BIOP211. Session 2. Pharmacology Pharmacodynamics continued Pharmacokinetics. Department of Bioscience.
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1 BIOP211 Session 2 Pharmacology Pharmacodynamics continued Pharmacokinetics Department of Bioscience
2 BIOP211 Pharmacology Session Overview Pharmacodynamics agonism and antagonism Pharmacokinetics o Routes of Administration o Absorption Endeavour College of Natural Health 2
3 Principles of Pharmacology ROUTE OF ADMINISTRATION ABSORPTION SYSTEMIC CIRCULATION DISTRIBUTION METABOLISM PHARMACODYNAMICS EXCRETION P H A R M A C O K I N E T I C S Endeavour College of Natural Health 3
4 Agonism & Antagonism o A drug s actions on its target can usually be described in the following way. o Agonist binds to and activates receptor to produce the response as the endogenous ligand. Can be partial agonists. Binding of an agonist causes a response. o Antagonist (also called blockers - binds to and blocks access to the endogenous ligand, diminishing the normal response. Competitive (reversible) or irreversible. Binding of an antagonist causes no effect, just a blocking of the interaction between receptor and endogenous substrate. Endeavour College of Natural Health 4
5 Agonism & Antagonism - Affinity o AFFINITY = Attraction of drug for a receptor. o High affinity low concentrations of the drug required to bind to the receptor. o Low affinity high concentrations of the drug are required to get any binding to the receptor. o No affinity no concentrations of the drug bind to the receptor. o Both Agonists and Antagonist have affinity. Endeavour College of Natural Health 5
6 Agonism & Antagonism - Efficacy EFFICACY (INTRINSIC ACTIVITY) = EFFECT Drug binds to receptor and has no effect = 0 Drug binds to receptor and at the higher concentrations can have the same maximum effect as the endogenous compound, efficacy = 1. Agonist - affinity & efficacy Antagonist affinity but no efficacy Remember that when an antagonist binds, nothing happens, but it does block the natural ligand from binding) Endeavour College of Natural Health 6
7 Drug Agonist o Relationship between concentration of drug and response is described by: E = Emax X C C + EC 50 o E = effect observed at a drug conc. of C. o E max = maximal response that the drug can produce. o EC 50 = Conc. at which the drug produces 50% of its maximal response. Endeavour College of Natural Health 7
8 Drug Potency (EC 50 ) o EC 50 reflects the affinity between the drug and the receptor (measure of drug potency). o Increasing [drug] above 80% maximal response little extra therapeutic effects and risk of adverse effects Endeavour College of Natural Health 8
9 Maximal Drug Efficacy Maximum response a drug can produce. Drugs may have the same potency (EC 50 ) but differ in their efficacy (% maximal response). Effectiveness of a drug depends on its maximal efficacy NOT potency. Endeavour College of Natural Health 9
10 Drug Antagonists o These types of drugs bind to receptors without eliciting a response (no efficacy), but by doing so, prevent the binding of the endogenous agonist. β -blockers (β adrenoceptor antagonists) blocks action of circulating adrenaline reduction in heart rate o 2 types of antagonism: Competitive reversible irreversible Non-competitive Endeavour College of Natural Health 10
11 Competitive (reversible) Antagonist o Interfere with binding of endogenous agonist. o Can bind to the same site on receptor as agonist. o the concentration of the antagonist concentration of the agonist bound to the receptor and its effect. o Action overcome by concentration of the agonist. o Degree of inhibition of a receptor by a competitive antagonist depends on plasma [antagonist]. Agonist Receptor Competitive Reversible Antagonist Endeavour College of Natural Health 11
12 Competitive Antagonism Endeavour College of Natural Health 12
13 Irreversible Antagonists o Target receptor becomes permanently unavailable for binding of endogenous agonist. o Action is prolonged and not terminate until the receptors are relaced by new receptors. o Duration of inhibition times depends on receptor turnover rate. o Pharmacological effect influenced by absorption, distribution, metabolism and excretion of drug. Endeavour College of Natural Health 13
14 Non-competitive Antagonists o Otherwise known as Functional antagonist. o Endogenous compounds and agonists have readily reversible (electrostatic) binding to receptor. o Bind at site other than the receptor for the endogenous compound to inhibit the response. o Site could be an ion channel opened by stimulation of the receptor. AGONIST RECEPTOR FUNCTIONAL ANTAGONIST ION CHANNEL ACTION Endeavour College of Natural Health 14
15 Pharmacokinetics and route of administration The pharmacokinetics, site of action, and chemistry of the drug will help determine what formulation of the drug is used Endeavour College of Natural Health 15
16 Routes of Administration ROUTES OF ADMINISTRATION ORAL Digestive tract Buccal Sublingual ENTERAL RECTAL OTHER Inhalation Dermal Ocular Nasal Otologic Urogenital PARENTERAL Subcutaneous Intravenous Intramuscular Intrathecal Intradermal Epidural Endeavour College of Natural Health 16
17 Oral Drug Administration DRUG RELEASE FROM DOSAGE FORM DRUG DISSOLUTION MEMBRANE TRANSPORT DIFFUSION DRUG ABSORPTION Endeavour College of Natural Health 17
18 SUBLINGUAL ADMINISTRATION Sublingual Superior Vena Cava Heart Organs (Kidney, adrenals) Liver Tissues (limbs, muscles) o Sub-lingual route bypasses first pass metabolism. o (1 st pass = drugs absorbed into blood stream from GIT. travel to the liver first via portal circulation). o - Liver involved in clearing active drug from blood. o - Often amount of active drug that leaves body is less than amount of drug absorbed from GIT. Endeavour College of Natural Health 18
19 Pulmonary Absorption/Inhalation o Gaseous and volatile drugs. o Aerosols o Absorbed across the pulmonary epithelium and mucous membrane of respiratory tract. o Rapid access to the circulation. o Solution of drugs can be atomised and the aerosol inhaled. o Difficult to regulate dose accurately. Endeavour College of Natural Health 19
20 Topical Administration o Local effect to skin, eye, nose, throat, vagina, ears. o Avoids 1 st pass metabolism. o Few drugs penetrate the intact skin. o Depends on lipid solubility and surface area. o Absorption enhanced by suspending drug in oil and rubbing it into the skin. o Efficacy variable and unpredictable. o Can cause systemic effects. Endeavour College of Natural Health 20
21 Pharmacokinetics and Drug Drug Bioavailability Bioavailability o the fraction of unchanged drug reaching the systemic circulation following administration by any route (Katzung, 2007 p. 40) o Following oral administration, bioavailability will be less than 100% due to factors such as incomplete absorption, metabolism by gut, absorption, liver biotransformation (first pass elimination) Endeavour College of Natural Health 21
22 Bioavailability Factors affecting bioavailability o Extent of absorption Lack of absorption from the gut (too hydrophilic /lipophilic) Reverse transporter associated with P-glycoprotein. o First pass elimination Endeavour College of Natural Health 22
23 Bioavailablility Route Bioavailability Characteristics Intravenous (IV) 100 Most rapid onset. Intramuscular (IM) 75 to < 100 Large volumes, may be painful. Subcutaneous (SC) 75 to < 100 Smaller volumes than IM, may be painful. Oral (PO) 5 to < 100 Most convenient, first-pass effect may be significant. Rectal (PR) 30 to < 100 Less first-pass effect than oral. Inhalation 5 to < 100 Often very rapid onset. Transdermal 80 to < 100 Usually very slow absorption, used for lack of first. Prolonged action. (Katzung 2007 p.41) Endeavour College of Natural Health 23
24 Distribution o Once a drug has been absorbed into the systemic circulation (blood), it is distributed to various sites of action within the body pharmacodynamics. o Distribution refers to the process of reversible transfer of a drug between one site and another within the body (one of which is usually blood). Endeavour College of Natural Health 24
25 Factors Affecting Distribution Factors affecting distribution: o Plasma protein binding o Tissue binding o Blood brain barrier (BBB) o Placental barrier o Blood supply o Capillary permeability o Cardiovascular function Endeavour College of Natural Health 25
26 Distribution Plasma Protein Binding o On entry into the vascular system, portion of free drug molecules bind to proteins to form drug-protein complex. o Protein binding decreases the concentration of free drug available for distribution to the site of action. o Reversible and dynamic process with bound and unbound drug in equilibrium. o When free drug is eliminated dissociation of drugprotein complex to maintain equilibrium. o Only free or unbound drug is able to exert a pharmacological effect. Endeavour College of Natural Health 26
27 Distribution Plasma Protein Binding and Affinity o The extent of binding depends on affinity of the drug for the protein o Acidic drugs bind mainly to albumin o Basic drugs bind mainly to a glyco-protein o Two drugs can compete with each other for the same binding site and displace each other BINDING SITE Plasma Protein DRUG A DRUG B Endeavour College of Natural Health 27
28 Factors that Affect Distribution o Decrease in blood proteins increase in free drug concentration and effects Dietary protein insufficiency Liver disease decrease synthesis of plasma proteins Burns o Increase in blood proteins decrease in free drug concentration and effects Multiple myeloma excessive production of immunoglobulin proteins Endeavour College of Natural Health 28
29 Plasma Protein Binding PLASMA PROTEIN DRUG DRUG Systemic Circulation Site of Action DRUG PHARMACODYNAMICS Endeavour College of Natural Health 29
30 Distribution Tissue Binding o Lipid soluble/ lipophilic drugs (toxins) have a high affinity for adipose tissue (fat) which is where these drugs are stored. o They are slowly released from fat tissue. o Some drugs have an affinity for bone e.g tetracycline. Endeavour College of Natural Health 30
31 Barriers to Drug Distribution Blood Brain Barrier o Comprised of a layer of endothelial cells covered by a fatty sheath of glial cells joined by tight intercellular junctions (lipid layer). o Allows only lipid-soluble drugs to enter the brain and cerebrospinal fluid (CSF). o Serves as a defence mechanism to protect the brain from toxins. o It can become more leaky under disease conditions which allows access of drugs that would not normally penetrate. Endeavour College of Natural Health 31
32 Distribution Placental Barrier o Membrane that separates the blood vessels of the mother and foetus. o Less selective than BBB. o Non-selective passage of drugs. o Permeable to a number of water soluble drugs which can affect the foetus. Endeavour College of Natural Health 32
33 Summary Tutorial Session 2 Activity Lifestyle Factors, Pharmacotherapy and CM And True / False Questions Case Study Tutorial Session 2: Janice is 92 years old and is on multiple drugs for hypertension, diabetes and depression. She is experiencing dizziness when standing and has had some falls of late that have resulted in minor bruises but no broken bones. She has not had her medications reviewed for a year and is still on the same dosages as she was 20 years ago. What might be contributing to her increased incidence of falls? As a Natural Health Practitioner, what recommendations might you give to her regarding her medication regime? What systems/organs are affected in old age and how do these alter the pharmacokinetics of drugs in Janice's case? Endeavour College of Natural Health 33
34 Bibliography and Acknowledgements Begg EJ. 2008, Instant clinical pharmacology, 2nd edition, Blackwell Publishing Ltd Braun L, Cohen M. 2010, Herbs and natural supplements: An Evidence-based guide, 3rd edition, Elsevier Mosby, Sydney Bauer, L., 2014, echapter 5. Clinical pharmacokinetics and pharmacodynamics. In DiPiro J., Talbert R., Yee G., Matzke G., Wells B., Posey L (Eds), Pharmacotherapy: A pathophysiologic approach, 9th edition. Retrieved October 22, 2014 from Mobile Systems Inc. 2014, Dorland s medical dictionary for health consumers, v , viewed 22 October 2014, Brunton, L. Chabner, B. and Knollmann, B Goodman and Gilman s The pharmacological. basis of therapeutics, 12th edn, McGraw-Hill Publishing, NY Katzung, B, Masters, S and Trevor, A, 2014, Basic and clinical pharmacology (Lange Basic Science), 13th edn, Appleton and Lange, Stamford, USA. Lullman, H, 2010, Pocket atlas of pharmacology, 4th edition, Thieme, Stuttgart Page C, Hoffman, B, Curtis M, Walker M & Hoffman B 2006, Integrated pharmacology, 3rd Edition, Elsevier/Mosby, London. World Health Organization. (1969). WHO Expert Committee on Drug Dependence. Sixteenth report. (Technical report series. No. 407).World Health Organization, Geneva. References Bryant, B & Knights, K 2007, Pharmacology for health professionals, 2 nd edn, Mosby, Sydney Huether, S., and McCance, K., 2008, Understanding pathophysiology, 4 th edition, Elsevier. Robas, N., O'Reilly, M., Katugampola, S. and Fidock, M.,2003, Maximizing serendipity: strategies for identifying ligands for orphan G-protein-coupled receptors. Curr. Opin. Pharmacol. 3, Thibodeau G., Patton K. 2007, Anatomy & physiology, 6th edition, Mosby, St Louis Therapeutic Goods Administration (TGA), 2012, Complementary medicine reforms, viewed 20 November Endeavour College of Natural Health 34
35 COMMONWEALTH OF AUSTRALIA Copyright Regulations 1969 WARNING This material has been reproduced and communicated to you by or on behalf of the Endeavour College of Natural Health pursuant to Part VB of the Copyright Act 1968 (the Act). The material in this communication may be subject to copyright under the Act. Any further reproduction or communication of this material by you may be the subject of copyright protection under the Act. Do not remove this notice. Endeavour College of Natural Health 35
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