This document discusses pharmacodynamics, which refers to how drugs act on the body. It covers several mechanisms of drug action, including receptor-mediated and non-receptor mediated effects. Receptor-mediated actions can be further broken down based on the type of receptor, such as ligand-gated ion channels, G-protein coupled receptors, enzymatic receptors, nuclear receptors, and Jak-Stat binding receptors. Non-receptor mediated effects occur through physical, chemical, or enzymatic actions. The document also briefly discusses concepts of drug affinity, intrinsic activity, and the combination effects of synergism and antagonism.

1. PADMASHREE DR.D.Y.PATIL
COLLEGE OF PHARMACY AKURDI
SUBJECT NAME – ADVANCE PHARMACOLOGY
TOPIC NAME- PHARMACODYNAMIC
GUIDED BY- DR.D.S.SHIRODE
PRESENTED BY – DHANASHRI PRAKASH
SONAVANE

2. • PHARMACODYNAMIC
Pharmaco=Drug
Dynamic=Power
• It covers all the aspects relating to "What a drug does to the body"
Mechanism of action.
• Drug act either by receptor or by non receptor or by targeting specific
genetic changes.
• Mechanism of Action of Drugs
1. Receptor Mediated
2. Non Receptor Mediated

3. A. Non receptor Mediated
(1) By physical action
(a) Osmosis-Mannitol
(b) Adsorption-Activated charcoal for poisoning
(c) Demulcent-Cough syrups
(d) Radioactivity in hyperthyroidism
(2) By chemical action
(a) Antacids- Neutralizing gastric acid
(b) Chelating agent- Dimercaprol (BAL) in arsenic and mercury
poisoning.

4. (3) Through enzymes
(a) Competitive-
Physostigmine and neostigmine completes with acetylcholine for
cholinesterase
(b) Non-Competitive-
Acetazolamide Carbonic anhydrase
(4) Through ion channel - Local anesthetic Block Na+ channel in
neuronal membrane to produce local anesthesia.
(5) Through antibody production Vaccines.
(6) Transporters- Selective serotonin reuptake inhibitor
(SSRI)Antidepressants effect - Bind to 5HT transporter & block
reuptake

5. B. Receptor Mediated
• Receptor are macromolecules, present either on the cell surface,
cytoplasm or in the nucleus with the drug binds and interacts to
produce cellular changes.
• Receptors ore mostly proteins.
• Affinity-Ability to bind to the receptor.
• Intrinsic activity-Ability to produce action after binding.
• If there is no affinity, no intrinsic activity All drug have affinity, but
different intrinsic activity
DRUG RECEPTOR
DRUG
RECEPTOR
COMPLEX Response

6. 1. Based on intrinsic activity:
i. Agonist-Have both affinity and maximal intrinsic activity.
ii. Antagonist-Have affinity but no intrinsic activity
iii. Partial agonist - Have affinity and sub maximal intrinsic activity.
- Produce Submaximal effect but antagonize the action of full
agonist.
i. Inverse agonist-Have affinity but opposite Intrinsic activity.
- Produce an effect in opposite direction to agonist.
i. Non-competitive inhibitors with the same affinity to [E] and [E-
S] -the inhibitor binds at the allosteric site independently of
substrate binding
ii. Competitive inhibitors-which have bind to same receptor site and
progressively inhibit the agonist response.
-but not intrinsic activity.

7. Receptor Families’
1. LIGAND-GATED ION CHANNEL (INOTROPIC
RECEPTOR):
• This drug binds directly to the receptor located on an ion channel
without mediated by G-Protein.
• Wherever drugs bind the channels open and ions can enter.
• This type of receptor are fastest acting receptor.
• Binding of drug to inotropic receptor  Opens the ion channel-
(Na, K,Ca,CI) Flow of ions through channel Hyperpolarization
/Depolarization Tissue response.

9. 2. G-Protein Coupled Receptor
• It also known as heptahelical/serpentine receptor.
• It is largest family of cell membrane receptor.
• G protein are membrane protein and have 3 sub units alpha ,beta
,gamma heterotrimer.
• When all are join together G-protein coupled receptor is
inactive.GPCRs control cell function via Adenyl cyclase,
Phospholipase c and ion channel when drug binds to the receptor
which is turns activates a g protein that may result in activation or
inhibition of---
I. Adenyl cyclase
II. Phospholipase c
III. Ion channel
• This act on Gs,Gi,Gq receptors.

11. 3. Enzymatic Receptor
• Enzymes are Stimulated at outer end.
The drug binds to the extracellular
sites. The intracellular sites has
enzymatic activity.
• Ex: Prolactin, insuline, Growth
Harmone,Cytokinine
(Interleukine,Interferon,TGF
Transforming Growth Factor ).

12. 4. Nuclear Receptor
• This type of receptor is slowest acting receptor.
• Only lipid soluble drug can also act on it.
• If the drug bind to nuclear receptor, then they bind with DNA and act on
translation, transcription, replication and these process become slower.
• Both type of receptor finally act on nuclear mechanism by affecting
transcription.
• Two type of nuclear receptor
i. Cytoplasmic receptor: Glucocorticoids, Mineralocorticoids, Progestin
ii. Nuclear Receptor:T3,T4,Vitamin A,D ,Estrogen.

14. Jak-Stat Binding Receptors
• The Jak-Stat (Janus Kinase-Signal transducer and activator of
transcription) signaling pathway transmits information from
chemical signals outside the cell which cause DNA transcription
• Contain 3 main Components:
I. Receptor
II. JAK-Janus Kinase
III. STAT- Signal transducer and activator of transcription.

16. Neurotransmitter and their receptors

17. Combination Effect of Drug
• Synergism
An interaction between two or more drugs that causes the total effect of
the drugs to be greater than the sum of the individual effects of each
drug.
• Antagonism
antagonism occurs when a drug binds to a different receptor and
produces a physiological response that opposes the effect of the agonist-
bound receptor.