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1. Objectives
• Explain about posology
• Understand types of Drug-Receptor Interactions
• Understand pharmacodynamics like mechanism of
drug action, dose-response relation ship
• Understand about drug interaction and adverse drug
reaction
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2. Posology
• Posology ▪ Derived from the Greek word Posos-how
much, and logos-science is the branch of
pharmacology dealing with doses.
• Dose : is the quantity(amount)administered or taken
by a patient for the intended medicinal effect.
Factors affecting the drug dose
1.Age : Elderly individuals may also respond abnormally
to the usual amount of a drug because of
changes in drug-receptor sensitivity or because
of age-related alterations in target tissues and
organs.
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3. Factors affecting the drug dose
Body Weight:
 The official usual doses for drugs are considered
suitable for 70 kg individuals. The ratio between the
amount of drug administered and the size of the
body influences the drug concentration at the site of
action.
 Therefore, drug dosage may require adjustment.
3. Sex
 women are more susceptible to the effects of certain
drugs than are men.
 Pregnant women and nursing mothers should use
drugsonly with the advise and under the guidance of
theirphysician. 3

4. Factors affecting the drug dose…
4.Pathological state ▪
 The effects of certain drugs may be modified by the
pathological condition of the patient and must be
considered in determining the dose.
5.Tolerance
 The ability to endure the influence of a drug,
particularly when acquired by a continued use of
the substance
6.Drug-Drug interactions
 The effects of a drug may be modified by the
concurrent administration of another drug.
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5. Factors affecting the drug dose…
7.Routes of administration
 Drugs administered iv enter the blood stream
directly and thus the full amount administered is
present in the blood.
 Thus, a lesser parenteral dose of a drug is required
than the oral dose to achieve the same blood levels
of drug.
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6. Pharmacodynamics
• Study of action of drugs to the body
– mechanism of action of the drug
• Mainly concerned on interaction of the drug with
receptors
– What the drug does to the body
antacids
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7. Selectivity vs Specificity in Drug Action
• Drug Selectivity
– number of receptor types or subtypes that the drug binds to
in the body
– affinity of the drug
• Drug Specificity
– the number of effects that the drug is capable of producing
in the body
– In order to be specific, the drug has to produce a single
specific effect in the body
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8. Concept of efficacy, potency and affinity
 Intrinsic activity(Efficacy):is the ability of a drug to elicit the
pharmacologic response.
 Potency of a drug: the amount of drug required to produce a
given effect.
 Affinity: is the ability of drug to bind to specific target
site(recepter)
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9. Types of Drug-Receptor Interactions
 Agonists
– bind to and activate the receptor
• bring about the pharmacological effect
– Direct acting and indirect acting
• Full agonists
– maximal pharmacologic effect when administered at
sufficiently high concentrations
• Partial agonists
– are drugs that bind and activate the receptor
• not as high as the effect obtained from the binding of
a ‘full’ agonist
– may act as either an ‘agonist’ (in the absence of a full
agonist) or as an ‘antagonist’ (in the presence of a full
agonist)
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10. • Inverse agonists
– bind to the receptor and stabilize it in its inactive
(nonfunctional) conformation
• opposite of the effects produced by conventional
agonists at the receptor
• Allosteric agonists (Allosteric Activators)
– enhance the efficacy/binding affinity of the receptor
agonist by binding to allosteric sites on the receptor
molecule
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12. • Antagonists (blockers)
– are drugs that bind to the same binding site of the
agonist on the receptor molecule without activating the
receptor
• ‘Competitive Antagonists’
– Competition of agonist and antagonist for same site
in receptor
– concentration dependent (Reversible)
• Allosteric antagonists(Noncompetitive Antagonists)
– inhibit/reduce the efficacy/binding affinity of the
receptor agonist by binding to allosteric sites on the
receptor molecule
– not concentration dependent
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13. 13

14. Dose – response relationship
• Two types of dose response curve
1. Graded dose response
2. Quantal dose response
1. Graded dose response curve
– Graded response : the response increase as the
administered dose continuously increase
Death
Coma
Anesthesia
Hypnosis
Sedation
Response
Phenobarbital Dose 14

15. Graded dose response(Individual dose
relationship)
inhibition
dose
log
dose
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16. 2. Quantal relationship
– Show the effect of d/t dose on response among all (
many) individuals taking the drug
– Show individual variation in response for a given dose
– Usually done on animals than humans
Quantal Dose-Response Curves
• A quantal dose-response curve represents the percentage
of individuals (or laboratory animals) under study
– who exhibit a specified drug effect
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17. Quantal Dose-Response Curves
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ED 50:- the dose that
produces response in
50% of the individual
LD 50:- the dose
that cause death in
50% of the animal

18. Median Toxic Dose (TD50), is the drug dose required to
produce a particular toxic effect in 50% of individuals or
laboratory animals.
Therapeutic index (TI) = LD50/ED50
• Therapeutic index is used to measure safety of a given
chemical. The value Therapeutic index can be <1 or >1
• TI > 1 mean the drug is safer(larger TI indicates clinically
safer drug.
can also be calculated as:
Therapeutic index (TI) = TD50/ED50
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19. • Desensitization (seconds to minutes)
– a rapid and reversible process that desensitizes the
tissue to further receptor-agonist interaction for only a
few minutes
• Down-Regulation
– exposure of cells to the agonist over a long period of
time (hours to days)
– involves degradation of receptor molecules present in
the cell
– may cause relative tolerance to the effects of a drug
agonist
Receptor Regulation
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20. Receptor Regulation….
• Tolerance
– refers to a decrease in the intensity of the response to a
given dose of a drug as a consequence of continued
drug administration over an extended period of time
• Up-Regulation of the receptor
– occurs when receptor activation is blocked for
prolonged periods of time (usually several days) by
pharmacologic antagonists.
Major receptor families
• These receptors may be divided into four families
1) ligand-gated ion channels
2) G protein–coupled receptors
3) enzyme–linked receptors
4) intracellular receptors
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21. 21

22. Drug interactions
• Drug could have an interaction with other agents
that are administered to body concomitantly
– Other drugs
– Foods taken
– Beverages
– Herbs
• Drug interaction could be significantly important
or harmful
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23. 23
• Type of interaction
Drug –drug interaction
Drug-food interaction
Eg -antacid Vs ketoconazole --- ketoconazole
need acidic env’t- antacid?-↓absorption
Grape fruit juice Vs phenytoin ---- grape fruit
juice cyp 3A4 enzyme inhibitor

24. 24
Eg – benzodiazepine Vs Alcohol---both have CNS
depression, sedation
-- MAOI Vs wine ----wine have tyramin which
have sympathetic effect and increase the synthesis of
NE + MAOI inhibit the metabolism of NE---have
excess NE---hypertensive crises
E.g. Saint John's Vs warfarin ---Saint John's is
liver microsomal enzyme inducer
Drug – beverage interaction
Drug-herbal interaction

25. Based on level of interaction: drug- interaction
classified as:-
• Pharmacokinetic level interaction
– Absorption
• TTC + Ca2+ containing foods or drugs --- ↓ absorption
of TTC
– Distribution level interaction
• Main factor for this interaction is:
– high plasma protein binding capacity
» displacement of these drugs by other highly
plasma protein binding drug ---- ↑plasma
level-----toxicity
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26. • Biotransformation level interaction
– Cimetidine + Warfarin ----- bleeding …??
Phenobarbital + OCP-----pregnancy….??
• Excretion level interaction
• Tubular secretion :- since there is carrier case
– probencide + pencillin :
• Tubular reabsorption:
– weak acid drug + bicarbonate ----- ↑ excretion
Enzyme inducer
Phenobarbital
Carbamazepine
Phenytoin
Rifampin
NVP &EFV
Gresofulvin
Enzyme inhibitor
Cimetidine
Ketoconazole
Erythromycin
Isoniazide
CAF
Omeprazole
Grape fruit juice
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27. • Pharmacodynamic interaction
I. Agonizing interaction
II. Antagonizing interaction
I. Agonizing interaction
1. Additive – Occurs when the combined effect of two
drugs is equal to the sum of the effects of each agent
given alone
• 1 + 1 = 2
• H1antagonist + CNS depressant
2. Potentiation:-
• a situation where by one drug enhance the action of
another drug without having an effect by itself
– 0 + 1 > 1
– Caffeine + ergotamine
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28. I. Agonizing interaction…
3. Synergism
• when the combined effects of two drugs are much
greater than the sum of the effects of each agent
given alone
• 1 + 1 >>> 2
• penicillin + amino glycosides
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29. I. Antagonizing interaction
– Chemical antagonism
• Involve direct chemical interaction b/n agonist and
antagonist
• chelating agent (dimercaprol) + heavy metals(Hg,
Au…)
– Functional (physiologic) antagonism
• Involve interaction of two agonist that act
independently of each other but happen to cause
opposite effect
• acetylcholine + epinephrine
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30. I. Antagonizing interaction…
 Competitive antagonism
• Is most frequently encountered type of drug antagonism
in clinical practice
• Is competition of agonist and antagonist for same site in
receptor
– Reversible ( equilibrium) competitive antagonism
Non-competitive antagonism
– Irreversible (not equilibrium) competitive
antagonism
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31. Competitive antagonism
Antagonist Receptor
Antagonist-Receptor
Complex
DENIED!
Competitive
Inhibition
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32. 32

33. 33

34. Agonist Receptor
Antagonist
‘Inhibited’-Receptor
DENIED!
Non-competitive antagonism
Non-competitive
Inhibition
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