The document explains the definition and principles of pharmacology, specifically focusing on drug interactions with biological systems. It describes drug targets, including receptors, enzymes, and transporters, and distinguishes between agonists and antagonists in terms of their effects on receptors. Additionally, it addresses mechanisms of drug resistance and their implications for treatment effectiveness.

1. ‫االختصاص‬ ‫الصيدالني‬
‫مصطفى‬ ‫حبيب‬ ‫فريدون‬
Respiropharmacologist

2. Drug
can be defined as a chemical
substance of known structure,
other than a nutrient or an
essential dietary ingredient,
which, when administered to a
living organism, produces a
biological effect.

3. Pharmacology
 Can be defined as the study of the effects of drugs on
the function of living systems
 One of the basic tenets of pharmacology is that drug
molecules must exert some chemical influence on
one or more constituents of cells in order to
produce a pharmacological response.
 Pharmacological effects, therefore, require, in
general, the non-uniform distribution of the drug
molecule within the body or tissue.
 Most drug targets are protein molecules

4. PROTEIN TARGETS FOR DRUG
BINDING
 Four main kinds of regulatory protein are
commonly involved as primary drug targets,
namely:
 receptors
 enzymes
 carrier molecules (transporters)
 ion channels.

5. DRUG RECEPTORS
 Receptor (by the action of adrenaline
(epinephrine) on the heart. Adrenaline first
binds to a receptor protein (the β adrenoceptor,
that serves as a recognition site for adrenaline
and other catecholamines.
 When it binds to the receptor, a train of reactions
is initiated leading to an increase in force and
rate of the heartbeat. In the absence of
adrenaline, the receptor is functionally silent

6.  Drugs acting on receptors may be agonists or
antagonists.
 Agonists initiate changes in cell function,
producing effects of various types; antagonists
bind to receptors without initiating such
changes.
 Agonist potency depends on two parameters:
affinity (i.e. tendency to bind to receptors) and
efficacy (i.e. ability, once bound, to initiate
changes that lead to effects).
 For antagonists, efficacy is zero.

7.  Full agonists (which can produce maximal effects)
have high efficacy
 Partial agonists (which can produce only
submaximal effects) have intermediate efficacy.
 According to the two-state model, efficacy reflects
the relative affinity of the compound for the resting
and activated states of the receptor. Agonists show
selectivity for the activated state; antagonists show
no selectivity. This model, although helpful, fails to
account for the complexity of agonist action.
 Inverse agonists show selectivity for the resting
state of the receptor, this being of significance only
in unusual situations where the receptors show
constitutive activity

8.  Drug antagonism occurs by various mechanisms:
 Chemical antagonism (interaction in solution)
 Pharmacokinetic antagonism (one drug affecting
the absorption, metabolism or excretion of the
other)
 Competitive antagonism (both drugs binding to
the same receptors); the antagonism may be
reversible or irreversible
 Non-competitive antagonism (the antagonist
interrupts receptor-effector linkage)
 Physiological antagonism (two agents producing
opposing physiological effects).

10. Drug resistance
 is a term used to describe the loss of
effectiveness of antimicrobial or antitumor
drugs.
 Many different mechanisms can give rise
resistance

11.  Change in receptors
 Loss of receptors
 Exhaustion of mediators
 Increased metabolic degradation of the drug
 Physiological adaptation
 Active extrusion of drug from cells

12.  Mechanisms that operate mainly over a short
timescale (milliseconds to hours), particularly
excitation, contraction and secretion, which
account for many physiological response.