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USMLE - Pharm
Kaplan Section 6 - Inflammatory Drugs - ASA, NSAIDs
| Question | Answer |
|---|---|
| How does ASA (aspirin) inhibit COX? | Causes irreversible inhibition of COX by forming covalent bond via acetylation. |
| T or F: ASA actions are dose dependent. | TRUE |
| What is the effect of low dose ASA? | 1/2 tablet daily. Blocks thromboxane synthesis --> inhibits platelet aggregation. (basis for post-MI prophylaxis) |
| What is the dose and mechanism of ASA used as an analgesic? | 2 tablets - moderate dose. Inhibit formation of prostaglandins --> no sensitization of peripheral pain receptors to pain mediators such as bradykinin and histamine |
| What is the dose and mechanism of ASA used as an antipyresis? | 2 tablets - moderate dose. Pyrogens --> inc IL-1 --> inc PGE2 synthesis in hypothalamus --> inc temp set point. ASA dec set point back to nl in hyPERthermia. |
| What is the dose and mechanism of ASA used as an antiinflammatory? | moderate to high dose. Inflammation induces COX2 expression. ASA inhibits COX2. Also interferes with selectin and integrin formation --> no infiltration into tissue through EC jxns |
| What ASA dose causes hyperuricemia and what dose causes uricosuria? | low to moderate --> dec tubular secretion --> more urea kept in blood --> hyperuricemia; high --> dec tubular reabsorption --> more urea lost in urine --> uricosuria. |
| What happens to acid/base/electrolyte balance at high therapeutic doses? | uncoupling of oxidative P --> inc respiration --> blow off CO2 --> dec pCO2 --> RESP ALKALOSIS --> renal compensation by inc HCO3- elmination --> compensated resp alkalosis (nl pH, dec HCO3-, dec pCO2). Stable in adults; toxic in kids. |
| What happens to acid/base/electrolyte balance at toxic doses? | resp center inhibited --> dec resp --> inc CO2 in blood --> inc pCO2 --> RESP ACIDOSIS (dec pH, dec HCO3-, nlzation of pCO2) + inhib of Krebs cycle + severe uncoupling of oxid P--> dec ATP ==> MET ACIDOSIS, hyperTHERM, hypoK+ |
| Adverse effects of ASA: | 1. GI irritation (gastritis, ulcers, bleeding), 2. salicylism, 3. bronchoconstriction, 4. hypersensitivity triad, 5. Reye's syndrome, 6. anti-platelet action (inc PT and bleeding times), 7. renal dysfxn and hypoglycemia with chronic use |
| What is salicylism? | First signs of ASA toxicity: tinnitus, vertigo, dec hearing |
| What is the triad of hypersensitivity in ASA toxicity? | asthma, nasal polyps, rhinitis |
| What is Reye's Syndrome? | causes fatty liver with minimal inflammation, and severe encephalopathy (with swelling of the brain); associated with ASA consumption by children |
| What are some adverse effects of chronic ASA use? | Renal dysfunction (prostaglandins inhibited); hypoglycemia |
| What happens if you take ASA with EtOH? | increased GI bleeding |
| What happens if you take ASA with uricosurics? | Decreases the effectiveness of uricosurics |
| What are the effects of ASA OD? | vasomotor collapse, resp and renal failure |
| What is the antidote to ASA OD? | no specific antidote. 1. gastric lavage (+/- activated charcoal), 2. ventilatory support, 3. sx treatment of acid/base/elec imbalance, 4. manage hyperthermia and resulting dehydration |
| What should you doto the urine to help in ASA elimination? | 1. increase urine volume (diuretic), 2. alkalinization |
| At toxic doses, what "order" elimination kinetics? | zero-order |
| What is the actual dose of ASA associated with toxicity in adults? In children? | adults - 150 mg/kg (30 tablets in 70 kg person); child (10 to 12 kg) toxic dose is 4 to 6 tablets! |
| What do ibuprofen, naproxen, indomethacin, ketorolac, and sulindac have in common? | They are all NSAIDs. |
| Put these in order of strongest analgesic effect: ASA, ibuprofen, ketorolac, naproxen. | ketorolac > ibuprofen/naproxen > ASA |
| Do NSAIDs cause GI irritation? | yes, but less than ASA does |
| How do NSAIDs affect uric acid elimination? | none |
| What are the effects of chronic NSAID usage? | 1. nephritis, 2. nephritic syndrome, 3. acute renal failure (via dec formation of PGE2 and PGI2, which normally maintain RBF and GFR) |
| What NSAID does not cause renal failure? | sulindac |
| NSAIDs dec the activity of which types of drugs? | 1. ACE inhibitors, 2. loop diuretics, 3. beta blockers |
| What happens in indomethacin toxicity? | NSAID. 1. thrombocytopenia (low platelets), 2. agranulocytosis (low granulocytes -- neutrophils, basophils and eosinophils), 3. CNS effects |
| What happens in sulindac toxicity? | NSAID. pancreatitis |
| What happens in diclofenac toxicity? | NSAID. hepatotoxicity |
| What drugs selectively inhibit COX2? | Celecoxib and rofecoxib |
| How do selective COX2 inhibitors compare to NSAIDs as anti-inflammatory agents? | equal. |
| What are the primary differences between selective COX2 inhibitors and NSAIDs? | 1. less GI toxicity, 2. less anti-platelet action for COX2-inhib's |
| What do selective COX2 inhibitors do to prothrombin time? | increase PT time when used with warfarin. Inhibit EC fxn --> prothrombic effects. |
| Mechanism of acetominophen | Inhibit COX in CNS --> equiv analgesic and antipyretic to ASA. Does NOT inhibit COX in peripheral tissues --> no anti-inflammatory effects. |
| How good is acetominophen as an anti-platelet? | Unlike ASA, acetominophen has no antiplatelet activity |
| T or F: ASA and acetominophen are implicated in Reye's Syndrome | False. Only ASA is implicated - not acetominophen! |
| How does acetominophen affect uric acid levels? | No effect on uric acid levels. |
| Is acetominophen a bronchodilator or bronchoconstrictor? | neither. Not bronchospastic (ASA is). |
| Which causes more GI distress? ASA or acetominophen? | ASA. GI distress is minimal at low to moderate acetominophen doses. |
| Describe acetominophen metabolism. | 2 pathways: 1. metabolized by liver glucuronyl transferase --> inactive conjugate. 2. minor pathway: metabolized by CYP450 --> reactive metabolite (N-acetylbenzoquinoneimine) --> inactivated by glutathione (GSH) |
| What happens in acetominiphen OD? | stores of GSH are depleted --> can't inactivate the active acetominophen metabolite made through the CYP450 pathway --> metabolite reacts with hepatocytes --> N,V, abd pain, liver failure (centrilobar necrosis) |
| How does the chronic use of EtOH affect acetominophen usage? | EtOH induces CYP450 --> increase production of active acetominophen metabolite --> enhances liver toxicity |
| How do you manage liver toxicity due to acetominophen? | administer N-acetylcysteine (supplies -SH groups) within first 12 h |
Created by:
christinapham
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