Pharmacology Basics
What are controlled substances?
Controlled substances are drugs regulated by the government due to abuse potential . In the US, the DEA classifies them into Schedules I–V : I (highest abuse, no medical use — heroin, LSD), II (high abuse — opioids, amphetamines), III–V (decreasing abuse potential).
Aspirin (acetylsalicylic acid) irreversibly inhibits COX-1 and COX-2 by acetylating a serine residue . At low doses (81 mg), it primarily inhibits platelet COX-1, preventing thromboxane A2 synthesis and platelet aggregation (antiplatelet effect). At higher doses, it has analgesic and anti-inflammatory effects.
Phase IV surveillance monitors drug safety after FDA approval in the general population . It detects rare adverse effects not seen in clinical trials, evaluates long-term effects, and can lead to black box warnings, restricted use, or withdrawal from the market.
Pharmacology is the study of drugs and their effects on living organisms . It encompasses how drugs are absorbed, distributed, metabolized, and excreted (pharmacokinetics), as well as how they produce their effects (pharmacodynamics).
Pharmacology Basics
What are the main classes of antidepressants?
Drug allergies are immune-mediated reactions to medications . Type I (immediate/anaphylaxis): IgE-mediated, occurs within minutes (penicillin allergy). Type IV (delayed): T-cell mediated, occurs after days (drug rash). True allergies require prior sensitization and are distinct from side effects.
Antidepressant classes: SSRIs (fluoxetine — first-line), SNRIs (venlafaxine — serotonin + norepinephrine), TCAs (amitriptyline — older, more side effects), MAOIs (phenelzine — dietary restrictions), atypical (bupropion, mirtazapine). All take 4–6 weeks for full effect.
Antivirals target specific steps in viral replication . Examples: acyclovir (herpes — inhibits viral DNA polymerase), oseltamivir (influenza — neuraminidase inhibitor), antiretrovirals (HIV — multiple classes). Vaccines are generally preferred for prevention.
Phase II metabolism involves conjugation reactions that attach a polar molecule (glucuronic acid, sulfate, acetyl, methyl, or glutathione) to the drug or its Phase I metabolite. This makes the compound more water-soluble and easier to excrete via kidneys or bile.
Pharmacology Basics
What is the difference between narrow and wide therapeutic index drugs?
Drug excretion is the removal of drugs and metabolites from the body . The kidneys are the primary route (via glomerular filtration, tubular secretion, and reabsorption). Other routes: bile/feces, lungs (volatile anesthetics), sweat, saliva, and breast milk.
Antifungals target fungal cell components not found in human cells . Classes: azoles (fluconazole — inhibit ergosterol synthesis), polyenes (amphotericin B — bind ergosterol), echinocandins (caspofungin — inhibit cell wall glucan), and allylamines (terbinafine).
Dosage forms include: tablets, capsules, solutions, suspensions, injections, suppositories, patches (transdermal), inhalers, creams/ointments, eye/ear drops, sublingual tablets, and lozenges . Each form affects onset of action, duration, bioavailability, and patient compliance.
Narrow TI drugs (warfarin, lithium, digoxin, phenytoin) have small margins between therapeutic and toxic doses, requiring close monitoring and blood level checks. Wide TI drugs (amoxicillin, ibuprofen) have large safety margins and require less monitoring.
Pharmacology Basics
What is the mechanism of aspirin?
Anaphylaxis is a severe, life-threatening allergic reaction involving multiple organ systems : airway swelling, hypotension, urticaria, bronchospasm. Treatment: epinephrine (adrenaline) IM immediately , followed by antihistamines and corticosteroids. Common triggers: penicillin, NSAIDs, latex.
Aspirin (acetylsalicylic acid) irreversibly inhibits COX-1 and COX-2 by acetylating a serine residue . At low doses (81 mg), it primarily inhibits platelet COX-1, preventing thromboxane A2 synthesis and platelet aggregation (antiplatelet effect). At higher doses, it has analgesic and anti-inflammatory effects.
Macrolides (erythromycin, azithromycin, clarithromycin) inhibit bacterial protein synthesis by binding to the 50S ribosomal subunit . They are bacteriostatic and used for respiratory infections, skin infections, and as penicillin alternatives. Common side effect: GI upset.
Warfarin inhibits vitamin K epoxide reductase, blocking the recycling of vitamin K needed to activate clotting factors II, VII, IX, and X. It has a narrow therapeutic index monitored by INR (target 2.0–3.0) . Many drug and food interactions (vitamin K-rich foods).
Pharmacology Basics
What are antiviral drugs?
Antivirals target specific steps in viral replication . Examples: acyclovir (herpes — inhibits viral DNA polymerase), oseltamivir (influenza — neuraminidase inhibitor), antiretrovirals (HIV — multiple classes). Vaccines are generally preferred for prevention.
Anaphylaxis is a severe, life-threatening allergic reaction involving multiple organ systems : airway swelling, hypotension, urticaria, bronchospasm. Treatment: epinephrine (adrenaline) IM immediately , followed by antihistamines and corticosteroids. Common triggers: penicillin, NSAIDs, latex.
An agonist is a drug that binds to a receptor and activates it, producing a biological response . Full agonists produce a maximal response; partial agonists produce a submaximal response even at full receptor occupancy. Example: morphine is a full agonist at opioid receptors.
Volume of distribution is a theoretical volume that relates the total amount of drug in the body to its plasma concentration : Vd = dose/plasma concentration. A large Vd indicates the drug distributes extensively into tissues; a small Vd suggests it stays mostly in plasma.
Pharmacology Basics
How do beta-blockers work?
Drug dependence is a state where discontinuation causes withdrawal symptoms . Physical dependence : physiological adaptation requiring continued use. Psychological dependence : emotional craving. Both can occur with opioids, benzodiazepines, alcohol, and other substances.
The therapeutic index (TI) is the ratio of the toxic dose to the therapeutic dose : TI = TD50/ED50. A narrow therapeutic index means there is a small margin between effective and toxic doses (e.g., warfarin, lithium, digoxin). These drugs require careful monitoring.
Antiemetics prevent nausea and vomiting . Classes: 5-HT3 antagonists (ondansetron — chemotherapy-induced), D2 antagonists (metoclopramide — also prokinetic), NK1 antagonists (aprepitant), antihistamines (meclizine — motion sickness), cannabinoids (dronabinol).
Beta-blockers (metoprolol, atenolol, propranolol) block beta-adrenergic receptors . β1 blockade: reduces heart rate, contractility, and cardiac output. β2 blockade: can cause bronchoconstriction. Used for hypertension, heart failure, arrhythmias, angina, and anxiety.
Pharmacology Basics
What is the difference between a tablet and a capsule?
An antagonist is a drug that binds to a receptor but does not activate it, blocking the action of agonists . Competitive antagonists compete for the same binding site (can be overcome by more agonist). Non-competitive antagonists bind elsewhere and cannot be overcome.
Tablets : compressed powder, can be scored/split, may have enteric coating; slower dissolution. Capsules : powder/liquid in a gelatin shell; faster dissolution, easier to swallow, can mask taste. Some capsules can be opened and sprinkled on food.
Benzodiazepines (diazepam, lorazepam, alprazolam) enhance GABA-A receptor activity, increasing chloride influx and neuronal inhibition . Used for anxiety, insomnia, seizures, and muscle spasms. Risks: sedation, tolerance, dependence, respiratory depression (especially with opioids).
ARBs (losartan, valsartan, candesartan) block angiotensin II type 1 (AT1) receptors , preventing vasoconstriction and aldosterone release. Similar benefits to ACE inhibitors but without the dry cough . Used when patients cannot tolerate ACE inhibitors.
Pharmacology Basics
What is OTC vs prescription drugs?
A dose-response curve plots drug dose (x-axis) against the magnitude of response (y-axis) . Key parameters: potency (position on x-axis — how much drug is needed), efficacy (maximum response achievable), ED50 (dose for 50% effect).
IV administration delivers drugs directly into the bloodstream , providing 100% bioavailability and immediate effect. It is used for emergencies, drugs with poor oral absorption, precise dosing, and when rapid onset is needed. Disadvantages: infection risk, cannot be easily reversed.
OTC (over-the-counter) drugs can be purchased without a prescription and are generally considered safe for self-treatment at recommended doses. Prescription drugs require a healthcare provider's authorization due to greater risks, need for monitoring, or potential for abuse.
Drug allergies are immune-mediated reactions to medications . Type I (immediate/anaphylaxis): IgE-mediated, occurs within minutes (penicillin allergy). Type IV (delayed): T-cell mediated, occurs after days (drug rash). True allergies require prior sensitization and are distinct from side effects.
Pharmacology Basics
What is ADME?
Tablets : compressed powder, can be scored/split, may have enteric coating; slower dissolution. Capsules : powder/liquid in a gelatin shell; faster dissolution, easier to swallow, can mask taste. Some capsules can be opened and sprinkled on food.
Steady state is achieved when the rate of drug administration equals the rate of elimination , resulting in consistent plasma concentrations. It takes approximately 4–5 half-lives to reach steady state with repeated dosing.
A dose-response curve plots drug dose (x-axis) against the magnitude of response (y-axis) . Key parameters: potency (position on x-axis — how much drug is needed), efficacy (maximum response achievable), ED50 (dose for 50% effect).
ADME stands for Absorption, Distribution, Metabolism, and Excretion — the four processes that determine how a drug moves through the body. Together they determine the drug's concentration at the site of action and its duration of effect.
Pharmacology Basics
What is a black box warning?
A black box warning is the FDA's strongest warning placed on a drug's label , indicating serious or life-threatening risks. Examples: SSRIs (suicidality in young adults), fluoroquinolones (tendon rupture), rosiglitazone (heart failure). It does not mean the drug is banned.
Fluoroquinolones (ciprofloxacin, levofloxacin) inhibit bacterial DNA gyrase and topoisomerase IV , preventing DNA replication. They are broad-spectrum and bactericidal. Used for UTIs, respiratory infections. Side effects include tendon rupture and QT prolongation.
Antihistamines block histamine H1 receptors, reducing allergic symptoms (sneezing, itching, runny nose). First generation (diphenhydramine): cross BBB, causing drowsiness. Second generation (cetirizine, loratadine): don't cross BBB significantly, less sedating.
A CYP enzyme inducer increases the production of CYP enzymes, leading to faster drug metabolism and potentially reduced drug effectiveness. Examples: rifampin, carbamazepine, phenytoin, St. John's Wort . They can cause therapeutic failure of co-administered drugs.
Pharmacology Basics
What are the main dosage forms?
Dosage forms include: tablets, capsules, solutions, suspensions, injections, suppositories, patches (transdermal), inhalers, creams/ointments, eye/ear drops, sublingual tablets, and lozenges . Each form affects onset of action, duration, bioavailability, and patient compliance.
Tablets : compressed powder, can be scored/split, may have enteric coating; slower dissolution. Capsules : powder/liquid in a gelatin shell; faster dissolution, easier to swallow, can mask taste. Some capsules can be opened and sprinkled on food.
Potency refers to the amount of drug needed to produce an effect (lower dose = more potent). Efficacy refers to the maximum effect a drug can produce regardless of dose. Efficacy is generally more clinically important than potency.
A loading dose is a higher initial dose given to rapidly achieve therapeutic plasma concentrations before switching to maintenance doses. It is used for drugs with long half-lives where waiting for steady state would be impractical (e.g., digoxin, amiodarone).
Pharmacology Basics
What is the first-pass effect?
The first-pass effect is the metabolism of an orally administered drug by the liver before it reaches systemic circulation . The drug is absorbed from the GI tract into the portal vein, passes through the liver, and may be significantly metabolized, reducing bioavailability.
Drug absorption is the movement of a drug from its site of administration into the bloodstream . Factors affecting absorption: route of administration, drug solubility, pH, blood flow to absorption site, surface area, and drug formulation.
A generic drug contains the same active ingredient, dose, route, and dosage form as the brand-name drug . It must demonstrate bioequivalence. Generics are typically 80–85% cheaper and are approved after the brand's patent expires (usually 20 years).
A maintenance dose is the regular dose given to maintain the drug concentration at steady state . It equals the amount of drug eliminated per dosing interval. It depends on clearance, bioavailability, and target concentration.
Pharmacology Basics
What is an adverse drug reaction (ADR)?
Tablets : compressed powder, can be scored/split, may have enteric coating; slower dissolution. Capsules : powder/liquid in a gelatin shell; faster dissolution, easier to swallow, can mask taste. Some capsules can be opened and sprinkled on food.
An ADR is an unwanted, harmful effect caused by a drug at normal therapeutic doses . Type A (augmented): dose-dependent, predictable, related to pharmacology (e.g., bleeding with anticoagulants). Type B (bizarre): dose-independent, unpredictable, often immune-mediated (e.g., drug allergy).
Metformin is the first-line oral drug for type 2 diabetes . It reduces hepatic glucose production, increases insulin sensitivity, and decreases intestinal glucose absorption. It does not cause hypoglycemia when used alone. Main side effect: GI upset. Rare but serious: lactic acidosis.
Pharmacogenomics studies how genetic variation affects drug response . Genetic differences in CYP enzymes, drug transporters, and receptors explain why patients respond differently to the same drug. It enables personalized medicine — selecting drugs and doses based on genetic profile.
Pharmacology Basics
How do thiazide diuretics work?
Thiazides (hydrochlorothiazide, chlorthalidone) inhibit the Na-Cl cotransporter in the distal convoluted tubule , promoting sodium and water excretion. This reduces blood volume and blood pressure. Side effects: hypokalemia, hyperuricemia, hyperglycemia.
An agonist is a drug that binds to a receptor and activates it, producing a biological response . Full agonists produce a maximal response; partial agonists produce a submaximal response even at full receptor occupancy. Example: morphine is a full agonist at opioid receptors.
Phase I metabolism involves oxidation, reduction, or hydrolysis reactions that modify the drug molecule. The cytochrome P450 (CYP) enzyme system in the liver is the most important. Key CYP enzymes: CYP3A4 (metabolizes ~50% of drugs), CYP2D6, CYP2C9, CYP2C19, CYP1A2.
A CYP enzyme inducer increases the production of CYP enzymes, leading to faster drug metabolism and potentially reduced drug effectiveness. Examples: rifampin, carbamazepine, phenytoin, St. John's Wort . They can cause therapeutic failure of co-administered drugs.
Pharmacology Basics
What are laxatives and their types?
Warfarin inhibits vitamin K epoxide reductase, blocking the recycling of vitamin K needed to activate clotting factors II, VII, IX, and X. It has a narrow therapeutic index monitored by INR (target 2.0–3.0) . Many drug and food interactions (vitamin K-rich foods).
Bactericidal antibiotics kill bacteria directly (penicillins, cephalosporins, fluoroquinolones, aminoglycosides). Bacteriostatic antibiotics inhibit growth, relying on the immune system to clear infection (tetracyclines, macrolides, sulfonamides). The distinction matters in immunocompromised patients.
Drug excretion is the removal of drugs and metabolites from the body . The kidneys are the primary route (via glomerular filtration, tubular secretion, and reabsorption). Other routes: bile/feces, lungs (volatile anesthetics), sweat, saliva, and breast milk.
Laxatives treat constipation. Types: bulk-forming (psyllium — absorb water), osmotic (lactulose, PEG — draw water into bowel), stimulant (bisacodyl, senna — increase motility), stool softeners (docusate — reduce surface tension). Osmotic and bulk-forming are first-line.
Pharmacology Basics
What is drug metabolism (biotransformation)?
NSAIDs (ibuprofen, naproxen, aspirin) work by inhibiting cyclooxygenase (COX) enzymes (COX-1 and COX-2) , reducing prostaglandin synthesis. Prostaglandins mediate pain, inflammation, and fever. Side effects: GI irritation, kidney issues, bleeding risk.
A drug interaction occurs when one drug affects the activity of another . Types: pharmacokinetic (altered ADME — e.g., CYP inhibition) and pharmacodynamic (additive, synergistic, or antagonistic effects at receptors). Drug interactions can increase toxicity or reduce efficacy.
Drug metabolism is the chemical modification of drugs by the body , primarily in the liver. It typically converts lipophilic drugs into more water-soluble metabolites for excretion. Metabolism occurs in two phases: Phase I (oxidation, reduction, hydrolysis) and Phase II (conjugation).
Narrow TI drugs (warfarin, lithium, digoxin, phenytoin) have small margins between therapeutic and toxic doses, requiring close monitoring and blood level checks. Wide TI drugs (amoxicillin, ibuprofen) have large safety margins and require less monitoring.
Pharmacology Basics
What is post-marketing surveillance (Phase IV)?
A partial agonist binds to and activates a receptor but produces only a partial response compared to a full agonist, even at maximum occupancy. It can act as an antagonist in the presence of a full agonist (by competing for receptors). Example: buprenorphine.
Phase IV surveillance monitors drug safety after FDA approval in the general population . It detects rare adverse effects not seen in clinical trials, evaluates long-term effects, and can lead to black box warnings, restricted use, or withdrawal from the market.
NSAIDs (ibuprofen, naproxen, aspirin) work by inhibiting cyclooxygenase (COX) enzymes (COX-1 and COX-2) , reducing prostaglandin synthesis. Prostaglandins mediate pain, inflammation, and fever. Side effects: GI irritation, kidney issues, bleeding risk.
Antivirals target specific steps in viral replication . Examples: acyclovir (herpes — inhibits viral DNA polymerase), oseltamivir (influenza — neuraminidase inhibitor), antiretrovirals (HIV — multiple classes). Vaccines are generally preferred for prevention.
Pharmacology Basics
What is an antagonist?
An antagonist is a drug that binds to a receptor but does not activate it, blocking the action of agonists . Competitive antagonists compete for the same binding site (can be overcome by more agonist). Non-competitive antagonists bind elsewhere and cannot be overcome.
An enteric-coated tablet has a coating that resists stomach acid but dissolves in the alkaline pH of the small intestine . Used to protect drugs destroyed by stomach acid (e.g., omeprazole), protect the stomach from irritation (e.g., aspirin), or target drug release to the intestine.
Bronchodilators relax airway smooth muscle to open the airways . Types: short-acting beta-2 agonists (SABA) like albuterol (rescue), long-acting beta-2 agonists (LABA) like salmeterol (maintenance), and anticholinergics like ipratropium. Used for asthma and COPD.
Anaphylaxis is a severe, life-threatening allergic reaction involving multiple organ systems : airway swelling, hypotension, urticaria, bronchospasm. Treatment: epinephrine (adrenaline) IM immediately , followed by antihistamines and corticosteroids. Common triggers: penicillin, NSAIDs, latex.
Pharmacology Basics
What is a drug's mechanism of action?
COX-1 is constitutive (always present): protects stomach lining, maintains kidney function, supports platelet aggregation. COX-2 is inducible: produced during inflammation and pain. Non-selective NSAIDs inhibit both; selective COX-2 inhibitors (celecoxib) spare COX-1.
Antihypertensives lower blood pressure. Major classes: ACE inhibitors (-pril), ARBs (-sartan), calcium channel blockers (-dipine), beta-blockers (-olol), thiazide diuretics (-thiazide) , alpha-blockers, and direct vasodilators. Treatment choice depends on patient comorbidities.
Mechanism of action (MOA) describes the specific biochemical interaction through which a drug produces its effect . Most drugs work by binding to receptors, enzymes, ion channels, or transport proteins. Understanding MOA helps predict effects, side effects, and interactions.
Laxatives treat constipation. Types: bulk-forming (psyllium — absorb water), osmotic (lactulose, PEG — draw water into bowel), stimulant (bisacodyl, senna — increase motility), stool softeners (docusate — reduce surface tension). Osmotic and bulk-forming are first-line.
Pharmacology Basics
What is an enteric-coated tablet?
Controlled substances are drugs regulated by the government due to abuse potential . In the US, the DEA classifies them into Schedules I–V : I (highest abuse, no medical use — heroin, LSD), II (high abuse — opioids, amphetamines), III–V (decreasing abuse potential).
An enteric-coated tablet has a coating that resists stomach acid but dissolves in the alkaline pH of the small intestine . Used to protect drugs destroyed by stomach acid (e.g., omeprazole), protect the stomach from irritation (e.g., aspirin), or target drug release to the intestine.
Drug allergies are immune-mediated reactions to medications . Type I (immediate/anaphylaxis): IgE-mediated, occurs within minutes (penicillin allergy). Type IV (delayed): T-cell mediated, occurs after days (drug rash). True allergies require prior sensitization and are distinct from side effects.
Drug tolerance is a decreased response to a drug after repeated use, requiring higher doses for the same effect . Types: pharmacokinetic (increased metabolism), pharmacodynamic (receptor desensitization), and behavioral. Example: opioid tolerance develops rapidly, requiring dose escalation.
Pharmacology Basics
What is a prodrug?
Phase I trials test safety, dosing, and side effects in a small group (20–100) of healthy volunteers . The primary goal is to determine the drug's pharmacokinetic profile, maximum tolerated dose, and identify adverse effects. ~70% of drugs pass Phase I.
Antiemetics prevent nausea and vomiting . Classes: 5-HT3 antagonists (ondansetron — chemotherapy-induced), D2 antagonists (metoclopramide — also prokinetic), NK1 antagonists (aprepitant), antihistamines (meclizine — motion sickness), cannabinoids (dronabinol).
Drug allergies are immune-mediated reactions to medications . Type I (immediate/anaphylaxis): IgE-mediated, occurs within minutes (penicillin allergy). Type IV (delayed): T-cell mediated, occurs after days (drug rash). True allergies require prior sensitization and are distinct from side effects.
A prodrug is an inactive compound that is converted to its active form in the body through metabolism . Examples: enalapril → enalaprilat, codeine → morphine, levodopa → dopamine. Prodrugs are used to improve oral absorption, reduce side effects, or target specific tissues.
Pharmacology Basics
What are diuretics?
SSRIs (selective serotonin reuptake inhibitors: fluoxetine, sertraline, escitalopram) block serotonin reuptake in the synapse, increasing serotonin availability . First-line treatment for depression and anxiety. Take 4–6 weeks for full effect. Side effects: sexual dysfunction, GI upset, insomnia.
Diuretics increase urine output by promoting sodium and water excretion from the kidneys . Types: loop diuretics (furosemide — most potent), thiazides (hydrochlorothiazide — mild), potassium-sparing (spironolactone — aldosterone antagonist). Used for hypertension, heart failure, edema.
Antihistamines block histamine H1 receptors, reducing allergic symptoms (sneezing, itching, runny nose). First generation (diphenhydramine): cross BBB, causing drowsiness. Second generation (cetirizine, loratadine): don't cross BBB significantly, less sedating.
Naloxone (Narcan) is an opioid antagonist that rapidly reverses opioid overdose . It competitively binds to opioid receptors, displacing opioids. Given IV, IM, or intranasally. Its effects last 30–90 minutes (shorter than most opioids), so redosing may be needed.
Pharmacology Basics
What are bronchodilators?
Phase IV surveillance monitors drug safety after FDA approval in the general population . It detects rare adverse effects not seen in clinical trials, evaluates long-term effects, and can lead to black box warnings, restricted use, or withdrawal from the market.
Bronchodilators relax airway smooth muscle to open the airways . Types: short-acting beta-2 agonists (SABA) like albuterol (rescue), long-acting beta-2 agonists (LABA) like salmeterol (maintenance), and anticholinergics like ipratropium. Used for asthma and COPD.
Corticosteroids (prednisone, dexamethasone, hydrocortisone) are synthetic analogs of cortisol with potent anti-inflammatory and immunosuppressive properties . They inhibit phospholipase A2 and NF-κB pathways. Used for asthma, autoimmune diseases, allergies. Long-term risks: osteoporosis, diabetes, adrenal suppression.
Antifungals target fungal cell components not found in human cells . Classes: azoles (fluconazole — inhibit ergosterol synthesis), polyenes (amphotericin B — bind ergosterol), echinocandins (caspofungin — inhibit cell wall glucan), and allylamines (terbinafine).
Pharmacology Basics
What is a Phase I clinical trial?
A CYP enzyme inhibitor decreases CYP enzyme activity, leading to slower drug metabolism and potentially increased drug levels/toxicity. Examples: ketoconazole, erythromycin, grapefruit juice (CYP3A4), fluoxetine (CYP2D6) . They can cause dangerous drug accumulation.
Phase I trials test safety, dosing, and side effects in a small group (20–100) of healthy volunteers . The primary goal is to determine the drug's pharmacokinetic profile, maximum tolerated dose, and identify adverse effects. ~70% of drugs pass Phase I.
A side effect is any effect other than the intended one (can be positive or negative). An adverse effect is specifically a harmful, undesired effect. Example: drowsiness from an antihistamine is a side effect; severe liver damage from acetaminophen overdose is an adverse effect.
CCBs block L-type calcium channels in vascular smooth muscle and cardiac cells . Dihydropyridines (amlodipine, nifedipine): primarily vasodilate. Non-dihydropyridines (verapamil, diltiazem): slow heart rate and reduce contractility. Used for hypertension, angina, arrhythmias.
Pharmacology Basics
What are fluoroquinolones?
A black box warning is the FDA's strongest warning placed on a drug's label , indicating serious or life-threatening risks. Examples: SSRIs (suicidality in young adults), fluoroquinolones (tendon rupture), rosiglitazone (heart failure). It does not mean the drug is banned.
Phase I metabolism involves oxidation, reduction, or hydrolysis reactions that modify the drug molecule. The cytochrome P450 (CYP) enzyme system in the liver is the most important. Key CYP enzymes: CYP3A4 (metabolizes ~50% of drugs), CYP2D6, CYP2C9, CYP2C19, CYP1A2.
Penicillin works by inhibiting bacterial cell wall synthesis . It binds to penicillin-binding proteins (PBPs) and blocks cross-linking of peptidoglycan, weakening the cell wall. The bacteria swell and lyse due to osmotic pressure. It is bactericidal.
Fluoroquinolones (ciprofloxacin, levofloxacin) inhibit bacterial DNA gyrase and topoisomerase IV , preventing DNA replication. They are broad-spectrum and bactericidal. Used for UTIs, respiratory infections. Side effects include tendon rupture and QT prolongation.
Pharmacology Basics
What are antifungal drugs?
Laxatives treat constipation. Types: bulk-forming (psyllium — absorb water), osmotic (lactulose, PEG — draw water into bowel), stimulant (bisacodyl, senna — increase motility), stool softeners (docusate — reduce surface tension). Osmotic and bulk-forming are first-line.
Antifungals target fungal cell components not found in human cells . Classes: azoles (fluconazole — inhibit ergosterol synthesis), polyenes (amphotericin B — bind ergosterol), echinocandins (caspofungin — inhibit cell wall glucan), and allylamines (terbinafine).
Statins (atorvastatin, rosuvastatin, simvastatin) inhibit HMG-CoA reductase, the rate-limiting enzyme in cholesterol synthesis . This reduces LDL cholesterol by 30–50%. They also stabilize atherosclerotic plaques and reduce inflammation. Side effects: myalgia, rare rhabdomyolysis.
OTC (over-the-counter) drugs can be purchased without a prescription and are generally considered safe for self-treatment at recommended doses. Prescription drugs require a healthcare provider's authorization due to greater risks, need for monitoring, or potential for abuse.
Pharmacology Basics
What is the difference between COX-1 and COX-2?
Insulin is a hormone produced by pancreatic beta cells that lowers blood glucose by promoting cellular glucose uptake. Injectable insulin types vary by onset/duration: rapid-acting (lispro, 15 min), short-acting (regular, 30 min), intermediate long-acting (glargine, 24h).
Opioids bind to mu (μ), delta (δ), and kappa (κ) opioid receptors in the CNS and periphery. Mu receptors mediate analgesia, euphoria, respiratory depression, and constipation. They inhibit pain signal transmission by reducing neurotransmitter release.
COX-1 is constitutive (always present): protects stomach lining, maintains kidney function, supports platelet aggregation. COX-2 is inducible: produced during inflammation and pain. Non-selective NSAIDs inhibit both; selective COX-2 inhibitors (celecoxib) spare COX-1.
Bioavailability is the fraction of an administered drug that reaches the systemic circulation in active form . IV drugs have 100% bioavailability. Oral drugs have lower bioavailability due to incomplete absorption and first-pass metabolism.
Pharmacology Basics
How do calcium channel blockers work?
A maintenance dose is the regular dose given to maintain the drug concentration at steady state . It equals the amount of drug eliminated per dosing interval. It depends on clearance, bioavailability, and target concentration.
Antiemetics prevent nausea and vomiting . Classes: 5-HT3 antagonists (ondansetron — chemotherapy-induced), D2 antagonists (metoclopramide — also prokinetic), NK1 antagonists (aprepitant), antihistamines (meclizine — motion sickness), cannabinoids (dronabinol).
An enteric-coated tablet has a coating that resists stomach acid but dissolves in the alkaline pH of the small intestine . Used to protect drugs destroyed by stomach acid (e.g., omeprazole), protect the stomach from irritation (e.g., aspirin), or target drug release to the intestine.
CCBs block L-type calcium channels in vascular smooth muscle and cardiac cells . Dihydropyridines (amlodipine, nifedipine): primarily vasodilate. Non-dihydropyridines (verapamil, diltiazem): slow heart rate and reduce contractility. Used for hypertension, angina, arrhythmias.
Pharmacology Basics
What is anaphylaxis?
Phase III trials are large-scale studies (1,000–3,000+ patients) comparing the new drug to standard treatment or placebo . They confirm efficacy, monitor side effects, and collect data for FDA review. These are randomized, controlled, often double-blind studies. ~25–30% of drugs pass Phase III.
Penicillin works by inhibiting bacterial cell wall synthesis . It binds to penicillin-binding proteins (PBPs) and blocks cross-linking of peptidoglycan, weakening the cell wall. The bacteria swell and lyse due to osmotic pressure. It is bactericidal.
Anaphylaxis is a severe, life-threatening allergic reaction involving multiple organ systems : airway swelling, hypotension, urticaria, bronchospasm. Treatment: epinephrine (adrenaline) IM immediately , followed by antihistamines and corticosteroids. Common triggers: penicillin, NSAIDs, latex.
Phase II metabolism involves conjugation reactions that attach a polar molecule (glucuronic acid, sulfate, acetyl, methyl, or glutathione) to the drug or its Phase I metabolite. This makes the compound more water-soluble and easier to excrete via kidneys or bile.
Pharmacology Basics
What is a drug interaction?
AEDs prevent seizures by modulating ion channels, enhancing GABA activity, or reducing glutamate activity . Examples: phenytoin (sodium channels), valproic acid (multiple mechanisms), levetiracetam (SV2A protein), carbamazepine (sodium channels). Many have narrow therapeutic indices.
Potency refers to the amount of drug needed to produce an effect (lower dose = more potent). Efficacy refers to the maximum effect a drug can produce regardless of dose. Efficacy is generally more clinically important than potency.
A drug interaction occurs when one drug affects the activity of another . Types: pharmacokinetic (altered ADME — e.g., CYP inhibition) and pharmacodynamic (additive, synergistic, or antagonistic effects at receptors). Drug interactions can increase toxicity or reduce efficacy.
A generic drug contains the same active ingredient, dose, route, and dosage form as the brand-name drug . It must demonstrate bioequivalence. Generics are typically 80–85% cheaper and are approved after the brand's patent expires (usually 20 years).
Pharmacology Basics
What are antihypertensive drugs?
Drug excretion is the removal of drugs and metabolites from the body . The kidneys are the primary route (via glomerular filtration, tubular secretion, and reabsorption). Other routes: bile/feces, lungs (volatile anesthetics), sweat, saliva, and breast milk.
Tachyphylaxis is a rapid decrease in drug response after repeated doses in a short period . It occurs faster than typical tolerance and may involve receptor desensitization or depletion of neurotransmitter stores. Example: repeated use of nasal decongestant sprays (rebound congestion).
Phase I metabolism involves oxidation, reduction, or hydrolysis reactions that modify the drug molecule. The cytochrome P450 (CYP) enzyme system in the liver is the most important. Key CYP enzymes: CYP3A4 (metabolizes ~50% of drugs), CYP2D6, CYP2C9, CYP2C19, CYP1A2.
Antihypertensives lower blood pressure. Major classes: ACE inhibitors (-pril), ARBs (-sartan), calcium channel blockers (-dipine), beta-blockers (-olol), thiazide diuretics (-thiazide) , alpha-blockers, and direct vasodilators. Treatment choice depends on patient comorbidities.
Pharmacology Basics
What are macrolide antibiotics?
Antifungals target fungal cell components not found in human cells . Classes: azoles (fluconazole — inhibit ergosterol synthesis), polyenes (amphotericin B — bind ergosterol), echinocandins (caspofungin — inhibit cell wall glucan), and allylamines (terbinafine).
Polypharmacy refers to the use of five or more medications simultaneously , common in elderly patients. It increases the risk of drug interactions, adverse effects, medication non-adherence, falls, and cognitive impairment. Regular medication review is essential.
Macrolides (erythromycin, azithromycin, clarithromycin) inhibit bacterial protein synthesis by binding to the 50S ribosomal subunit . They are bacteriostatic and used for respiratory infections, skin infections, and as penicillin alternatives. Common side effect: GI upset.
Pharmacology is the study of drugs and their effects on living organisms . It encompasses how drugs are absorbed, distributed, metabolized, and excreted (pharmacokinetics), as well as how they produce their effects (pharmacodynamics).
Pharmacology Basics
What are antihistamines?
Polypharmacy refers to the use of five or more medications simultaneously , common in elderly patients. It increases the risk of drug interactions, adverse effects, medication non-adherence, falls, and cognitive impairment. Regular medication review is essential.
ADME stands for Absorption, Distribution, Metabolism, and Excretion — the four processes that determine how a drug moves through the body. Together they determine the drug's concentration at the site of action and its duration of effect.
Tachyphylaxis is a rapid decrease in drug response after repeated doses in a short period . It occurs faster than typical tolerance and may involve receptor desensitization or depletion of neurotransmitter stores. Example: repeated use of nasal decongestant sprays (rebound congestion).
Antihistamines block histamine H1 receptors, reducing allergic symptoms (sneezing, itching, runny nose). First generation (diphenhydramine): cross BBB, causing drowsiness. Second generation (cetirizine, loratadine): don't cross BBB significantly, less sedating.
Pharmacology Basics
What is bioequivalence?
An enteric-coated tablet has a coating that resists stomach acid but dissolves in the alkaline pH of the small intestine . Used to protect drugs destroyed by stomach acid (e.g., omeprazole), protect the stomach from irritation (e.g., aspirin), or target drug release to the intestine.
Bioequivalence means that a generic drug has the same rate and extent of absorption as the brand-name drug . The FDA requires generics to be within 80–125% of the brand's bioavailability. This ensures comparable clinical effects.
Mechanism of action (MOA) describes the specific biochemical interaction through which a drug produces its effect . Most drugs work by binding to receptors, enzymes, ion channels, or transport proteins. Understanding MOA helps predict effects, side effects, and interactions.
An antagonist is a drug that binds to a receptor but does not activate it, blocking the action of agonists . Competitive antagonists compete for the same binding site (can be overcome by more agonist). Non-competitive antagonists bind elsewhere and cannot be overcome.
Pharmacology Basics
What are SSRIs?
Routes include: oral (PO), intravenous (IV), intramuscular (IM), subcutaneous (SC), sublingual (SL), transdermal, inhalation, rectal, topical, and intrathecal . Each route has different absorption rates, bioavailability, and clinical applications.
SSRIs (selective serotonin reuptake inhibitors: fluoxetine, sertraline, escitalopram) block serotonin reuptake in the synapse, increasing serotonin availability . First-line treatment for depression and anxiety. Take 4–6 weeks for full effect. Side effects: sexual dysfunction, GI upset, insomnia.
A drug interaction occurs when one drug affects the activity of another . Types: pharmacokinetic (altered ADME — e.g., CYP inhibition) and pharmacodynamic (additive, synergistic, or antagonistic effects at receptors). Drug interactions can increase toxicity or reduce efficacy.
Drug distribution is the process by which a drug moves from the bloodstream to body tissues . Factors: blood flow, drug lipophilicity, protein binding, tissue permeability, and the blood-brain barrier. Highly perfused organs (heart, liver, kidneys) receive drugs first.
Pharmacology Basics
What is metformin?
SSRIs (selective serotonin reuptake inhibitors: fluoxetine, sertraline, escitalopram) block serotonin reuptake in the synapse, increasing serotonin availability . First-line treatment for depression and anxiety. Take 4–6 weeks for full effect. Side effects: sexual dysfunction, GI upset, insomnia.
Polypharmacy refers to the use of five or more medications simultaneously , common in elderly patients. It increases the risk of drug interactions, adverse effects, medication non-adherence, falls, and cognitive impairment. Regular medication review is essential.
Metformin is the first-line oral drug for type 2 diabetes . It reduces hepatic glucose production, increases insulin sensitivity, and decreases intestinal glucose absorption. It does not cause hypoglycemia when used alone. Main side effect: GI upset. Rare but serious: lactic acidosis.
A maintenance dose is the regular dose given to maintain the drug concentration at steady state . It equals the amount of drug eliminated per dosing interval. It depends on clearance, bioavailability, and target concentration.
Pharmacology Basics
What are benzodiazepines?
OTC (over-the-counter) drugs can be purchased without a prescription and are generally considered safe for self-treatment at recommended doses. Prescription drugs require a healthcare provider's authorization due to greater risks, need for monitoring, or potential for abuse.
The placebo effect is a beneficial health outcome from an inert treatment due to the patient's belief in its efficacy . It can involve real physiological changes (endorphin release, dopamine changes). Clinical trials use placebo controls to distinguish true drug effects from placebo responses.
Drug excretion is the removal of drugs and metabolites from the body . The kidneys are the primary route (via glomerular filtration, tubular secretion, and reabsorption). Other routes: bile/feces, lungs (volatile anesthetics), sweat, saliva, and breast milk.
Benzodiazepines (diazepam, lorazepam, alprazolam) enhance GABA-A receptor activity, increasing chloride influx and neuronal inhibition . Used for anxiety, insomnia, seizures, and muscle spasms. Risks: sedation, tolerance, dependence, respiratory depression (especially with opioids).
Pharmacology Basics
What is the difference between bactericidal and bacteriostatic antibiotics?
Bactericidal antibiotics kill bacteria directly (penicillins, cephalosporins, fluoroquinolones, aminoglycosides). Bacteriostatic antibiotics inhibit growth, relying on the immune system to clear infection (tetracyclines, macrolides, sulfonamides). The distinction matters in immunocompromised patients.
Benzodiazepines (diazepam, lorazepam, alprazolam) enhance GABA-A receptor activity, increasing chloride influx and neuronal inhibition . Used for anxiety, insomnia, seizures, and muscle spasms. Risks: sedation, tolerance, dependence, respiratory depression (especially with opioids).
IV administration delivers drugs directly into the bloodstream , providing 100% bioavailability and immediate effect. It is used for emergencies, drugs with poor oral absorption, precise dosing, and when rapid onset is needed. Disadvantages: infection risk, cannot be easily reversed.
A side effect is any effect other than the intended one (can be positive or negative). An adverse effect is specifically a harmful, undesired effect. Example: drowsiness from an antihistamine is a side effect; severe liver damage from acetaminophen overdose is an adverse effect.
Pharmacology Basics
What are antipsychotic drugs?
Phase IV surveillance monitors drug safety after FDA approval in the general population . It detects rare adverse effects not seen in clinical trials, evaluates long-term effects, and can lead to black box warnings, restricted use, or withdrawal from the market.
Pharmacology is the study of drugs and their effects on living organisms . It encompasses how drugs are absorbed, distributed, metabolized, and excreted (pharmacokinetics), as well as how they produce their effects (pharmacodynamics).
Drug allergies are immune-mediated reactions to medications . Type I (immediate/anaphylaxis): IgE-mediated, occurs within minutes (penicillin allergy). Type IV (delayed): T-cell mediated, occurs after days (drug rash). True allergies require prior sensitization and are distinct from side effects.
Antipsychotics treat schizophrenia and psychotic disorders . First generation/typical (haloperidol): block D2 receptors, risk of extrapyramidal side effects. Second generation/atypical (risperidone, olanzapine, quetiapine): block D2 and 5-HT2A, fewer movement side effects but metabolic risks.
Pharmacology Basics
What are anticoagulants?
Mechanism of action (MOA) describes the specific biochemical interaction through which a drug produces its effect . Most drugs work by binding to receptors, enzymes, ion channels, or transport proteins. Understanding MOA helps predict effects, side effects, and interactions.
COX-1 is constitutive (always present): protects stomach lining, maintains kidney function, supports platelet aggregation. COX-2 is inducible: produced during inflammation and pain. Non-selective NSAIDs inhibit both; selective COX-2 inhibitors (celecoxib) spare COX-1.
The therapeutic index (TI) is the ratio of the toxic dose to the therapeutic dose : TI = TD50/ED50. A narrow therapeutic index means there is a small margin between effective and toxic doses (e.g., warfarin, lithium, digoxin). These drugs require careful monitoring.
Anticoagulants prevent blood clot formation by interfering with the coagulation cascade . Examples: warfarin (blocks vitamin K), heparin (activates antithrombin III), DOACs (rivaroxaban, apixaban — directly inhibit factor Xa or thrombin). Used for DVT, PE, atrial fibrillation.
Pharmacology Basics
What is the dose-response curve?
SSRIs (selective serotonin reuptake inhibitors: fluoxetine, sertraline, escitalopram) block serotonin reuptake in the synapse, increasing serotonin availability . First-line treatment for depression and anxiety. Take 4–6 weeks for full effect. Side effects: sexual dysfunction, GI upset, insomnia.
Antihistamines block histamine H1 receptors, reducing allergic symptoms (sneezing, itching, runny nose). First generation (diphenhydramine): cross BBB, causing drowsiness. Second generation (cetirizine, loratadine): don't cross BBB significantly, less sedating.
The FDA (Food and Drug Administration) regulates the development, approval, manufacturing, and marketing of drugs in the United States. It ensures drugs are safe and effective through clinical trial oversight, facility inspections, and post-marketing surveillance. It also manages drug labeling and recalls.
A dose-response curve plots drug dose (x-axis) against the magnitude of response (y-axis) . Key parameters: potency (position on x-axis — how much drug is needed), efficacy (maximum response achievable), ED50 (dose for 50% effect).
Pharmacology Basics
What are the phases of drug development?
Antidepressant classes: SSRIs (fluoxetine — first-line), SNRIs (venlafaxine — serotonin + norepinephrine), TCAs (amitriptyline — older, more side effects), MAOIs (phenelzine — dietary restrictions), atypical (bupropion, mirtazapine). All take 4–6 weeks for full effect.
Pharmacokinetics (PK): what the body does to the drug (ADME: absorption, distribution, metabolism, excretion). Pharmacodynamics (PD): what the drug does to the body (mechanism of action, effects, dose-response relationships).
Bronchodilators relax airway smooth muscle to open the airways . Types: short-acting beta-2 agonists (SABA) like albuterol (rescue), long-acting beta-2 agonists (LABA) like salmeterol (maintenance), and anticholinergics like ipratropium. Used for asthma and COPD.
Drug development: Preclinical (lab/animal testing) → Phase I (safety in 20–100 healthy volunteers) → Phase II (efficacy in 100–300 patients) → Phase III (large-scale efficacy in 1000–3000 patients) → FDA approval → Phase IV (post-marketing surveillance).
Pharmacology Basics
What are the main routes of drug administration?
AEDs prevent seizures by modulating ion channels, enhancing GABA activity, or reducing glutamate activity . Examples: phenytoin (sodium channels), valproic acid (multiple mechanisms), levetiracetam (SV2A protein), carbamazepine (sodium channels). Many have narrow therapeutic indices.
The CYP450 system is a family of liver enzymes responsible for metabolizing the majority of drugs . CYP3A4 is the most abundant and metabolizes ~50% of all drugs. CYP enzyme activity varies between individuals due to genetics, age, and drug interactions (induction/inhibition).
Steady state is achieved when the rate of drug administration equals the rate of elimination , resulting in consistent plasma concentrations. It takes approximately 4–5 half-lives to reach steady state with repeated dosing.
Routes include: oral (PO), intravenous (IV), intramuscular (IM), subcutaneous (SC), sublingual (SL), transdermal, inhalation, rectal, topical, and intrathecal . Each route has different absorption rates, bioavailability, and clinical applications.
Pharmacology Basics
What is half-life (t½)?
Diuretics increase urine output by promoting sodium and water excretion from the kidneys . Types: loop diuretics (furosemide — most potent), thiazides (hydrochlorothiazide — mild), potassium-sparing (spironolactone — aldosterone antagonist). Used for hypertension, heart failure, edema.
Half-life is the time required for the plasma concentration of a drug to decrease by 50% . It determines dosing frequency. After ~4–5 half-lives, a drug reaches steady state (with repeated dosing) or is essentially eliminated (after discontinuation).
Bactericidal antibiotics kill bacteria directly (penicillins, cephalosporins, fluoroquinolones, aminoglycosides). Bacteriostatic antibiotics inhibit growth, relying on the immune system to clear infection (tetracyclines, macrolides, sulfonamides). The distinction matters in immunocompromised patients.
Common opioid side effects: constipation (most common, doesn't resolve with tolerance), respiratory depression (most dangerous), nausea/vomiting, sedation, pruritus (itching), urinary retention, miosis (pinpoint pupils) , and physical dependence/addiction risk.
Pharmacology Basics
What are antiepileptic drugs (AEDs)?
TDM involves measuring drug blood levels to maintain concentrations within the therapeutic range . It is essential for narrow therapeutic index drugs (warfarin, lithium, phenytoin, digoxin, aminoglycosides, vancomycin). It guides dose adjustments to maximize efficacy and minimize toxicity.
Antihypertensives lower blood pressure. Major classes: ACE inhibitors (-pril), ARBs (-sartan), calcium channel blockers (-dipine), beta-blockers (-olol), thiazide diuretics (-thiazide) , alpha-blockers, and direct vasodilators. Treatment choice depends on patient comorbidities.
AEDs prevent seizures by modulating ion channels, enhancing GABA activity, or reducing glutamate activity . Examples: phenytoin (sodium channels), valproic acid (multiple mechanisms), levetiracetam (SV2A protein), carbamazepine (sodium channels). Many have narrow therapeutic indices.
Antihistamines block histamine H1 receptors, reducing allergic symptoms (sneezing, itching, runny nose). First generation (diphenhydramine): cross BBB, causing drowsiness. Second generation (cetirizine, loratadine): don't cross BBB significantly, less sedating.
Pharmacology Basics
How does acetaminophen (paracetamol) work?
The placebo effect is a beneficial health outcome from an inert treatment due to the patient's belief in its efficacy . It can involve real physiological changes (endorphin release, dopamine changes). Clinical trials use placebo controls to distinguish true drug effects from placebo responses.
Acetaminophen's exact mechanism is not fully understood . It likely inhibits COX enzymes in the CNS (reducing pain and fever) but has minimal peripheral anti-inflammatory activity. It does not cause GI irritation. Hepatotoxicity at doses >4 g/day is the major risk.
Corticosteroids (prednisone, dexamethasone, hydrocortisone) are synthetic analogs of cortisol with potent anti-inflammatory and immunosuppressive properties . They inhibit phospholipase A2 and NF-κB pathways. Used for asthma, autoimmune diseases, allergies. Long-term risks: osteoporosis, diabetes, adrenal suppression.
Fluoroquinolones (ciprofloxacin, levofloxacin) inhibit bacterial DNA gyrase and topoisomerase IV , preventing DNA replication. They are broad-spectrum and bactericidal. Used for UTIs, respiratory infections. Side effects include tendon rupture and QT prolongation.