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Pharmacokinetics The study of how the body deals with a drug in terms of the way it is absorbed, distributed and eliminated.
Pharmacodynamics The analysis of what the drug does to the body, including the mechanism by which the drug exerts its effect.
Pharmacotherapeutics The area of pharmacology that refers to the use of specific drugs to prevent, treat, or diagnose a disease. Divided into two functional areas: pharmacokinetics and pharmacodynamics.
Toxicology The study of the harmful effects of chemicals.
Pharmacology The study of drugs
Drug Any substance that, when taken into a living organism, may modify one or more of its functions. Any substance that alters physiologic function in an organism.
Pharmacy The preparation and dispensation of medications.
Chemical name Refers to the specific compound's structure, when discussing a drug.
Generic ("Official") Name Name of a drug derived from the chemical name. Aka nonproprietary.
Trade ("Brand") Name Name of a drug assigned by the pharmaceutical company.
Generic Drugs Produce the same effects as the brand name drug if they are bioequivalent. Less expensive than their brand name counterparts.
FDA Food and Drug Administration. Responsible for monitoring the use of existing drugs as well as developing and approving of new ones through their Center for Drug Evaluation and Research.
FDA Mission Assure the safety, efficacy and security of drugs.
FDA role pertaining to drugs Product approvals. Classification (and labeling). Drug manufacturing standards.
Drug Approval Process Is expensive and time consuming. Made up of several phases: Preclinical Testing, Human (Clinical) Testing (Phase I, Phase II, Phase III) and Phase IV.
Preclinical Testing During the drug approval process it is initial laboratory tests to determine drug effects and safety. Done on laboratory animals and usually occurs over 1-2 years.
Human (Clinical) Testing If the results from the preclinical studies in the drug approval process are favorable and the IND is approved then testing of a drug can occur in humans. It is divided into 3 phases.
IND Investigational New Drug. An application filed by a drug sponsor with the FDA, once animal testing has favorably occurred and they want to start testing with humans.
Phase I of Human (Clinical) Testing In the drug approval process the drug is tested on a small (~20) number of healthy volunteers for about a year. The purpose is to determine the effects, safe dosage and pharmacokinetics of the drug.
Phase II of the Human (Clinical) Testing In the drug approval process the drug is tested on a limited number (~10-150) of patients with the targeted disorder for 2 years. The purpose is to assess the drug's effectiveness in treating the specific disease/disorder.
Phase III of Human (Clinical) Testing In the drug approval process the drug is tested on a large number (~1000-3000) of patients with the target disorder. The purpose is to assess safety and effectiveness in a larger patient population.
NDA New Drug Application. After a drug has successful been tested at both the Preclinical and Clinical Levels the sponsor fills out this application. If the FDA approves then the drug can be marketed and prescribed for use.
Postmarketing surveillance Phase IV in drug approval process. After the NDA is approved this is all of the methods used to continue monitoring drug safety. As the drug is now in the general population it may cause a rare adverse rxn at any time that may pull it from the market.
Special Provisions in the FDA drug approval process Drugs designed to treat serious and life-threatening conditions have a shorter time course through the development and review process.
Over-the-counter Drugs Drugs that can be purchased by the consumer directly and without a prescription. Used to treat relatively minor problems and make the consumer more comfortable. Judged to be safe for use by the consumer without medical supervision.
Prescription Drugs Drugs that may be ordered or dispensed only by an authorized practitioner (i.e., physician, dentist, or other appropriate health care provider). These are drugs that treat more serious problems and their use requires more direct medical supervision.
Controlled Substances Act (1970) Placed drugs into specific categories or "schedules" according to their potential for abuse. Restrictions on prescription renewal and penalties for possession based on different categories. Highest potential for abuse, schedule I, to lowest potential, schedule V.
Dose-Response Curve The relationship between incremental doses of a drug and the magnitude of the reaction that those doses will cause. Provides information about the dosage range over which the drug is effective, as well as the peak response.
Threshold Dose Point in dose response curve in which there is a response to the drug.
Schedule I In the Controlled Substances Act these drugs are regarded as having the highest potential for abuse, and are not typically used as an acceptable medical treatment in the US. Examples are Heroin, Marijuana, LSD.
Schedule II In the Controlled Substances Act these drugs are approved for specific therapeutic purposes but still have a high potential for abuse and possible addiction. Examples are Morphine, Barbituates, Amphetamines.
Schedule III In the Controlled Substance Act these drugs have a lower abuse potential than those in Schedules I and II but still possibility of moderate dependence so for therapeutic purposes. Examples are opioids and non-opioids such as Vicaden and Percocet.
Schedule IV In the Controlled Substances Act these drugs supposedly have lower potential for abuse and are approved for therapeutic purposes. Examples are Benzodiazepines.
Schedule V In the Controlled Substances Act these drugs have the lowest relative abuse potential. Drugs in this category consist primarily of low doses of opioids that are used in cough medications and antidiarrheal preparations.
Ceiling Effect AKA maximal efficacy. The point at which no further increase in response occurs as a drug dose is progressively increased; this effect is represented by a plateau on the drug's dose-response curve.
Potency The dose of a drug that produces a given response in a specific amplitude. When two drugs are compared, the more potent drug will produce a given response at a lower dose.
Quantal Dose-Response Curves The relationship between the dose of the drug and the occurrence of a certain response measured in a large group of people. Two measures are the median effective dose and the median toxic dose.
Median Effective Dose A reference point in the quantal dose-response curve. The dose at which 50% of the population respond to the drug in a specified manner.
Median Toxic Dose A reference point in the quantal dose-response curve. The dose at which 50% of the group exhibits the adverse effect.
Therapeutic Index A ratio used to represent the relative safety of a particular drug; the larger the therapeutic index, the safer the drug. It is calculated as the median toxic dose divided the median effective dose.
Routes of Drug Administration Enteral. Parenteral. New Techniques(other)
Enteral A route of drug administration that is through the alimentary canal(gastrointestinal tract). The types are oral, sublingual/buccal, and rectal. Advantage - easier to administer. Disadvantage - less predictable.
First-pass Effect The phenomenon in which drugs absorbed from the stomach and small intestine must pass through the liver before reaching the systemic circulation. Certain drugs undergo extensive hepatic metabolism because of this first pass through the liver.
Parenteral administration Administration of drugs by routes other than via the alimentary canal. Types are inhalation, injection(subcutaneous, intramuscular, intrathecal, intravenous, intra-arterial), topical and transdermal.
New Techniques for Drug Delivery A route of drug administration that is not enteral or parenteral. Examples are controlled release preparations, implanted drug delivery system,and targeting drug delivery to specific cells and tissues.
Bioavailability The extent to which a drug reaches the systemic circulation.
Factors affecting bioavailability of a drug Route of administration. Chemical composition and tissue permeability. Blood flow. Binding to plasma proteins. Binding to subcellular components.
Volume of distribution A ratio used to estimate the distribution of a drug within the body relative to the total amount of fluid in the body. It is calculated as the amount of drug administered divided by the plasma concentration of the drug.
Drug storage sites in the body Adipose (primary site). Bone. Muscle. Organs(liver or kidneys).
Adverse effects of drug storage in the body Local damage to the storage sites. Site "soaks up" the drug, preventing it from reaching target site. Redistribution of the drug.
Biotransformation Biochemical changes that occur to a drug within the body, usually resulting in the breakdown and inactivation of the drug, drug metabolism. The goal is to terminate the drug after it has exerted it's pharmacological effect and create a more polar compound to aid excretion.
Drug elimination Via biotransformation and excretion.
Cellular mechanisms of biotransformation Oxidation(O added or H removed). Reduction(O removed or H added). Hydrolysis. Conjugation.
Organs responsible for biotransformation Liver(primary site). Lungs. Kidneys. Gastrointestinal epithelium. Skin.
Enzyme Induction The process wherein some drugs provoke cells to synthesize more drug metabolizing enzymes, thus leading to accelerated biotransformation. Done through an increase of enzyme synthesis and decrease enzyme degradation. Contributes to tolerance.
Excretion Part of drug elimination that involves getting rid of the drug from the body.
Organs responsible fro drug excretion Kidneys(primary site). Lungs. GI tract. Sweat, saliva, breast milk.
Drug elimination rates Significant in determining the amount and frequency of dosage of a drug. Two of the primary measurements are clearance and half-life.
Clearance Refers to the ability of a single organ or tissue or all organs and tissues to eliminate a drug. Depends on blood flow to organ(s) and the ability of the organ(s) to extract drug from blood.
Half-life The amount of time required for 50% of the drug remaining in the body to be eliminated. A function of both clearance and volume of distribution.
Dosing schedules It is desirable to bring plasma concentrations of a drug up to a certain level and maintain it there. Easy to do with CONTINUOUS administration, which matches rate of administration to rate of elimination. In contrast, administration at INTERVALS adjusts the dosage to provide an average concentration over the dosage period but has highs and lows.
Factors affecting pharmacokinetics 1)Genetics. 2)Disease. 3)Drug interactions. 4)Age. 5)Diet. 6)Gender. 7)Other, such as environmental/occupational hazards, smoking and alcohol consumption, and exercise, obesity, SCI.
Drug Receptors A component of a cell to which a drug binds, thereby initiating a chain of biochemical events. Primarily the component is a protein. Location of the receptor is either on the cell surface or intracellular.
Cell surface receptors Bind to substances that can't readily enter the cell such as amino acids, peptides, and amine compounds.
Intracellular receptors Are located in the cytoplasm or nucleus and bind to substances that readily enter the cell. Example in the cytoplasm is steroids and in the nucleus is thyroid hormones.
Cell surface receptor mechanism of action They can affect cell function (1)by acting as an ion channel and directly altering cell membrane permeability, (2)by acting enzymatically to directly influence function in the cell, (3) by being linked to regulatory proteins that control other chemical and enzymatic processes in the cell.
Intracellular receptor mechanism of action Bind to specific genes in the DNA and cause changes in DNA expression messenger RNA expression. Alter protein synthesis.
Affinity The mutual attraction between a drug and a specific cellular receptor. High affinity-binds readily to open receptors, even if drug concentration is relatively low. Low affinity requires a higher drug concentration.
Factors that affect a drug's ability to bind to a receptor in drug-receptor interactions Size and shape of the drug relative to receptor. Electrostatic attraction. Affinity. Status of receptor via local regulators and environment of membrane.
Functional aspects of drug-receptor interaction Drug selectivity, a selective drug affects only one type of cell or tissue and produces a specific physiological response. Dose-response, related to number of receptors bound by the drug. Classification: Agonist vs Antagonist.
Receptor regulation Receptor responses are not static and can be altered. In general, a prolonged increase in the stimulation of various receptors will lead to a decrease in receptor function, and a decreased stimulation will lead to an increase in receptor numbers or sensitivity.
Nonreceptor drug mechanisms 1)Become incorporated into the manufacture of specific cellular components. 2)Chemical reactions. 3)Directly alter enzyme function. 4)Bind to harmful compounds and prevent them from exerting toxic effects.
Receptor Overstimulation Brief and transient response is to desensitize and decrease "active" receptors. Slow and prolonged response is to down-regulate and decrease number of receptors.
Receptor decreased stimulation Brief and transient response is to become supersensitive and increase "active"receptors. Slow and prolonged response is to up-regulate and increase number of receptors.
Opioid Analgesics Used to be called narcotics. A pain reliever that causes sedation, but the sedation is not the purpose of the drug but a side-effect.
Source of Opioid Analgesics 1)Natural and semisynthetic agents derived from the opium poppy. 2)Synthetic agents derived from basic chemical components in the lab. 3)endogenous opioids - peptides with analgesic properties.
The families of endogenous opioids Endorphins. Enkephalins. Dynorphins.
Typical agent categories for Opioids Classified according to their interaction with receptors. 1)Strong Agonists. 2)Mild-to-Moderate Agonists. 3)Mixed Agonists-Antagonists. 4)Antagonists.
Mechanism of action of Opioids Stimulate the Opioid receptors that decrease ascending pain transmission and activate descending pathways that reduce pain.
Routes of administration of Opioids Enteral-oral, rectal. Parenteral-injection(IV, IM, Subcutaneous, Intrathecal), transdermal, other.
Distribution of Opioids To all tissues but exert primary effect after reaching CNS.
Elimination of Opioids Metabolism via the liver (as well as kidneys, lungs, CNS). Excretion via the kidneys.
Location of Opioid receptors In the CNS, spinal cord-neurons that transmit nociceptive info and brain-regions associated with pain transmission and interpretation. In peripheral sites, primarily afferent neurons.
Cholinergic Use acetylcholine in the synapse. Both the parasympathetic and sympathetic efferent limbs in the preganglionic-postganglionic synapse and the parasympathetic postganglionic-effector synapse are such.
Adrenergic Refers to synapses or physiologic responses involving epinephrine and norepinephrine. The synapse in the sympathic nervous system between the postganglionic neuron and the effector cell.
Cholinergic receptors Located at AcH synapses. Subdivided into 2 categories; muscarinic and nicotinic.
Nicotinic receptors A cholinergic receptor of the ANS. Located at the junction between preganglionic and postganglionic neurons in the sympathetic and parasympathetic pathways.
Muscarinic receptors A category of cholinergic receptor of the ANS. Located on all parasympathetic effector cells: visceral and bronchiole smooth muscle, cardiac muscle, exocrine glands and sweat glands. They generally contract blood vessels, decrease HR, and increase secretion
Alpha receptors Adrenergic receptors of the SNS. Alpha 2 receipts a subtype that acts like a negative feedback loop decreasing all sympathetic response.
Beta receptors Adrenergic receptors of the SNS. Beta1 is in cardiac muscle and increases HR and contractility. Beta2 is in bronchioles smooth muscle and cause bronchodilation.
Diuretics Drugs that increase the formation and excretion of urine. Often the first drug used to treat HTN, by decreasing fluid in the body the BP decreases. Also used in CHF to reduce cardiac workload.
Drugs to treat HTN. Stepped -care approach. Drugs used include: diuretics, sympatholytics, vasodilators, renin-angiotensin inhibitors, and calcium channel blockers. Often pts begin on one drug, such as the diuretic, and then further drugs from different classes are added as needed.
Typical diuretic agents Thiazides diuretics - lasix. Loop diuretics. Potassium-sparing diuretics.
Mechanism of action of diuretics Site in the kidneys. Inhibits Na+ reabsorption. Increase Na+ and water excretion. Decrease fluid volume in vasculature to decrease cardiac workload.
Adverse effects of diuretics Fluid depletion: reflexive increase of cardiac workload, orthostatic hypotension. Electrolyte imbalance: Na and K depletion which may lead to metabolic and cardiac problems. Other: impaired glucose and lipid metabolism, GI disturbances.
Sympatholytic Drugs Drugs that interfere with sympathetic discharge, useful for HTN. Classified according to where and how interrupt sympathetic activity. One type, Beta Blockers, also useful in treating angina, arrhythmias, and CHF.
Types of Sympatholytic Drugs Beta Blockers, selective and nonselective. Alpha blockers. Presynaptic adrenergic inhibitors. Centrally acting agents. Ganglionic blockers. All but centrally acting agent can have orthostatic hypotension as an adverse reaction.
Vasodilators Drugs that directly vasodilator the peripheral nervous system will produce an antihypertensive effect by decreasing peripheral vascular resistance. Also used in CHF.
Mechanism of action of vasodilators Site - peripheral vasculature smooth muscle. Effects - inhibit contractile process, keep diameter of vessels open.
Adverse effects of vasodilators Reflex tachycardia. Orthostatic Hypotension. Dizziness.
Inhibition of renin-angiotensin system Keep blood vessels from opening by stopping the renin-angiotensin process, via ACE inhibitors or angiotensin II inhibitors.
ACE Inhibitors A renin-angiotensin inhibitor, used for HTN and CHF. Works in the peripheral vasculature and inhibits the angiotensin converting enzyme so that angiotensin II is not produced.
Angiotensin II Inhibitor A renin-angiotensin inhibitor, used for HTN. Works in the peripheral vasculature and decreases vascular resistance by blocking angiotensin II effects.
Adverse effects from Renin-Angiotensin inhibitors Allergic reactions. Hematologic effects and renal problems
Calcium Channel Blockers Drugs that selectively block calcium entry into vascular smooth-muscle cells Were originally developed to treat angina and arrhythmias but now also used for HTN.
Calcium channel blockers mechanism of action In the peripheral vasculature smooth muscle cells. Blocks calcium entry into the cells thereby inhibiting the contractile process (vasodilation, decreased vascular resistance). Also have an effect on the heart, decreased HR and contraction.
Adverse effects of calcium channel blockers Excessive vasodilation, reflex tachycardia, orthostatic hypotension, abnormalities in HR and pedal edema.
Angina Pain in the chest region that occurs during ischemic heart disease. Types: stable, variant, unstable.
Drugs used to treat Angina Organic Nitrates, general vasodilation. Beta blockers, decrease cardiac work and O2 demand. Calcium channel blockers, increase myocardial O2 and decrease O2 demand. Anticoagulants, prevent further artery blockage.
Organic Nitrates Drug precursors that become nitrous oxide in the blood and causes vasodilation of smooth muscle in peripheral vasculature by inhibiting contra toon. Good to treat angina.
Adverse effects of organic nitrates Orthostatic hypotension. Tolerance.
Angina specific treatments Only treating symptoms. Stable, organic nitrate or beta blocker. Variant, calcium channel blocker. Unstable, combo.
Cardiac arrhythmias Any significant deviation from normal cardiac rhythm. Abnormal impulse generation and/or conduction. Classified to site of origin, nature of disturbed heart beat or impairment of cardiac conduction.
Drugs to treat cardiac arrhythmias Sodium channel blockers, uses Na to help control cardiac conduction. Drugs that prolong repolarization, slows and stabilizes HR. Beta blockers, slow HR and conduction through heart. Calcium channel blockers, alter excitability and conduction of cardiac tissues.
Sodium channel blockers Bind to membrane sodium channels in the myocardium. Normalize rate Na into heart cells and thereby controls cardiac excitation and conduction. May cause an increase in other arrhythmias.
Drugs that prolong repolarization Drugs that delay the depolarization of cardiac cells, which prolongs the effective refractory period of the cardiac action potential. Slows and stabilizes HR. May increase rhythm disturbances even if used for cardiac arrhythmias.
Drugs to treat CHF Drugs that increase myocardial contraction. ACE Inhibitors, decrease vascular resistance. Beta Blockers, prevent sympathetic-induced overload to the heart. Diuretics, decrease fluid volume, thereby decreasing cardiac workload. Vasodilators, decrease cardiac workload.
Drugs that increase myocardial contraction Used to treat CHF. Improves cardiac pumping ability. Types: cardiac glycosides, beta agonists, and phosphodiesterase inhibitors.
Cardiac Glycosides A drug that increases myocardial contraction and is used to treat CHF(and arrhythmias). Drug name known Digitalis. In the heart it increases intracellular Ca and facilitates the contractile process. May have toxicity issues.
Beta Agonists A drug that increases myocardial contraction used in acute heart failure or hypotension and advanced cases of CHF when other drugs have failed. Works on the beta1 receptors of the heart to increase HR and contractility. May cause chect pain arrhythmias, and SOB.
Phosphodiesterase inhibitors A drug that increases myocardial contraction for CHF. Increases intracellular calcium in the heart to facilitate contractile process. May cause arrhythmias and HA.
Drugs to treat overactive clotting Anticoagulants. Antithrombotics. Thrombolytics.
Anticoagulants Used to prevent abnormal clot formation by targeting clotting factors. Heparin is administered by IV. Warfarin/Coumadin is administered orally and impairs hepatic synthesis of clotting factors. May cause hemorrhage.
Antithrombotics Inhibits the function of platelets to prevent clot formation. Aspirin inhibits the biosynthesis of pro platelet aggregation substances. Plavix inhibits ADP receptor on the platelet membrane. May cause hemorrhage.
Thrombolytics Meds that break up clots. Converts profibrinolysin to fibrinolysin, which breaks down fibrin clots. May cause hemorrhage, fever, allergic reactions.