02a: Pharmacodynamics Flashcards
The GABA receptor is a(n) (X)-gated (Y) (transporter/channel/ATPase).
X = ligand
Y = Cl (ion)
Channel
T/F: Drug effect on enzymes is usually inhibitory.
True
Cocaine (stimulates/inhibits) which processes?
Inhibiting;
Reuptake of serotonin, NE, and DA
Local anesthetics work by (stimulating/inhibiting):
Inhibiting;
Voltage-gated Na channels
List the two types of dose-response curves.
- Dose-intensity (how much effect?)
2. Dose-frequency (how many affected?)
In Dose-Intensity curve, what’s the y-axis?
% effect
In Dose-Frequency curve, what’s the y-axis?
% subjects responding
The mathematical model that describes [drug] and R occupancy can also be applied to dose and response if which conditions are met?
- Drug:R bind in 1:1 stoichiometry
2. Drug effect proportional to drug binding
EC50 is also measure of drug (X). What does it represent?
X = potency
[Drug] that gives 50% of max effect
EC(max) is also called (X) of drug. What does it represent?
X = efficacy
Max effect of drug (achievable at high dose)
T/F: EC50 is directly correlated to drug potency.
False - indirectly (higher EC50, lower potency)
How well drug binds receptor is (potency/efficacy). How well drug produces effect is (potency/efficacy). Star the one that’s more relevant to clinicians.
Potency; efficacy*
Increasing number of spare receptors will (increase/decrease) potency of drug.
Increase (decrease EC50)
Chemical antagonist exerts its effect by:
Interacts with agonist to render it inactive (i.e. Etanercept)
Pharmacokinetic antagonist exerts its effect by:
Accelerating metabolism/elimination of agonist
Physiological antagonist exerts its effect by:
Activating mechanism that opposes agonist’s effect
Competitive and noncompetitive antagonism are examples of which type of antagonism? This occurs at the level of (ligand/receptor/beyond).
Pharmacological;
Receptor
Reversible competitive antagonist: how does dose-response curve change? And ED50?
Shift right; Higher EC50 (reduced potency)
Competitive antagonism (is/isn’t) surmountable, which means (X).
Is;
X = can overcome inhibition by increasing [agonist]; efficacy unchanged
Non-competitive antagonism: (potency/efficacy) change in which way(s)?
Decrease efficacy (max effect); no change in potency (EC50)
Irreversible competitive antagonism: (potency/efficacy) change in which way(s)?
Decrease efficacy (max effect); no change in potency (EC50)
Why might a dose-effect curve be bell-shaped? Give an example.
Multiple receptors with different affinity and opposing effects;
Ex: Epi (low dose) binds beta2-R, vasodilation; Epi (high dose) binds alpha1-R, vasoconstriction
Positive cooperativity (i.e. Hemoglobin) changes shape of dose-effect curve in which way(s)?
Steeper curve
Spare receptors: you have (same/different) response with (same/different) receptor occupancy. How is the dose-response curve changed?
Same; different (less % occupancy)
Shifts left, same max