Pharmacology Basics

This deck offers a friendly introduction to the foundational concepts of pharmacology, the science of how drugs interact with living systems. You'll work through core definitions, learn what pharmacokinetics and pharmacodynamics actually mean, and explore the key processes that determine what happens to a drug once it enters the body. Topics like absorption, bioavailability, distribution, metabolism, and the role of the cytochrome P450 system are broken down into clear, manageable questions to help you build a solid mental framework.

It's well suited for anyone just starting out in pharmacology, whether you're a nursing, pharmacy, medical, or biology student, or simply curious about how medicines work. If you're preparing for exams, beginning clinical rotations, or reviewing for the first time after a break, these cards can help you get oriented before moving on to more detailed or specialized material.

Because pharmacology builds heavily on interconnected concepts, try spacing your reviews over several short sessions rather than cramming everything at once. As you study, pay attention to how the ideas link together. For example, seeing how absorption connects to distribution and metabolism can make the whole picture easier to remember. Revisiting the cards regularly will help these foundational terms become second nature, giving you a reliable base to grow on as your studies continue.

Pharmacology is the study of drugs and their effects on living organisms. It is traditionally divided into two complementary branches. Pharmacokinetics describes what the body does to a drug and is summarized by the acronym ADME: Absorption, Distribution, Metabolism, and Excretion. These four processes together determine how much active drug reaches its site of action and how long it remains there. Pharmacodynamics, in contrast, describes what the drug does to the body, including its mechanism of action, the relationship between dose and response, and the resulting therapeutic and adverse effects. Most drugs produce their effects by binding to specific molecular targets, most commonly receptors, enzymes, ion channels, or transport proteins, and this binding is the basis of a drug's mechanism of action.

Recognizing drug names by their suffixes is a useful practical skill in pharmacology because the ending of a generic name usually reveals its class. For example, suffixes such as -olol denote beta-blockers, -pril indicates ACE inhibitors, -sartan indicates angiotensin receptor blockers, -statin indicates HMG-CoA reductase inhibitors, -prazole indicates proton pump inhibitors, -dipine indicates calcium channel blockers, -cillin indicates penicillins, and -azole indicates antifungal azoles. In the United States, the Food and Drug Administration oversees the development, approval, manufacturing, and marketing of drugs, ensuring that marketed medications have demonstrated both safety and efficacy through rigorous preclinical and clinical testing.

Absorption is the movement of a drug from its site of administration into the bloodstream. The rate and extent of absorption depend on the route of administration, drug solubility, pH at the absorption site, blood flow, surface area, and the drug's formulation. Bioavailability refers to the fraction of an administered dose that reaches the systemic circulation in active form. Intravenous administration delivers the drug directly into the bloodstream and therefore has 100 percent bioavailability, while oral drugs typically have lower bioavailability because of incomplete absorption and the first-pass effect, in which the drug is absorbed from the gastrointestinal tract into the portal circulation and metabolized by the liver before reaching the rest of the body. Common routes of administration include oral, intravenous, intramuscular, subcutaneous, sublingual, transdermal, inhalation, rectal, topical, and intrathecal, each with characteristic absorption rates, bioavailabilities, and clinical uses.

Once in the bloodstream, a drug is distributed to body tissues. The rate and extent of distribution depend on blood flow to tissues, the drug's lipophilicity, the extent of plasma protein binding (mainly to albumin), tissue permeability, and specialized barriers such as the blood-brain barrier. Only the unbound or free fraction of a drug is pharmacologically active, and competition between drugs for protein binding sites can lead to clinically important drug interactions. The volume of distribution (Vd) is a theoretical volume that relates the total amount of drug in the body to its plasma concentration, calculated as Vd = dose / plasma concentration. A large Vd indicates extensive distribution into tissues, while a small Vd suggests that the drug remains largely confined to the plasma.

Drug metabolism, also called biotransformation, primarily occurs in the liver and converts lipophilic drugs into more water-soluble metabolites that can be more readily excreted. Phase I reactions involve oxidation, reduction, or hydrolysis and are largely carried out by the cytochrome P450 enzyme system, with CYP3A4 being the most important enzyme because it metabolizes roughly half of all drugs, followed by CYP2D6, CYP2C9, CYP2C19, and CYP1A2. Phase II reactions conjugate the drug or its Phase I metabolite with a polar group such as glucuronic acid, sulfate, acetyl, methyl, or glutathione, further increasing water solubility. CYP enzyme activity can be increased by inducers such as rifampin, carbamazepine, phenytoin, and St. John's Wort, which accelerate drug metabolism and can reduce therapeutic effect, or decreased by inhibitors such as ketoconazole, erythromycin, grapefruit juice, and fluoxetine, which slow metabolism and can lead to toxic accumulation. Finally, excretion removes drugs and metabolites from the body, principally through the kidneys via glomerular filtration, tubular secretion, and tubular reabsorption, with secondary contributions from bile, feces, the lungs (for volatile anesthetics), sweat, saliva, and breast milk.

The half-life of a drug, denoted t½, is the time required for the plasma concentration of the drug to decrease by 50 percent, and it is one of the most clinically important pharmacokinetic parameters because it determines appropriate dosing frequency. After approximately four to five half-lives of repeated dosing, the rate of drug administration equals the rate of elimination and the drug reaches a steady state, in which plasma concentrations fluctuate within a consistent therapeutic range rather than continuing to rise. After a drug is discontinued, the same four to five half-life rule applies in reverse, so that the drug is essentially eliminated from the body after that time interval.

Two dosing strategies are used to manage the delay before steady state is achieved. A loading dose is a higher initial dose given to rapidly achieve therapeutic plasma concentrations and is particularly useful for drugs with long half-lives, such as digoxin and amiodarone, where waiting for steady state through maintenance dosing alone would be clinically impractical. A maintenance dose is the regular dose given thereafter to keep the drug at therapeutic concentrations and is calculated to replace the amount of drug eliminated during each dosing interval, depending on the drug's clearance, bioavailability, and target concentration.

For drugs with a narrow therapeutic index, including warfarin, lithium, digoxin, phenytoin, and the aminoglycoside and glycopeptide antibiotics, therapeutic drug monitoring is used to measure blood levels and adjust doses so that concentrations remain within the narrow range between efficacy and toxicity. This is in contrast to drugs with a wide therapeutic index, such as amoxicillin and ibuprofen, which have a large safety margin and generally do not require blood-level monitoring.

Pharmacodynamics describes how a drug produces its effects at the molecular, cellular, and whole-organism level. The dose-response curve plots the drug dose on the x-axis against the magnitude of the response on the y-axis and allows two important properties to be visualized: potency, reflected by the position of the curve along the x-axis and indicating how much drug is needed to produce an effect, and efficacy, reflected by the maximum height of the curve and indicating the largest effect the drug can produce regardless of dose. The ED50 is the dose that produces 50 percent of the maximum effect. Although a more potent drug is sometimes assumed to be clinically superior, efficacy is generally considered more important than potency because it represents the maximum therapeutic benefit that can be achieved.

Most drugs act by binding to specific receptors, and the nature of this binding determines the type of drug-receptor interaction. An agonist binds to a receptor and activates it to produce a biological response, with full agonists producing a maximal response and partial agonists producing only a submaximal response even when all available receptors are occupied. An antagonist binds to a receptor but does not activate it, instead blocking the action of agonists; competitive antagonists bind to the same site as the agonist and their effect can be overcome by increasing the agonist concentration, whereas non-competitive antagonists bind elsewhere and cannot be overcome in this way. A partial agonist can also act as an antagonist in the presence of a full agonist by competing for the same receptors, as seen with buprenorphine at opioid receptors.

The therapeutic index (TI) quantifies the safety margin of a drug and is defined as the ratio of the toxic dose to the effective dose, often expressed as TI = TD50 / ED50, where TD50 is the dose that produces toxicity in 50 percent of subjects and ED50 is the dose that produces the desired effect in 50 percent. A high therapeutic index indicates a wide margin between effective and toxic doses, while a narrow therapeutic index, as is found for warfarin, lithium, digoxin, and phenytoin, means that small changes in dose or blood concentration can produce toxicity, so these drugs require careful dose titration and often therapeutic drug monitoring.

A drug interaction occurs when one drug alters the activity of another. Pharmacokinetic interactions arise when absorption, distribution, metabolism, or excretion is altered, for example when one drug inhibits or induces a CYP450 enzyme and changes the blood levels of another. Pharmacodynamic interactions arise at the site of action and may be additive, synergistic, or antagonistic. Synergism occurs when two drugs together produce an effect greater than the sum of their individual effects, as seen with trimethoprim and sulfamethoxazole, which block successive steps in bacterial folate synthesis. Antagonism occurs when one drug reduces or blocks the effect of another; naloxone, for example, antagonizes morphine by competitively binding to opioid receptors and is used clinically as an antidote in opioid overdose.

Adverse drug reactions are unwanted, harmful effects that occur at normally therapeutic doses and are classified into types. Type A (augmented) reactions are dose-dependent, predictable from the drug's pharmacology, and are illustrated by bleeding with anticoagulants. Type B (bizarre) reactions are dose-independent, unpredictable, and often immune-mediated, as in drug allergy. A side effect is any effect other than the intended therapeutic effect and may be neutral, beneficial, or harmful, whereas an adverse effect specifically denotes a harmful and undesired outcome. Repeated drug exposure can also lead to drug tolerance, a decreased response that requires higher doses for the same effect, which may be pharmacokinetic in origin (such as increased metabolism), pharmacodynamic in origin (such as receptor desensitization), or behavioral. Tachyphylaxis is a particularly rapid form of tolerance that develops after repeated doses over a short period, as in the rebound congestion seen with prolonged use of nasal decongestant sprays. Drug dependence refers to a state in which discontinuation produces withdrawal symptoms and may be physical, with physiological adaptation, or psychological, with emotional craving, and is characteristic of opioids, benzodiazepines, and alcohol.

Several additional safety concepts complete this picture. Drug allergies are immune-mediated reactions, with Type I immediate IgE-mediated reactions producing anaphylaxis within minutes, as can occur with penicillins, and Type IV delayed T-cell-mediated reactions producing rashes days after exposure. Anaphylaxis itself is a severe, life-threatening, multi-system allergic reaction involving airway swelling, hypotension, urticaria, and bronchospasm, and it is treated with immediate intramuscular epinephrine, followed by antihistamines and corticosteroids. Polypharmacy, generally defined as the simultaneous use of five or more medications, is common in older adults and increases the risk of drug interactions, adverse effects, non-adherence, falls, and cognitive impairment, so regular medication review is essential. A black box warning is the strongest caution the FDA places on a drug label and indicates serious or life-threatening risks, such as suicidality in young adults taking SSRIs, tendon rupture with fluoroquinolones, or heart failure with rosiglitazone, although it does not mean that the drug is banned. Pharmacogenomics studies how genetic variation affects drug response by altering CYP enzymes, transporters, and receptors, and it underlies the move toward personalized medicine, in which drug choice and dose are tailored to a patient's genetic profile. A related concept is the prodrug, an inactive compound that is converted to its active form by metabolism in the body, with examples including enalapril to enalaprilat, codeine to morphine, and levodopa to dopamine, often designed to improve absorption or target delivery.

Antibiotics are drugs that either kill bacteria (bactericidal) or inhibit their growth (bacteriostatic), and they target structures or processes that are specific to bacteria, such as the cell wall, ribosomes, or DNA replication enzymes. Penicillins and cephalosporins are beta-lactam antibiotics that inhibit bacterial cell wall synthesis by binding to penicillin-binding proteins and blocking cross-linking of peptidoglycan, ultimately leading to osmotic lysis of the bacterium. Cephalosporins are classified into generations, with first-generation agents such as cephalexin mainly active against gram-positive organisms, second-generation agents such as cefuroxime having broader coverage, third-generation agents such as ceftriaxone covering many gram-negative organisms, and fourth-generation agents such as cefepime providing broad coverage of both gram-positive and gram-negative bacteria. Macrolides such as erythromycin, azithromycin, and clarithromycin are bacteriostatic antibiotics that bind the 50S ribosomal subunit and inhibit bacterial protein synthesis, and they are commonly used for respiratory and skin infections and as alternatives in patients allergic to penicillin. Fluoroquinolones such as ciprofloxacin and levofloxacin are bactericidal drugs that inhibit DNA gyrase and topoisomerase IV, blocking DNA replication, and are used for urinary tract and respiratory infections, with notable adverse effects including tendon rupture and QT prolongation. Antibiotic resistance arises when bacteria evolve mechanisms such as beta-lactamase production, altered target sites, efflux pumps, and decreased permeability, and it is driven by overuse and misuse of these drugs. In immunocompromised patients, the distinction between bactericidal and bacteriostatic antibiotics becomes especially important, because bactericidal agents are often preferred when host defenses are impaired.

Antifungal drugs similarly target structures specific to fungi. Azoles such as fluconazole inhibit the synthesis of ergosterol, a key component of the fungal cell membrane; polyenes such as amphotericin B bind directly to ergosterol and disrupt the membrane; echinocandins such as caspofungin inhibit the synthesis of cell wall glucan; and allylamines such as terbinafine inhibit squalene epoxidase, also in ergosterol synthesis. Antiviral drugs target specific steps in viral replication, including acyclovir, which inhibits viral DNA polymerase in herpesvirus infections, oseltamivir, a neuraminidase inhibitor used in influenza, and the multiple classes of antiretrovirals used in HIV, although vaccines remain the preferred strategy for prevention.

Analgesics relieve pain through several distinct mechanisms. Non-opioid analgesics include the nonsteroidal anti-inflammatory drugs (NSAIDs) and acetaminophen. NSAIDs such as ibuprofen, naproxen, and aspirin inhibit cyclooxygenase enzymes, reducing the production of prostaglandins that mediate pain, inflammation, and fever. COX-1 is a constitutive enzyme that protects the stomach lining, supports kidney function, and promotes platelet aggregation, while COX-2 is induced at sites of inflammation and pain; non-selective NSAIDs inhibit both, whereas selective COX-2 inhibitors such as celecoxib spare COX-1. Aspirin is unique in that it irreversibly acetylates COX-1 and COX-2; at low doses of about 81 mg, this produces an antiplatelet effect by preventing thromboxane A2 synthesis, while higher doses are required for analgesic and anti-inflammatory action. Acetaminophen is believed to act primarily in the central nervous system by inhibiting COX enzymes, producing analgesia and antipyresis with little peripheral anti-inflammatory effect and minimal gastrointestinal irritation, although hepatotoxicity becomes a serious concern at doses above about 4 g per day. Opioids such as morphine, codeine, and oxycodone bind to mu, delta, and kappa opioid receptors, particularly mu receptors, which mediate analgesia as well as respiratory depression, sedation, and the most common side effect, constipation. Naloxone is a competitive opioid antagonist used to rapidly reverse opioid overdose, given intravenously, intramuscularly, or intranasally, with the caveat that its duration of action is shorter than that of most opioids, so redosing may be required.

Antihypertensive drugs lower blood pressure through several distinct mechanisms, and the choice of agent often depends on patient comorbidities. ACE inhibitors such as lisinopril, enalapril, and ramipril block the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone secretion, with characteristic side effects of dry cough, hyperkalemia, and rare angioedema. Angiotensin receptor blockers such as losartan, valsartan, and candesartan block the angiotensin II type 1 receptor and provide similar benefits without the dry cough, making them useful alternatives when ACE inhibitors are not tolerated. Beta-blockers such as metoprolol, atenolol, and propranolol block beta-adrenergic receptors, with beta-1 blockade reducing heart rate, contractility, and cardiac output, and beta-2 blockade risking bronchoconstriction, so they are used in hypertension, heart failure, arrhythmias, and angina. Calcium channel blockers block L-type calcium channels in vascular smooth muscle and cardiac cells; dihydropyridines such as amlodipine and nifedipine act mainly as vasodilators, while non-dihydropyridines such as verapamil and diltiazem also slow heart rate and reduce contractility. Thiazide diuretics such as hydrochlorothiazide and chlorthalidone inhibit the sodium-chloride cotransporter in the distal convoluted tubule, promoting sodium and water excretion and reducing blood volume, with the side effects of hypokalemia, hyperuricemia, and hyperglycemia. Diuretics in general increase urine output by promoting sodium and water excretion, and include the more potent loop diuretics such as furosemide, the milder thiazides, and potassium-sparing agents such as spironolactone, which acts as an aldosterone antagonist.

Statins such as atorvastatin, rosuvastatin, and simvastatin inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis, lowering LDL cholesterol by 30 to 50 percent and additionally stabilizing atherosclerotic plaques and reducing inflammation, with myalgia and rare rhabdomyolysis as side effects. Anticoagulants prevent clot formation by interfering with the coagulation cascade and include warfarin, which inhibits vitamin K epoxide reductase and requires monitoring of the INR with a target of 2.0 to 3.0; heparin, which activates antithrombin III; and the direct oral anticoagulants (DOACs) such as rivaroxaban and apixaban, which directly inhibit factor Xa or thrombin. Proton pump inhibitors such as omeprazole, esomeprazole, and pantoprazole irreversibly inhibit the hydrogen-potassium ATPase proton pump in gastric parietal cells, reducing acid production by up to 90 percent and being used for gastroesophageal reflux disease, peptic ulcers, and Helicobacter pylori eradication, although long-term use carries risks of bone fractures and vitamin B12 deficiency.

Several important drug classes target the central nervous system. SSRIs such as fluoxetine, sertraline, and escitalopram block serotonin reuptake in the synapse, increasing serotonin availability, and are first-line treatment for depression and anxiety, although full effect takes four to six weeks and side effects include sexual dysfunction, gastrointestinal upset, and insomnia. SNRIs such as venlafaxine additionally inhibit norepinephrine reuptake, while older tricyclic antidepressants such as amitriptyline and MAO inhibitors such as phenelzine are used less often because of more side effects and dietary restrictions; atypical agents such as bupropion and mirtazapine offer alternative mechanisms. Benzodiazepines such as diazepam, lorazepam, and alprazolam enhance GABA-A receptor activity, increasing chloride influx and neuronal inhibition, and are used for anxiety, insomnia, seizures, and muscle spasms, with risks of sedation, tolerance, dependence, and respiratory depression especially when combined with opioids. Antipsychotics treat schizophrenia and other psychotic disorders; first-generation or typical agents such as haloperidol block dopamine D2 receptors and carry a high risk of extrapyramidal side effects, while second-generation or atypical agents such as risperidone, olanzapine, and quetiapine additionally block serotonin 5-HT2A receptors and have fewer movement side effects but greater metabolic risks. Antiepileptic drugs such as phenytoin, carbamazepine, valproic acid, and levetiracetam prevent seizures by modulating ion channels, enhancing GABA activity, or reducing glutamate activity, and many have narrow therapeutic indices that require monitoring. Corticosteroids such as prednisone, dexamethasone, and hydrocortisone are synthetic analogs of cortisol with potent anti-inflammatory and immunosuppressive effects, acting by inhibiting phospholipase A2 and NF-κB, and are used in asthma, autoimmune disease, and allergies, although long-term use risks osteoporosis, diabetes, and adrenal suppression. In respiratory and allergic disease, antihistamines block histamine H1 receptors, with first-generation agents such as diphenhydramine crossing the blood-brain barrier and causing drowsiness while second-generation agents such as cetirizine and loratadine do not; bronchodilators relax airway smooth muscle, including short-acting beta-2 agonists such as albuterol for rescue, long-acting beta-2 agonists such as salmeterol for maintenance, and anticholinergics such as ipratropium. In diabetes, metformin is the first-line oral agent for type 2 diabetes, reducing hepatic glucose production and increasing insulin sensitivity without causing hypoglycemia when used alone, while injectable insulin preparations are classified by onset and duration into rapid-acting (lispro), short-acting (regular), intermediate (NPH), and long-acting (glargine) forms. Finally, antiemetics such as ondansetron (a 5-HT3 antagonist), metoclopramide (a D2 antagonist and prokinetic), aprepitant (an NK1 antagonist), meclizine (an antihistamine for motion sickness), and dronabinol (a cannabinoid) prevent nausea and vomiting through different mechanisms, and laxatives for constipation include bulk-forming agents such as psyllium, osmotic agents such as lactulose and polyethylene glycol, stimulants such as bisacodyl and senna, and stool softeners such as docusate.

Drug development follows a structured sequence from laboratory research to general clinical use. Preclinical testing involves laboratory and animal studies to evaluate basic pharmacology and toxicology. Phase I clinical trials test safety, pharmacokinetics, and dosing in a small group of 20 to 100 healthy volunteers, identifying adverse effects and the maximum tolerated dose, with roughly 70 percent of drugs passing this stage. Phase II trials enroll 100 to 300 patients with the target disease to assess efficacy and further evaluate safety, while Phase III trials are large-scale studies in 1000 to 3000 or more patients, usually randomized, controlled, and often double-blind, comparing the new drug to standard treatment or placebo and generating the data on which FDA approval is based; about 25 to 30 percent of drugs pass Phase III. After approval, Phase IV post-marketing surveillance monitors the drug in the general population, detects rare adverse effects not seen in earlier trials, evaluates long-term outcomes, and can lead to black box warnings, restrictions, or in rare cases withdrawal from the market. Clinical trials also rely on the placebo effect, a beneficial response to an inert treatment produced by the patient's belief in its efficacy and accompanied by real physiological changes such as endorphin and dopamine release, which is why placebo controls are essential for distinguishing true drug effects.

Drugs are regulated according to their risk and abuse potential. Over-the-counter drugs can be purchased without a prescription and are considered safe for self-treatment at recommended doses, while prescription drugs require authorization from a healthcare provider because of greater risks, the need for monitoring, or potential for abuse. Controlled substances are drugs regulated by the government because of their potential for abuse and dependence; in the United States the Drug Enforcement Administration classifies them into five schedules, with Schedule I containing drugs of the highest abuse potential and no accepted medical use such as heroin and LSD, Schedule II containing drugs with high abuse potential such as opioids and amphetamines, and Schedules III through V containing substances with progressively lower abuse potential. A generic drug contains the same active ingredient in the same dose, route, and dosage form as the brand-name product and must demonstrate bioequivalence, meaning that its rate and extent of absorption fall within 80 to 125 percent of the brand product, so generics can usually be substituted while producing comparable clinical effects at substantially lower cost, typically 80 to 85 percent less, and they become available after the brand's patent, usually lasting about 20 years, expires.

The dosage form in which a drug is delivered affects its onset, duration, bioavailability, and patient adherence. Tablets are compressed powders that can be scored, split, or coated, while capsules contain powder or liquid in a gelatin shell, dissolve more rapidly, and may be easier to swallow. Enteric-coated tablets have a coating that resists acidic gastric pH and dissolves only in the alkaline environment of the small intestine, protecting acid-labile drugs such as omeprazole from destruction and protecting the stomach from irritant drugs such as aspirin. Sustained-release or extended-release formulations, often labeled SR, XR, or ER, release the drug slowly over an extended period to reduce dosing frequency and maintain stable blood levels, and they must never be crushed or chewed because disrupting the formulation can release the entire dose at once in a phenomenon called dose dumping. Other dosage forms include solutions, suspensions, injections, suppositories, transdermal patches, inhalers, creams and ointments, eye and ear drops, sublingual tablets, and lozenges, each suited to particular clinical situations and patient needs.