Week 1: Drug Action PDF

How do drugs act to cause their effects define the terms pharmacodynamics and pharmacokinetics - Pharmacokinetics: - rate processes such as absorption, distribution, metabolism, and excretion of a drug and the multiple interrelationships affecting same, such as incomp...

How do drugs act to cause their effects define the terms pharmacodynamics and pharmacokinetics - Pharmacokinetics: - rate processes such as absorption, distribution, metabolism, and excretion of a drug and the multiple interrelationships affecting same, such as incomplete absorption, saturability in transport, biotransformation, or binding. - What drug does to the body - Pharmacodynamics: the way in which drug interact with the body → therapeutic action to occur → what body does to drug discuss examples of non-specific ways in which drugs can produce therapeutic effects - Non-specific mechanisms - Chelating agents → remove heavy metal ions in cases of poisoning or disorders - Osmotic agents → fluid balance between body compartments - GIT - osmotic laxatives (eg magnesium citrate) - kidney - osmotic diuretics (eg mannitol) - Surfactants → reduce surfactant tension describe the four specific molecular targets of drug action - Specific cellular target - Target usually macromolecule - Usually protein/ DNA - The drug mimic/ block the actions of endogenous factors (target 1 target → 1 effect only) → drug can be compete with endogenous ligands - Drugs have the preference for 1 target over others → selectivity depends on: - Chemical structure - Molecular size - Electrical charge Selectivity is: - Reciprocal (certain class of drug bind certain target and the certain target recognize certain classes of drug)  - related to dose or concentration↑dose => ↑chance of interacting with other targets - Bind to particular component to get response Ion channels Found in all cells in the body - Maintain voltage gradient and ionic fluxes - Crucial in excitable cells Types: - Ligand-gated (=receptor) - Voltage-gated Drug can do: - Local anaesthetics - block voltage-gated Na+ → inhibit the transmission of nerve impulses (block nociception) - K+ channel openers → hyperpolarize the cell membrane → block Ca++ channel → Partial agonists > Antagonists. Affinity: Full agonists = Partial agonists (could be lower than full agonists - weaker bonds) = Antagonists (for the receptor binding site). Efficacy: Full agonists > Partial agonists > Antagonists. potency affinity efficacy Full agonist High - >> response Have affinity E = 1 - maximal response Partial agonist Medium Have affinity however E < 1 - not maximal usually weaker bonds response even in saturating conc Antagonist No - as produce no Have affinity E=0 response Competitive antagonist can be overcome by >> agonist conc (reversible) >< irreversible Non-competitive antagonist: - Physiological: opposing effects (contraction vs relaxation) - Chemical (inactivated) - bind to the active drug and inactivate - Pharmacokinetics - affects conc at target sites - Allosteric - bind to diff site on receptor to affect ligand binding/ stimulation of second messenger → tend to cancel one another out Highly potent drugs desirable: → maximum response→ >> efficacy (E) → biological effects discuss how the differences between competitive reversible and irreversible antagonist can be demonstrated experimentally give examples of clinically important drugs which act as agonists or antagonists Agonists Antagonists Ventolin(salbutamol) -βadrenoceptor Narcan(naloxone) -μ opioid receptor morphine –opioid receptor Claratyne(loratadine) –histamine receptor adrenaline –adrenoceptor