Pharmacodynamics. Dr. Alia Shatanawi
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1 Pharmacodynamics Dr. Alia Shatanawi
2 Drug Receptor Interactions Sep-17
3 Dose response relationships Graduate dose-response relations As the dose administrated to single subject or isolated tissue is increased, the pharmacologic effect will also increase. At a certain dose, the effect will reach a maximum level, which is called the ceiling effect or Emax.
4 Graduate dose-response curve
5 Graduate dose-response curve
6 Potency and efficacy Potency is a measure of the amount of drug necessary to produce an effect of a given magnitude. The concentration producing an effect that is the fifty percent of the maximum is used to determine potency (EC50). Efficacy is the maximum effect of a drug, Emax, and does depend on the number of drug-receptor complexes formed, and also on the efficiency of the of coupling of receptor activation to cellular responses. Aspirin and morphine produce the same pharmacologic effect (analgesia) but have very different levels of efficacy.
7 The smaller the EC50, the greater the potency. Efficacy is indicated by the height of the log dose response Log dose response curve
8 Relations between drug concentration and drug effect
9 Drug Receptors & Pharmacodynamics Receptors largely determine the quantitative relations between dose (or concentration) of the drug and pharmacologic effects. The receptor's affinity for binding a drug determines the concentration of drug required to form a significant number of drug-receptor complexes, The total number of receptors limits the maximal effect a drug can produce.
10 Relations between drug concentration and receptor-bound drug 28
11
12 KD: concentration at which binding site is 50% occupied. Affinity 1/Kd Dr. Shatanawi 2017
13 Relations between drug concentration and drug effect (A) or receptor-bound drug (B). The drug concentrations at which effect or receptor occupancy is halfmaximal are denoted by EC 50 and K d, respectively. Source: Drug Receptors & Pharmacodynamics, Basic & Clinical Pharmacology, 13e Citation: Katzung BG, Trevor AJ. Basic & Clinical Pharmacology, 13e; 2015 Available at: bookid=1193§ionid= Accessed: October 09, 2017 Copyright 2017 McGraw-Hill Education. All rights reserved
14 Even in intact animals or patients, responses to low doses o a drug usually increase in direct proportion to dose. As doses increase, however, the response increment diminishes. Finally, doses may be reached at which no further increase i response can be achieved. This relation between drug concentration and effect is traditionally described by a hyperbolic curve according to the following equation: 14
15 Two-state model of drug-receptor interaction Full agonists shift equilibrium fully towards the active conformation Partial agonists shift equilibrium partially towards the active conformation Sub-maximal effect with receptors completely occupied Dr. Shatanawi 2017
16 Two-state model of drug-receptor interaction The receptor is postulated to exist in the inactive, nonfunctional form (Ri) and in the activated form (Ra). Thermodynamic considerations indicate that even in the absence of any agonist, some of the receptor pool must exist in the Ra form some of the time and may produce the same physiologic effect as agonistinduced activity. Agonists have a much higher affinity for the Ra configuration and stabilize it, so that a large percentage of the total pool resides in the Ra D fraction and a large effect is produced 16
17 Constitutive Activity The effect of receptors, occurring in the absence of agonist, is termed constitutive activity. The recognition of constitutive activity may depend on the receptor density, the concentration of coupling molecules (if a coupled system), and the number of effectors in the system. 17
18 18
19 Inverse agonists: While antagonists are traditionally thought to have no functional effect in the absence of an agonist, some antagonists exhibit inverse agonist activity because they also reduce receptor activity below basal levels observed in the absence of any agonist at all. 19
20 Inverse agonists Inverse agonists shift equilibrium towards the inactive conformation Effect obvious if much constitutive activity
21 Competitive & Irreversible Antagonists Receptor antagonists bind to receptors but do not activate them The primary action of antagonists is to reduce the effects of agonists (other drugs or endogenous regulatory molecules) that normally activate receptors. 21
22 Competitive antagonists Bind agonist site Do not shift equilibrium towards active or inactive conformation Neutral antagonists
23 Types of Drug Receptor Interactions
24 Features of Graded Dose-Response Curves Maximal Efficacy. Potency. Slope or Shape of the Curve. Variability
25 Quantal Dose-Response Curves
26 Features of Quantal Dose-Effect Curves Involves all or non responses. Obeys Normal Frequency Distribution. When transformed into cumulative, will result in a sigmoid curve Can calculate Therapeutic Index= LD50/ED50
27 Quantal Dose-Effect Curves Effective Dose (ED50): is the dose at which 50% of individuals exhibit the specified quantal effect. Toxic Dose (TD50): is the dose required to produce a particular toxic effect in 50% of animals. Lethal Dose (LD50): is the dose required to produce death in 50% of the of the animals.
28 Therapeutic index and margin of safety
29 Therapeutic index and margin of safety Therapeutic index of a drug is a ratio of the dose that produces toxicity to the dose that produces a clinically desired or effective response in a population individuals: Where TD50 is the minimum dose that is lethal or toxic for 50% of the population, and ED50 is the minimum dose that is effective for 50% of the population. Ideally the TD50 Should be a much higher dose than the ED50 so that the therapeutic index would be large.
30 October 17 Munir Gharaibeh, MD, PhDm, MHPE 44
31 Agonist-Antagonist Relationships Competitive antagonist, higher concentrations of agonist are required to produce a given effect. High agonist concentrations can overcome inhibition by a competitive antagonist. Irreversible (or noncompetitive) antagonist, reduces the maximal effect the agonist can achieve, although it may not change its EC50.
32 Shift in the log-dose response Competitive antagonist Noncompetitive antagonist
33
34 Drug Antagonism Pharmacologic Antagonism: Competitive Antagonism Noncompetitive antagonism Physiologic Antagonism: Epinephrine in Anaphylaxis Chemical Antagonism: Antacids in heartburn.
35 Possibilities of Drug Combinations Antagonistic Effects Additive Effects Additive drug effect occurs if two drugs with the same effect, when given together produce an effect that is equal in magnitude to the sum of the effect. EAB = EA + EB = 2 Synergistic Effects: Interaction between two or more drugs or agents resulting in a pharmacologic response greater than the sum of individual responses to each drug or agent EAB > EA + EB > 2 Sulfamethoxazole + trimethoprim Potentiation Effects: Potentiation drug effect occurs if a drug lacking an effect of its own increase the effect of a second active drug. EAB > EA + EB > 2
36 Receptor Regulation Sensitization or Up-regulation 1. Prolonged/continuous use of receptor blocker 2. Inhibition of synthesis or release of hormone/ neurotransmitter - Denervation Desensitization or Down-regulation 1. Prolonged/continuous use of agonist 2. Inhibition of degradation or uptake of agonist Homologous vs. Heterologous Uncoupling vs. Decreased Numbers
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