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Pharm Lect 2 & 3
Pharm Lect 2&3
| Question | Answer |
|---|---|
| Drug Selectivity is | The ability to effect one tissue type/organ, but spare others. |
| Drug Selectivity depends on | 1.Dose. 2.Drug Distribution (where is the body it goes). 3.Receptor Distribution (Location of specific receptors). 4.Receptor Selectivity (specificity). |
| Chemical chirality: Enantiomers | more than half the useful drugs are chiral. Enantiomers can differ in pharmacological activity (one may be inactive or they both may have different uses). One may have longer/shorter duration of action (susceptable to metabolizing enzymes). |
| Drug Kd to receptors | Determines activity of the drug by how well it binds (affinity) to the receptor. Inversely proportional to the receptors affinity to the drug. **Lower the better |
| Antagonist | Binds, but doesn't activate a receptor. Prevent the agonist from binding to the receptor. **Have affinity but no intrinsic activity on receptor |
| Agonist | activates the signaling cascade upon binding a receptor. **Have affinity and intrinsic activity on receptor |
| Pharmacological Antagonist: Competitive | Degree of inhibition: concentration dependent. **higher [agonist] will out compete the competitive antagonist for the binding sites. |
| Pharmacological Antagonist: Noncompetitive | Elemenates available receptors. Independent of dose and affinity of the agonist. **Take away the drug and the effects will be reversed. |
| Pharmacological Antagonist: Irreversible | Covalently binds receptor. Body must now produce new receptors in order to reverse effects. **DRUG OVERDOSE |
| Physiological Antagonists Vs Chemical Antagonist | Phys: 2 drugs that produce opposing effects through different receptors. Chem: NO receptor required. two substances interacting directly and decreasing the effect of the active substance. |
| Affinity | The extent to which the ligand is capable of binding and remains bound to the receptor (Drug:receptor tightness). High:ligand binds well and activates receptor. Low:ligand doesn't bind as well and may not activate receptor. |
| Intrinsic Activity | **Same as RECEPTOR EFFICACY (Emax)** Extent to which the bound ligand activates the receptor. High IA: ligand produces large effect. Low IA: ligand produces small effect **Antagonist have no IA |
| Receptor Specificity | Receptor interacts with only one type of ligand. **Creates competition b/w ligands |
| Receptor Saturability | Since there are limited number of receptors, binding sites can become fully occupied. **Additional ligands can lead side effects |
| Full agonist | Drugs that bind and produce the full Intrinsic activity effect (Emax) in a system. **Will have the highest line on a dose-respose curve |
| Partial agonist | Drugs that cannot produce the full intrinsic activity effect in a system. **Will have lines below the Emax on a dose-response curve. |
| Potency | amount of drug needed to produce a given intensity of effect. More potent can determine by: 1.more left on a dose-response graph. 2.smaller EC50 or Kd. 3.High affinity of receptor for drug. 4.High Intrinsic Activity. **More potent = smaller dose ne |
| Law of mass action | magnitude of drug effect is directly proportional to the number of occupied receptors **Potency is related to affinity |
| EC50 | Dose concentration of a drug that produces 50% of max effect. **EC50 = Kd |
| Clinical Efficacy | depends on: 1.receptor-efficacy (ability to reach Emax). 2.the drugs ability to reach relavant receptors (route, absorption, distribution, clearane). |
| Effect on a dose-response curve by a Pharmacological Antagonist: Competitive | Decreases potency, shifting the curve to the right on the graph. |
| Effect on a dose-response curve by a Pharmacological Antagonist: Irreversible | The EC50 or Kd doesnt change, but the Emax decreases with increasing [irreversible antagonist]. |
| Effect on a dose-response curve by a Pharmacological Antagonist: Non-competitive | Reduces Efficacy (Emax) that will go away over time. Potency EC50 can also be decreased so it can shift to the Right |
| Advantages of irriversible inhibitors | Once bound to the receptor, the inhibitor no longer needs to be present to inhibit agonist. Therefore the duration of action of inhibitor is INDEPENDEANT of the rate of it's elimination; More dependent on the rate of turnover of receptors |
| Disadvantages of irriversible inhibitors | The blockage on the receptor can't be overcome by the removal of the antagonist OR by adding excess agonist. **Must make new receptors. |
| Spare Receptors | Determine tissue sensitivity to an agonist. Changing the number of spare receptors changes that target tissue's sensitivity. **Makes potency much higher(shifts graph to left) and prevents agonist overflow leading to side effects. |
| Is ED50 equal to Kd if spare receptors are present? | NO, the more spare receptors, the further away Kd moves from ED50 |
| Effect on a dose-response curve by a Pharmacological Antagonist: non-competitive with spare receptors present | First the potency with decrease (shift to the right) then the efficacy (Emax) with decrease. **the non-comp shows effects similar to comp antagonist at first b/c the agonist doesn't need all the receptors to reach Emax. |
| Therapeutic index | TI = LD50 / ED50. **Must be > 1 for drug to be usable. |
Created by:
WeeG
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