Pharmacodynamics is one the basic unit to understand the pharmacology subject. Pharmacodynamics (sometimes described as what a drug does to the body) is the study of the biochemical, physiologic, and molecular effects of drugs on the body and involves receptor binding (including receptor sensitivity), postreceptor effects, and chemical interactions. This ppt will be helpful for MBBS, Pharmacy, and Nursing Students.

1. Pharmacodynamics
Akash Agnihotri
Department of Pharmacology
Amrita School of Medicine, Faridabad
Pharmacodynamics 1

2. Overview
• Pharmacodynamics basics
• Principles of drug action
• Mechanism of drug action
• Potency & Efficacy
• Combined effects of drugs
• Adverse drug reactions
• Pharmacovigilance
• Drug-Drug Interactions
Pharmacodynamics 2

3. Pharmacokinetics and Pharmacodynamics
• What the body does to the body
• Movement of drug within the body
• Includes the process of ADME
Pharmacokinetics
• What drugs do the body & how
• Study of drugs, their mechanism of action,
pharmacological actions, and their adverse
effects
Pharmacodynamics
Pharmacokinetics by Akash Agnihotri 3

4. What is Pharmacodynamics?
• pharmakon= drug; dynamics=action/activity
• Study of effects of drugs on the body
• Mechanism of drug action
• Relationship between drug concentration and effect
Definition:
Pharmacodynamics is the study of the effects of drugs on the body
and mechanisms of the drug action and the relationship between
drug concentration and effect
Pharmacodynamics 4

5. Drugs Act by (Principles of drug action)
• Stimulation
• Depression
• Irritation
• Replacement
• Anti-infective or cytotoxic
• Modification of the immune status
Pharmacodynamics 5

6. Drugs Act by
• Stimulation: Increase cellular activities (Adrenaline stimulates heart; Salivary
glands stimulated by pilocarpine; metoclopramide increases GI motility-
diarrhea)
• Depression: Decrease cellular activities (Quinidine depresses heart;
Omeprazole depresses Acid Secretion; codeine causes constipation)
• Some drugs may stimulate one and depress other (Morphine depresses
CNS but stimulates vagus)
• Irritation: May result in inflammation, also can be helpful (counter irritation)
Pharmacodynamics 6

7. Drugs Act by
• Replacement: When there is deficiency of natural substances (hormones,
nutrients)
• Insulin in Diabetes Mellitus; Vitamin C in scurvy; Thyroid in hypothyroidism
• Anti-infective or cytotoxic: Drugs destroying infective organism (Penicillin)
• Modification of the immune status: Vaccines and Sera act by improving
immunity (Glucocorticoids), BCG vaccine, Polio vaccination
Pharmacodynamics 7

8. Mechanism of drug action
Pharmacodynamics 8
Physical Chemical
Cellular
Enzymes
Ion channels
Receptors
Transporters
Others (Antibodies formation, Placebo)

9. Drug action: Enzymes
• Almost all biological reactions are carried out under catalytic influence of
enzymes
• Drug may act by Inhibition of various enzymes
• Enzyme stimulation is relevant to some natural metabolites only
• Enzyme stimulation:
Adrenaline stimulates hepatic glycogen phosphorylase through β-receptor
and cAMP
• Enzyme Inhibition:
Allopurinol inhibits enzyme Xanthine Oxidase
Acetazolamide inhibits the Carbonic Anhydrase
Omeprazole inhibits Na+K+-ATPase pump
Pharmacodynamics 9

10. Stimulation vs Induction
Pharmacodynamics 10
Stimulation: Increases
affinity for the substrate
Induction- Synthesis of
more enzyme protein

11. Competitive vs Non-Competitive Inhibition
Pharmacodynamics 11
Competitive Inhibition Non-Competitive Inhibition
• Antagonist binds with the same receptor
• Same maximal response can be attained by
increasing dose of agonist
• e.g., Ach-Atropine; Morphine-Naloxone
• Binds to
another site
• Maximal
response is
suppressed
• E.g., Diazepam-
Bicuculline

12. Drug action: Ion channels
• Various ion channels located on cell membrane
• Participate in transmembrane signaling process
• Drugs may interfere with the movement of ions across specific channels
Pharmacodynamics 12
Drugs Action Ion Channel
Nifedipine Block L-type calcium
channel
Phenytoin Modulates Voltage sensitive
Na+ channels
Amiodarone Blocks Myocardial sodium,
potassium, and
calcium channels

13. Drug action: Ion channels
Pharmacodynamics 13

14. Receptors
• Drugs usually do not bind directly to the enzymes, channels, transporters or
structural proteins, but act through specific regulatory macromolecules –
receptors
• Definition: It is defined as a macromolecule or binding site located on the
surface or inside the effector cell that serves to recognize the signal
molecule/drug and initiate the response to it, but itself has no other
function.
Pharmacodynamics 14

15. Drug-Receptor occupation theory
Clark’s equation (1937)
“The Pharmacologic effect of the drug depends on the percentage
of the receptors occupied”
If receptors are occupied, maximum effect is obtained. It is also called as the
Occupation Theory
Pharmacodynamics 15

16. Drug-Receptor occupation theory
Clark’s equation (1937)
D + R [DR] Response (E)
Affinity: Capability of a drug to form the complex with its receptor
[DR]
Intrinsic Activity or Efficacy (E): Ability of a drug to trigger the
pharmacological response after making [DR]
Pharmacodynamics 16

17. Important terms: On the basis of affinity and
efficacy
• Agonist: Drug having both affinity and intrinsic activity is called as agonist
• Antagonist: An agent which does have any effect of its own, but prevents the
action of an agonist on a receptor
• Inverse agonist: An agent which activates a receptor to produce opposite
effect to that of an agonist
• Partial agonist: An agent which activates a receptor to produce submaximal
effect
Pharmacodynamics 17

18. Important terms: On the basis of affinity
and efficacy
Pharmacodynamics 18
E= +1
E= 0
E= -1
Agonist (IA=+1)
Partial Agonist (IA=~0.5)
Antagonist (IA=0)
Inverse Agonist (IA=-1)
Active state of
receptor (Ra)
In-active state of
receptor (Ri)

19. Agonist & Antagonist
Pharmacodynamics 19

20. Signal
Transduction
Pharmacodynamics 20
Highly complex multistep processes that
provide for amplification and integration of
concurrently received extra and intra-
cellular signals at each step.
5 major categories:
1. G-protein coupled receptors
2. Ion channel receptor
3. Transmembrane enzyme-
linked receptors
4. Transmembrane JAK-STAT
binding receptors
5. Receptors regulating gene
expression

21. G-protein coupled receptors (GPCR)
Pharmacodynamics 21
G-protein Associated Receptor Effector pathway
Gs (Stimulates
membrane bound
adenylate cyclase)
Βeta-adrenergic, Histamine H2,
Serotonin 5HT-4-7, Dopamine-D1
Increased adenylyl
cyclase activity;
increased cAMP
Gi (inhibits membrane
bound adenylate
cyclase)
α2- adrenoceptors, Muscarinic M2,
opioid receptor, 5HT1, Dopamine-D2
Decreased adenylyl
cyclase activity;
decreased cAMP
Gq/G12/13 (Activates
phospholipase-C)
α1- adrenoceptors, Muscarinic-M1,M3,
Histamine-H1, Angiotensin-AT1
Activates phospholipase-
C
Go M2, D2, α2- adrenergic, GABAB, 5HT1 Ca2+ channel inhibition
Serpentine receptor OR Seven-pass OR Hepta-helical receptors

22. Transmembrane signaling mechanisms
Pharmacodynamics 22

23. Transporters
• Specific carriers present on the cell membrane
• Purpose: Transporting substrate across cell membrane in concentration
gradient or the against the concentration gradient using metabolic energy
Pharmacodynamics 23
Metabolites Transporters Drugs
Serotonin Serotonin transporter neuron Selective serotonin reuptake
inhibitor (Escitalopram,
Fluoxetine)
Dopamine Dopamine transporter neuron Amphetamine
Acetylcholine Choline uptake neuron Hemicholinium
Noradrenaline Norepinephrine transporter
neuron
Cocaine

24. Drug action by physical action
Pharmacodynamics 24

25. Drug action by physical action
• Osmosis: Magnesium sulfate: Total bulk fluid of faeces is increased (Purgative
fluid retained in lumen)
• Adsorption: Kaolin adsorbs bacterial toxins in diarrheal
• Protectives: Dusting powders for local effects
• Astringents: Denature the mucosal protein and protect mucosa
• Placebo: Pharmacodynamically inert and harmless substance, which
resembles actual medicament in size, shape, color, and smell
Pharmacodynamics 25

26. Receptor
regulations
terminologies
Pharmacodynamics 26

27. Potency and Efficacy
Pharmacodynamics 27

28. Potency
• Amount of drug needed to produce a certain response
• Example: 10 mg of morphine produces equal analgesic effect as
produced by 100 mg of pethidine. It means that morphine is 10
times more potent than pethidine. Drug potency helps us to decide
the dose of a drug.
Pharmacodynamics 28

29. Which is more potent?
Pharmacodynamics 29
Drug A Drug B Drug C

30. Efficacy
• It refers to the maximum response, which can be elicited by a particular drug
• Example: Aspirin can never achieve the level of analgesic effect, which
can be achieved by morphine. This means that morphine is more
efficacious than aspirin
Pharmacodynamics 30

31. Which is more efficacious?
Pharmacodynamics 31

32. Potency and Efficacy Graphs
Pharmacodynamics 32

33. Potency vs Efficacy
Pharmacodynamics 33

34. Combined effects of drugs
Pharmacodynamics 34

35. Combined effects of drugs
• Most patient prescribed 2 or more drugs
• They may exhibit either Synergism or Antagonism
• This is due to interactions at Pharmacokinetic or Pharmacodynamic level
1. Synergism (Syn-together; ergon-work)
2. Antagonism (Anta-opposite; ergon-work)
Pharmacodynamics 35

36. Synergism
• Synergism: Action of one drug is increased by other
• Can be: Additive and Supraadditive (Potentiation)
• Additive drug combinations:
Aspirin + Paracetamol as analgesic/antipyretic
Amlodipine + Atenolol as antihypertensive
Ephedrine + Theophylline as bronchodilator
• Supraadditive drug combinations:
Levodopa + Carbidopa: Inhibition of peripheral metabolism
Sulfamethoxazole + Trimethoprim: Sequential blockade
Telmisartan + Chlorthalidone: For hypertension
Pharmacodynamics 36

37. Pharmacodynamics 37
Chemical Physiological Receptor Level Non-Competitive
Types Drug Antagonism
Drug Antagonism
• Reversible
• Irreversible

38. Drug Antagonism: Chemical
• Chemical Antagonism: 2 drugs react and result in inactivation of effect
 Chelating agents (BAL, Disodium Edetate) used in arsenic and lead
poisoning
 Antacids like aluminium hydroxide neutralize gastric acid
 Potassium permanganate in gastric lavage
 2 drugs should not be mixed in same syringes (like Heparin + Penicillin)
Pharmacodynamics 38

39. Drug Antagonism: Physiological
• 2 drugs act at different sites or receptor to produce opposite effects
• Histamine acts on H2 receptors to produce bronchospasm and
hypotension
• Adrenaline reverse these effects by acting on adrenergic receptor
• Insulin and Glucagon have opposite effects on the blood sugar level
Pharmacodynamics 39

40. Drug Antagonism: Receptor level
• One drug (antagonist) blocks receptor action of other drug (agonist)
• Such antagonism may be reversible or irreversible
• Reversible competitive antagonism: The agonist and antagonist compete for
same receptor
• Concentration of agonist Antagonism (can be overcome)
• E.g., Acetylcholine and atropine compete at muscarinic receptors
• D-tubocurarine and acetylcholine compete for the nicotinic receptors at the neuromuscular junction
Pharmacodynamics 40
(Increasing)
This is because of Reversible Antagonism

41. Drug Antagonism: Receptor level
Irreversible competitive antagonism:
• Antagonist binds to firmly by covalent bond to receptor that it dissociates
very slowly or not at all
• Thus, it blocks the action of agonist and the blockade cannot be overcome by
increasing the dose of agonist; hence it is irreversible
• Adrenaline and phenoxybenzamine at α-adrenergic receptors
Pharmacodynamics 41

42. Drug Antagonism: Receptor level
Noncompetitive Antagonism:
• The antagonism blocks at the level of receptor-effector linkage
• E.g., Verapamil blocks the cardiac calcium channels and inhibits the entry of
Ca++ (Calcium ion)
• Thereby antagonizes the effect of cardiac stimulants, such as Isoprenaline
and Adrenaline
Pharmacodynamics 42

43. Antagonism- Other type
• One drug decreases or abolish the action of other
• Physical antagonism: Because of physical property of drug
Adsorption-charcoal adsorbs alkaloids in alkaloid poisoning
Pharmacodynamics 43

44. Adverse Drug Reactions
Pharmacodynamics 44

45. Adverse Drug Reactions
• Side Effects: Undesirable effects observed even with therapeutic doses of
drug and are mild and manageable
• Example: Dicyclomine (Anticholinergic) relieves pain of intestinal colic due to its
antispasmodic action (desirable) but side-by-side also causes dryness of mouth (side
effect)
• Levocetirizine: Sedation
• Toxicity: There are exaggerated form of side effects either due to overdose or
prolonged use of drug
• Bleeding due to high doses of heparin; coma-due to barbiturates; crystlurea; due to
sulfonamides
Pharmacodynamics 45

46. Adverse Drug Reactions (ADRs)
Pharmacodynamics 46
Type A Type B Type C Type D Type E
Augmented Bizarre Chronic Use Delayed End of use
Side Effects
Secondary Effects
Toxic Effects
Idiosyncratic reaction
Allergic Reactions
Type-I
(Anaphylaxis)
Penicillin, Lignocaine
Type-II
(Cytolytic Rxn)
Carbamazepine,
Phenytoin
Type-III
(Arthus Rxn)
Sulfonamides
Type-IV
(Delayed Hypersensitivity)
Penicillin

47. Pharmacovigilance
• WHO Definition: The science and activities related to the detection,
assessment, understanding, and prevention of adverse events or any
other drug-related problem.
• Aim: Ensure safe and rational use of medicine
• Reporting adverse reactions is the duty of all medical professionals
including, clinicians, nurses, pharmacists, dentists, and all
• Indian Pharmacopoeia Commission (IPC) Ghaziabad<<Uppsala
Monitoring Center, Sweden
Pharmacodynamics 47

48. ADR Form
Pharmacodynamics 48
A.Patient Information
B.Suspected adverse reaction
C. Suspected medications
D.Reporter details

49. Filled ADR From
Pharmacodynamics 49

50. Drug-Drug Interactions (DDIs)
• A change in a drug’s effect on the body when the drug is taken together with
a second drug
• Usually, the effect of one of the drugs gets either increased or decreased or
cause unexpected side effects
Pharmacodynamics 50
Consequences of DDIs

51. Pharmacodynamics 51
In Vitro
Incompatibility
In vivo Food - Drug
Interactions
Drug - Disease
Interactions
Drug-Drug Interactions
Mechanism of Drug-Drug Interactions
(DDIs)
• Pharmacokinetics
• Pharmacodynamics
Important
(Outside the body)
(During mixing of drug
before administration)
Precipitation, Effervescence,
Color change, Visual change
Changes in A,D,M,E

52. Summary
• Pharmacodynamics basics- What drugs do the body & how
• Principles of drug action- Stimulation, Depression, Irritation, Replacement
• Mechanism of drug action: (Physical, Chemical, Cellular: Receptors, Enzymes)
• Potency: Amount of drug needed to produce a certain response
• Efficacy: Refers to the maximum response
• Combined effects of drugs: (Synergism: Additive & Supraadditive, Antagonism:
Chemical, Physiological, Receptor (Competitive, Non-competitive)
• Adverse drug reactions: Type A, B, C, D, E
• Pharmacovigilance: Detection, Assessment, Understanding, and Prevention
of ADR
• Drug – Drug Interactions (DDIs): 1 drug Changes Pharmacokinetics or –dynamics
of other in the body
Pharmacodynamics 52

53. References
• Textbook of Pharmacology, Pathology & Genetics for Nurses-I, 2nd edition by
Suresh Sharma
• Pharmacology for nurses, 5th edition by Padmaja Udaykumar
• Textbook of Pharmacology for nursing student, 2nd edition by Joginder singh
pathania
• Principles of pharmacology, 4th edition by H. L. Sharma & K .K. Sharma; 2023
• Lippincott illustrated reviews pharmacology, 2nd SA edition by Sangeeta
Sharma; 2022
• Essentials of Medical Pharmacology, 9th edition by KD Tripathi; 2024
Pharmacodynamics 53

54. Thank You
Pharmacodynamics 54