN |
|
|
Term
| How are NSAIDs nephrotoxic? |
|
Definition
| Interfere w/ prostaglandin autoregulation of renal blood flow |
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|
Term
| What are examples of non-selective NSAIDs? |
|
Definition
| Aspirin, diclofenac, etodolac, ibuprofen, indomethacin, nabumetone, naproxen, ketorolac |
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|
Term
| What are examples of COX-2 selective NSAIDs? |
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Definition
|
|
Term
| Which NSAID is indicated for closure of patent ductus arteriosus (PDA)? |
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Definition
|
|
Term
| Which NSAID is only used acutely in the hospital setting? (no more than 5 days) |
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Definition
|
|
Term
| Which NSAID is most associated w/ photosensitivity? |
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Definition
|
|
Term
| Which NSAID is associated w/ liver abnormalities? |
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Definition
|
|
Term
| Which NSAID is most GI-protective? |
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Definition
|
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Term
|
Definition
| Irreversibly inhibits COX activity; changes structure of prostaglandin H synthase so prostaglandin H2 is not formed (PH2 would quickly convert to thromboxane A2 and prostaglandins) |
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|
Term
| How long does the antiplatelet effect of aspirin last? |
|
Definition
|
|
Term
| True or false: aspirin can exacerbate asthma |
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Definition
|
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Term
| Which NSAID is first-line analgesic in pregnancy? |
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Definition
|
|
Term
| At what stage of acetaminophen toxicity do we see abnormal LFTs? |
|
Definition
|
|
Term
| At what stage of acetaminophen toxicity do we see glucose, lactate, & phosphate abnormalities? |
|
Definition
|
|
Term
| What toxic metabolic pathway is activated once other pathways (glucuronidation, sulfation, glutathione) are saturated in acetaminophen toxicity? |
|
Definition
|
|
Term
| What does the Rumack-Matthew nomogram measure? |
|
Definition
| Plots Tylenol level vs. time since ingestion |
|
|
Term
| What is the antidote to acetaminophen toxicity? |
|
Definition
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