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USMLE - Pharm

Kaplan Section 6 - Inflammatory Drugs - ASA, NSAIDs

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