RR.Pharmacodynamics,PRESENTED BY ANSARI AASHIF RAZA MOHD IMTIYAZ PPT.pptx

PHARMACODYNAMICS

1. ANSARI AASHIF 1 TOPIC :- PHARMACODYNAMICS PRESENTED BY ANSARI AASHIF RAZA MOHD IMTIYAZ (I M.PHARM) DEPARTMENT OF PHARMACOLOGY

2. INTRODUCTION In pharmacodynamics comes from Greek word. The Greek word dynamics means power , means whats the drug does acting insides to the body,which is includes physiological and biochemical effects of drugs and their mechanisam of action to the organ system ,subcellular and macromolecular level. ANSARI AASHIF 2

3. MECHANISM OF DRUG ACTION Dose of drug eg : Prazosin Drug in systemic circulation systemic circulation Drug at site of action blood vessels Drug receptor action block 1 receptor Signal transduction vasodilation ( mechanism of action ) Clinical response 1]-postural hypotension 1]anti-hypertensive 2]-headache Adverse effect therapeutic effect 3]drowsiness   ANSARI AASHIF 3

4. Cont ……. Majority of drugs produce their effects by interacting with a discrete target biomolecule, which usually is a protein. Such mechanism confers selectivity of action to the drug. Functional proteins that are targets of drug action can be grouped into four major categories 1] enzymes 2]ion channels 3]transporters 4]receptors. ANSARI AASHIF 4

5. A. ENZYMES :- Generally all of the biological reaction are carried out by the catalytic influence of enzymes. And by the use of drugs enzymes get stimulated, which are truly foreign substance. Several enzymes are stimulated through receptors and second messengers, e.g. adrenaline stimulates hepatic glycogen phosphorylase through  receptors and cyclic AMP. Stimulation of an enzyme increases its affinity for the substrate so that rate constant ( kM ) of the reaction is lowered ANSARI AASHIF 5

6. Enzyme Inhibition :- Some chemicals (heavy metal salts, strong acids and alkalies ,formaldehyde, phenol, etc.) denature proteins and inhibit all enzymes non selectively. Enzyme will be activated in the presence of substrate and give the product E + S = P  I = NO PRODUCT There are three types of inhibition 1. Competitive Inhibition 2. Noncompetitive Inhibition 3. Uncompetitive Inhibition ANSARI AASHIF 6

7. Cont …….. 1. Competitive Inhibition :- In competitive inhibition inhibitior (molecule)very similar likes to the substrate molecule which binds to the enzyme active site and prevent to bind actual substrate and inhibiting the chemical reaction , eg ,Penicillin act as competitive inhibitor that block the active site of the enzyme and which caused the bacteria cell will be construct. in competitive inhibition k m value increase where as V max remain unchanged and V decrease. NOTE :- The inhibition can be over come by a high subtrate concentration. ANSARI AASHIF 7

8. Cont …. 2. Noncompetitive inhibition :- The inhibitor binds at the site but other in the active site on surface of the enzyme. In this inhibition there are no interference of the enzyme substrate binding but the catalysis is prevented due to the distruction in the enzyme confirmation . In the Noncompetitive inhibition the k m value is unchanged while V max is lowered and V decrease. ANSARI AASHIF 8

9. Cont ….. 3. Uncompetitive inhibition : :- In uncompetitive inhibitor, inhibitor binds only ES complex , not to the free enzyme and it yield E.S.I complex. E.g Drugs treating in the case of poisoing by methanol or ethylene glycol act as an uncompetitive inhibitors. In uncompetitive inhibition k m value decrease where as V max also decrease and V also decrease. ANSARI AASHIF 9

10. B. ION CHANNELS :- Proteins which act as ion selective channels participate in transmembrane signaling and regulate intracellular ionic composition. This makes them a common target of drug action. Drugs can affect ion channels, some of which actually are receptors, because they are operated by specific signal molecules either directly and are called ligand gated channels e.g. nicotinic receptor ,or through G-proteins and are termed G-protein regulated channels (e.g. cardiac β1 adrenergic receptor activated Ca2+ channel. ANSARI AASHIF 10

11. III. TRANSPORTERS Several substrates are translocated across membranes by binding to specific transporters (carriers) which either facilitate diffusion in the direction of the concentration gradient or pump the metabolite/ion against the concentration gradient using metabolic energy ANSARI AASHIF 11

12. IV. RECEPTORS The largest number of drugs do not bind directly to the effectors, viz. enzymes, channels, transporters, structural proteins, template biomolecules, etc. but act through specific regulatory macromolecules which control the above listed effectors. These regulatory macromolecules or the sites on them which bind and interact with the drug are called ‘receptors’ ANSARI AASHIF 12

13. Agonist :-An agent which activates a receptor to produce an effect similar to that of the physiological signal molecule. Inverse agonist An agent which activates a receptor to produce an effect in the opposite direction to that of the agonist. Antagonist :- An agent which prevents the action of an agonist on a receptor or the subsequent response, but does not have any effect of its own Partial agonist :-An agent which activates a receptor to produce submaximal effect but antagonizes the action of a full agonist. ANSARI AASHIF 13

14. Ligand :- (Latin: Ligare—to bind) Any molecule which attaches selectively to particular receptors or sites. The term only indicates affinity or ability to bind without regard to functional change: agonists and competitive antagonists are both ligands of the same receptor. ANSARI AASHIF 14

15. REFERENCE KD Tripathi Seventh Edition Dr .U. Satyanarayana and Dr .U. Chakrapani 4 th edition. ANSARI AASHIF 15

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