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18 Cards in this Set
- Front
- Back
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On the graded dose response curve which curve is more potent one that is sifted to the left or right?
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Curve that is shifted left = more potent = ie needs less drug for desired effect
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On the graded dose response curve which curve is more efficacious - shifted up or shifted down?
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Curve that is shifted up = higher efficacy = greater measured response
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What are the factors influencing efficacy
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1. Phamacokinetics(first pass can ↓ efficacy), 2. intrinsic properties of drug(partial agonist can ↓ efficacy), 3. patients state of health(hepatic/renal insufficiency can ↑ efficacy)
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In a graded dose response curve what are is the most dangerous?
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The one that shoots up to maximum efficacy in a small window of drug dose is the most dangerous
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Define: ED50, TD50, LD50, TI?
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ED50 = effective dose at which 50% of population is feeling the drugs effects, TD50 = toxic dose at which 50% of population is feeling it, LD50 = lethal dose at which 50% of population dies, TI = therepeutic index = margin of safety = LD50/ED50
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How do u calculate which drug is more potent? Ie Drug A = ED50 = 10mg/L, Drug B = ED50 = 150mg/ml
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150/10 = 15 thus Drug A is 15x more potent than drug B
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What is selectivity of drugs action?
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Depending on the dose of the drug Low or high dose u can get very different results. Ie Low dose = cough suppression but High dose = sedation even though it’s the same drug given
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Define:idiosyncratic drug response
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Unusual (unexpected) adverse drug response - angioedema when taking ACE inhibitor
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Define: hyporeactivity/hyperractivity
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Pt reacts more to drug
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Tolerance
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Nitrate used to treat angina - after time response decreases (ie u build up tolerance)
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Tachyphylaxis
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Depletion of NT involved in drugs action (ephidrine + scopolamine prevents sea sickness)
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What happens to an effective metabolizer persons CYP2D6 when they take proxetine?
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They become a poor metabolizer thus if they have to take codine or metoprolol they have ↓ metabolism thus its more efficacious and could have ↑ toxicity
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Why is a person w/pheochromocytoma more sensitive to beta-blocker vs a marathon runner?
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Pheochromocytoma = adrenal gland tumor and marathon runners secrete lots of adrenal hormones - but pheochromocytoma has more beta-receptors then a runner who is normal thus beta-blocker has more effect to have a larger ↓ in Heart Rate
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How do u get a person who has hyperthyroidism -> ↑ HR + Contractility when there are normal lvls of catecholamines?
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There are extra spare receptors
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What mechanism cancels out the drug terazosin over time?
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Comepensatory mechanism -Normally terazosin = anti-hypertensive thus bringing BP down but the central nervous system can override the drug and bring back the BP to elevated lvls
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What are the possible adverse effects of drugs?
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1. Direct extension of leading therapeutic effects(longer half-life), 2. mediated by identical receptors but in different tissues (side effect), 3. may be mediated by different types of receptors (unknown side effect)
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How to u minimize adverse drug effects
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1. Adjust dose (if bleeding too much w/anti-coagulant adjust dose), 2. change drugs(benzodiazepine instead of barbiturate for anxiety disorder), 3. introducing a second drug (beta-blocker + diuretics can minimixe doxazosin-induced orthostatic hypotension/edema)
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How to minimize undesired effects of drugs
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1. Lowest dose possible, 2. add an adjunct w/different mechanism of action + different toxicity profile, 3. change route of administration, 4. use newer drug w/imporved selectivity (albuterol is better then epi for asthma)
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