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19 Cards in this Set
- Front
- Back
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talk about non-competative antagonist:
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work at other receptor site, change its confirmation, or it binds to same pocket as the agonist but very very tightly/irreversibly.
this lowers the dose response curve (doesn't shift to the right as in a competative inhibitor). it's like a loss of sensitivity. |
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theraputic index? want it to be big or small?
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ED 50 = effective dose
TD 50 = toxic dose EC50 = effective concentration. theraputic index is TD50/ED50 want the index to be big? |
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in what do you measure the potency?
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EC50.
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drug disposition lecture:
what do you want a drug to look like to get into the blood stream? what groups do that? do opposite? |
lipid solubility up - use alkyl groups, ethyl groups, halogens, and especially sulfur.
opposite effect if you add hydroxyl groups, tertiary amines, carboxyl groups... |
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talk about pH and drug absorption:
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acidic drugs better absorbed in the stomach - in the acidic environment, you tend to not be ionized (hydrogen stays on). if the pH is 1 unit below the pKA, you have 90% un-ionized, with its hydrogen. 2 units below, 99% unionized.
weak bases, in acidic environment, end up charged - so they don't get absorbed. |
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talk about urine and kidney issues with drug excretion: how do you get rid of aspirin?
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if it's lipid soluble, it can be reabsorbed. meaning that if you want to increase the excretion, make it not reabsorbed - so protenate it (which makes it charged).
if it's an acid, make it charged - deprotenate it (put it in basic environment). to get rid of aspirin, it's an acid, use a weak base like bicarb to change the pH of the urine. |
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talk about digoxin -
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takes 6 hours to get to steady state levels in the heart, so it's a 2 comaprtment model. peripheral compartment takes awhile to get distributed.
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talk about chemical defense?
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brain, kidney, instestines, liver (pushing into bile) all have PGP to get rid of chemicals, keep them from getting into its compartment. maintains homeostasis.
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how are drugs altared by cp450?
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makes drugs more water soluble.
phase 1 is conjugation to help eliminate it. |
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chronic vs. acute metabolism?
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use alcohol as an example. EtOH has alcohol dehydrogenase, then p450 takes over later and can be induced.
acutely, it'll tie up p450 and inhibit it. if they're regularly heavy drinkers, gets induced. |
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inhibition vs. induction?
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inhibition is much faster than induction. induction requires days, weeks to reach steady state. take away, takes weeks to go back to normal
induction is just something binding to something. |
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co-administration of drugs that is bad?
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inhibitor of p450 includes cimetadine.
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pharmacokinetics: what equations sould we know?
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Vd = loading dose / [plasma]
dosing rate = Css * Cl T1/2 = .693 * Vd / Cl |
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if you double a dose that normally gives you a steady state, what happens?
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get a new steady state if 1st order elimination.
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what happens to clearance if kidney is blocked by protein?
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need to drop dose of drugs to match the reduced clearance.
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warfarin genetic differences in dosing comes from what genes?
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CYP2c9
and VKorC1. this is going to b e on the test. |
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what's a good target of h1 blocker?
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makes you sleepy! also good for nose running. tylenol PM has diphenhydramine.
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promethasine?
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it's phergan. if given IV, causes vasoconstriction and limbs fall off. meant to be IM.
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what do you do for flare ups?
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use cholcicine - good for screwing up white blood cells. and nsaids, but not aspirin (it's anti-uricosuric).
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