Therefore, there is a strong interaction between pharmacodynamics and pharmacokinetics
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1 PHRM20001: How Drugs Work TOPIC 1 Mechanism of Drug Action Lecture 1: Introduction Key principles learned from the history of pharmacology: - Risk vs Reward when treating people with a drug, many drugs will have adverse effects - Dose determines effect all drugs are poisons; the dose of the drug determines whether it is poisonous or not - Drugs bind to molecular targets drugs have to interact/bind with a target/receptor in the body for it to have an effect. It will not act unless bound What makes a drug safe and effective? 1) Identify target o Target = site of action to modify, resulting in a beneficial effect (eg heart, liver, etc.) o The drug must be at an effective concentration, bind, have an effect & be selective Agonist drug that binds to receptor and directly cause a response (by altering their conformation to an active form, causing a biological response) Antagonist bind & block receptor from interacting with another drug or endogenous stimulant 2) Getting the drug there o Drug must be absorbed, distributed & reach the target at an effective concentration 3) Getting the drug out of there o The drug has to be metabolised (usually by liver) & excreted (urine, faeces) o There is a balance of getting the drug to the target at a desired concentration and excreting it Drug that is not metabolised rapidly reaches a steady state, effect lasts for a prolonged period of time, does not get excreted immediately therefore don t have to consume drug constantly Drug that is metabolised rapidly effect lasts for a short while, acts acutely, excreted quickly Therefore, there is a strong interaction between pharmacodynamics and pharmacokinetics - Pharmacodynamics = the effect of the drug on the body (eg bind to receptor, increase heart rate ) - Pharmacokinetics = the effect of the body on the drug (eg how well the body absorbs, metabolises & excretes the drug) What is a drug? A drug is a chemical that affects physiological function in a specific way. It can either be: - Present endogenously in the body o Used for cellular communication: hormones, neurotransmitters second messengers, antibodies, genes o Eg adrenaline found in adrenal gland; first used as a bronchiole dilator to treat asthma, now used to treat anaphylactic shock (antigen reaction)
2 - Not normally found in the body o Synthetic drug or naturally occurring drug from other sources o Drugs that are not normally found in the human body is both a therapeutic agent and a poison o Effect of the drug depends on both its content & its dose o Eg atropine found in Atropa belladonna (Deadly Nightshade); used to dilate pupils to look more attractive; overdose led to loss of eyesight, dry mouth, hallucinations & death Drug names - Most marketed drugs have a trade name and a generic name - Generic name is the active compound of the drug Trade name Generic name Function Panadol Paracetamol Treat fever, headaches, minor aches Ventolin Salbutamol Treat asthma Prozac Fluoxetine Treat depression - Belongs in the SSRI (selective serotonin reuptake inhibitor) family *often, drug family names are used Overall, the principles of pharmacology are: - Where Site of action & selectivity - How much potency & efficacy - How often absorption & elimination Pharmacodynamics Pharmacokinetics Lecture 2 Drug Targets A drug will not work unless it is bound. Types of drug targets? 1) Ion channels - (Control flux of ion into or out of cells therefore controls its electrochemical gradient & excitability) - Drugs block or modulate channel openings. Eg nifedipine o Blocks Ca2+ channels results in reduced blood vessel constriction & reduced blood pressure 2) Carrier molecules/transporters - (Transport molecules across lipid membranes) - Eg. In normal conditions, molecule is removed from site of action (inactivation). When drug binds to transporters, drug blocks removal of molecules (activation) - Eg fluoxetine binds to serotonin carriers, prevents serotonin uptake into nerves, serotonin able to bind to its receptors, prolong serotonin action increases mood, treat depression
3 3) Enzymes - (Catalyse synthesis/breakdown of molecules) - Drugs may: o Inhibit enzymes bind directly to enzyme & inhibit its function Eg Aspirin binds to cyclo-oxygenase (COX) reducing the synthesis of pain/fever/inflammation mediators o Use enzymes prodrug binds to enzyme & produces an active drug Eg L-dopa used dopa decarboxylase enzyme to increase the synthesis of dopamine (break down L-dopa into dopamine). To treat Parkinsons disease o Use enzymes false substrate (drug) binds to enzyme to produce abnormal metabolite Eg fluorouracil (abnormal metabolite) replaces uracil as an intermediate in purine biosynthesis DNA synthesis is inhibited, cell division inhibited 4) Receptors - (recognition sites for molecules, drugs are selective to different types of receptors) - Drugs can activate or block receptors o Eg Morphine (agonist) activates opioid receptors to treat pain o Eg Nolaxone (antagonist) blocks opioid receptors to treat heroin overdose - Receptor = allows another molecule to bind and initiate a response within a cell; located in plasma membrane or cell cytoplasm - Ligand = anything (drug, hormone, neurotransmitter, toxin) that binds to a receptor and activates (agonist) or doesn t activate it (antagonist)
4 Nervous System Central Nervous System Peripheral Nervous System Brain & Spinal Cord Somatic Nervous System - Voluntary - Eg. Muscular system Neuromuscular junction (NMJ) Nicotinic receptor - ACh contraction Autonomic Nervous System - Involuntary, background Parasympathetic (rest, repose) Sympathetic (fight, flight) ACh NA Acetylcholine (ACh) Muscarinic receptors Only at sweat glands & adrenal gland induce secretion of sweat & adrenaline/noradrenaline (NA) Act on adrenoceptors muscle, blood vessel, airways Heart (β1) M3 (at smooth muscle & glands) M2 (at cardiac muscles) muscle (β2) relax Blood vessel, post junctional (α1) vasoconstrict Cardiac rate and force Airway contraction, GI secretion Cardiac rate and force Prejunctional receptor (α2) dampen neurotransmitter release
5 GPCR Ion Channel Adrenoceptors (NA, Adr) Muscarinic receptors Nicotinic - Sympathetic (ACh) receptors - Parasympathet ic Receptor α1 α2 β1 β2 M3 M2 Location Blood vessels & GI tract (post junctional receptors) Prejunctiona l receptor s Hear t muscles, airways muscles, glands Heart Natural Agonist Agonist drugs Noradrenaline, Adrenaline Acetylcholine ACh Phenylephr ine Clonidine Isopr enali ne Salbuta mol G-protein Gq Gi Gz Gs Gq Gi 2 nd IP3 & DAG cam IP3 & DAG messenger P Enzyme Phospholip ase C Phospholip ase C Conversion Overall action PIP2 IP3 + DAG Ca2+ ( ), Vasoconstr ict at unwanted sites Adenylat e cyclase ( ) Dampen NA release Aden ylate cycla se ATP cam P Hear t rate Adenyla te cyclase Ca2+ pumpe d out of cell, smooth muscle relax, bronch odilatio n PIP2 IP3 + DAG GI tract contract, secretion increase (SLUD) Adenylat e cyclase ( ) Cardiac rate Somatic skeletal muscle & ganglionic transmissio n Muscle contraction Antagonists Phentolamine Prazosin Propranolol Aten olol Atropine Suxametho nium, tubocurarin e
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