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Phrmacodynamics is the study of mechnism of action of drug i.e. what drug does to the body Modification of the effects of one drug by another drug & by other factors is also part of pharmacodynamics. Ligand(Drug) + Receptor = Ligand. Receptor L + R = L.R Slide 3: Principles of drug Action 1) Stimulation It is selective enhancement of the level of activity of specialized cell e.g. adrenaline stimulates heart Pilocarpine stimulates salivary galnd Excessive stimulation is often followed by depression of that function. Slide 4: 2) Depression: Principles of drug Action… It is selective diminution of activity of specialized cells e.g. barbiturates depress CNS, quinidine depressess heart 3) Irritation: Often noxious effect applied to less specialized cells e.g. bitter increase salivary and gastric secretion Counterirritant increase blood flow to the site. Slide 5: Principles of drug Action… 4) Replacement: This referes to the use of natural metabolites, hormones in Deficiency states. e.g. levodopa in parkinsonism Insulin in diabetes mellitus 5) Cytotoxic: Selective cytotoxic action for invading parasites or cancer cells. e.g. penicillin, chloroquine, mebendazole Slide 6: Mechanism of action of drug Mechanism of action of drug : Mechanism of action of drug 1) Physical action: 2) Chemical action 3) Through enzymes a) Inhibition i) Non Specific ii) Specific 4) Through Receptors Slide 8: 1) Physical action A physical property of drug is responsible for its drug action Slide 9: 2) Chemical Action: Drug react extracellurarly according to simple chemical equations e.g. Antacids(Aluminium hydroxide) neutalize gastric HCL Acidyfying(NH4Cl) & alkalinizing (NaHCO3) agents react with buffers in plasma & alter the pH of Urine. Oxidizing agents (KMnO4) are germicidal Chelating agents e.g. EDTA, BAL, Slide 10: 3) Through enzymes i) Inhibition Almost all biological reactions are carried out under catalytic influence of enzyme so enzymes are very important target of drug action A) Non specific: Drugs alter the tertiary structure of enzyme wit which they come in contact thus inhibit it. Slide 11: B) Specific Inhibition: Many drugs inhibit a particular enzyme without affecting others. i) Competitive e.g. physostigmine and neostigmine compete with acetylcholine for cholinesterase Sulphonamides compete with PABA for bacterial foalte synthetase. Slide 12: ii) Non competitive: e.g. Acetazolamide – carbonic anhydrase Aspirin – Cyclooxygenase Digoxin – Na+ K+ ATPase Theophylline – Phosphodiesterase. Slide 13: : Through Receptor Slide 14: Reconstruction of a neuron Cartoon of a neuron. Slide 15: The Neuron and Synapse Slide 16: Synapses are the connecting points between neurons Close-up of view of various synapses Slide 17: The Synapse and Neurotransmitters Release of neurotransmitter Exocytosis: The action potential triggers voltage gated Ca++ channels. Ca++ signals the release of neurotransmitter through exocytosis Slide 18: The Synapse and Release Release of neurotransmitter Exocytosis: Release: Neurotransmitter is spilled into the synapse. : The Synapse, Release and the Receptor Release of neurotransmitter Exocytosis Release Binding: neurotransmitter binds to receptors on the postsynaptic membrane. Slide 20: Pre Synaptic clefct Post The Receptor and Binding Slide 21: The Receptor and Binding Chemicals (ligands) must bind to the receptor and remain bound long enough for the receptor to be activated. Pre Synaptic cleft Post Slide 22: The Receptor - Specificity There are a number of specific ligands and a number of associated receptors. Pre Synaptic cleft Post Slide 23: The Receptor – Affinity Affinity: the extent to which the ligand is capable of binding and remains bound to a receptor. High Affinity – the ligand binds well and remains bound long enough to activate the receptor. Low Affinity – the ligand binds less well and may not remain bound long enough to activate the receptor. Slide 24: High Affinity Binding High Affinity – the ligand binds well and remains bound long enough to activate the receptor. Pre Synatic cleft Post High Affinity Binding : High Affinity Binding Low Affinity – the ligand binds less well and may not remain bound long enough to activate the receptor. Pre Synaptic cleft Post Slide 26: The Receptor – Intrinsic Activity Intrinsic Activity: the extent to which the ligand activates the receptor. High Intrinsic Activity – the ligand produces a large effect on the post synaptic cell. Low Intrinsic Activity – the ligand produces a small or inconsistent effect on the post synaptic cell. Slide 27: Classes of Ligands Agonist High affinity High intrinsic activity Antagonist: High affinity Low intrinsic activity Slide 28: Agonist High affinity High intrinsic activity Agonist Slide 29: Antagonist High affinity Low intrinsic activity Antagonist Classes of Ligands : Classes of Ligands Antagonist: Reversible: can be unbound from the receptor. Irreversible: cannot be unbound from the receptor. Competitive: competes with other ligands for biding to the receptor. Non-competitive: exerts its antagonist effects without competition for occupancy of the receptor. Reversible Antagonist : Reversible Antagonist High affinity Low intrinsic activity Antagonist Irreversible Antagonist : Irreversible Antagonist High affinity Low intrinsic activity Irreversible Antagonist Competitive Antagonist : Competitive Antagonist Noncompetitive Antagonist : Noncompetitive Antagonist References : References http://www.scripps.edu/~didonato/current.shtml 1) Pharmacology and Pharmacotheraprutics by Satoskar & Bhandarkar, 15th edition, Popular publication, Mumbai. 2) The pharmacological basis of therapeutics by Goodman & Gilman 9th edition, International publication. 3) Essentials of Medical Pharmacology by K.D. Tripathi, 5th edition, by Jaypee brothers, New Delhi. http://www.google.com Any Question ?????????? : Any Question ?????????? Lecture Finished : Lecture Finished Go home........ You do not have the permission to view this presentation. In order to view it, please contact the author of the presentation.