Title: Pharmacology Basics — LearnCoachAssist

Q: What is pharmacology?
A: 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).

Q: What is the difference between pharmacokinetics and pharmacodynamics?
A: 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).

Q: What is ADME?
A: 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.

Q: What is drug absorption?
A: 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.

Q: What is bioavailability?
A: 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.

Q: What is the first-pass effect?
A: 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.

Q: What are the main routes of drug administration?
A: 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.

Q: Why is the intravenous route used?
A: 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.

Q: What is drug distribution?
A: 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.

Q: What is protein binding?
A: Protein binding is when drugs bind to plasma proteins (mainly albumin) in the blood. Only the unbound (free) fraction is pharmacologically active. Highly protein-bound drugs (>90%) have a smaller free fraction. Drug interactions can occur when two drugs compete for binding sites.

Q: What is the volume of distribution (Vd)?
A: 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.

Q: What is drug metabolism (biotransformation)?
A: 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).

Q: What is Phase I metabolism?
A: 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.

Q: What is Phase II metabolism?
A: 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.

Q: What is the cytochrome P450 system?
A: 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).

Q: What is a CYP enzyme inducer?
A: 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.

Q: What is a CYP enzyme inhibitor?
A: 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.

Q: What is drug excretion?
A: 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.

Q: What is half-life (t½)?
A: 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).

Q: What is steady state?
A: 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.

Q: What is a loading dose?
A: 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).

Q: What is a maintenance dose?
A: 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.

Q: What is the therapeutic index?
A: 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.

Q: What is the dose-response curve?
A: 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).

Q: What is the difference between potency and efficacy?
A: 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.

Q: What is an agonist?
A: 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.

Q: What is an antagonist?
A: 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.

Q: What is a partial agonist?
A: 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.

Q: What are antibiotics?
A: Antibiotics are drugs that kill bacteria (bactericidal) or inhibit their growth (bacteriostatic). Major classes: penicillins, cephalosporins, macrolides, fluoroquinolones, tetracyclines, aminoglycosides, and sulfonamides. They target bacterial structures not found in human cells.

Q: What is the mechanism of penicillin?
A: 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.

Q: What is antibiotic resistance?
A: Antibiotic resistance occurs when bacteria evolve mechanisms to survive antibiotic exposure. Mechanisms include: enzyme production (beta-lactamase destroys penicillin), altered target sites, efflux pumps, and decreased permeability. Caused by overuse/misuse of antibiotics.

Q: What are cephalosporins?
A: Cephalosporins are beta-lactam antibiotics related to penicillins that inhibit cell wall synthesis. They are categorized by generations: 1st gen (cephalexin — gram-positive), 2nd gen (cefuroxime), 3rd gen (ceftriaxone — gram-negative), 4th gen (cefepime — broad).

Q: What are macrolide antibiotics?
A: 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.

Q: What are fluoroquinolones?
A: 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.

Q: What are analgesics?
A: Analgesics are pain-relieving drugs. Two main categories: non-opioid (NSAIDs like ibuprofen, acetaminophen) for mild-moderate pain, and opioid (morphine, codeine, oxycodone) for moderate-severe pain. They work through different mechanisms.

Q: How do NSAIDs work?
A: 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.

Q: What is the difference between COX-1 and COX-2?
A: 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.

Q: How does acetaminophen (paracetamol) work?
A: 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.

Q: How do opioids work?
A: 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.

Q: What are the side effects of opioids?
A: 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.

Q: What is naloxone?
A: 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.

Q: What are antihypertensive drugs?
A: 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.

Q: How do ACE inhibitors work?
A: ACE inhibitors (lisinopril, enalapril, ramipril) block angiotensin-converting enzyme, preventing conversion of angiotensin I to angiotensin II. This reduces vasoconstriction and aldosterone secretion, lowering blood pressure. Side effects: dry cough, hyperkalemia, angioedema (rare).

Q: How do ARBs work?
A: 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.

Q: How do beta-blockers work?
A: 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.

Q: How do calcium channel blockers work?
A: 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.

Q: How do thiazide diuretics work?
A: 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.

Q: What are statins?
A: 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.

Q: What are anticoagulants?
A: 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.

Q: How does warfarin work?
A: 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).

Q: What are proton pump inhibitors (PPIs)?
A: PPIs (omeprazole, esomeprazole, pantoprazole) irreversibly inhibit the H+/K+ ATPase proton pump in gastric parietal cells, reducing stomach acid production by up to 90%. Used for GERD, peptic ulcers, and H. pylori treatment. Long-term risks: bone fractures, vitamin B12 deficiency.

Q: What are SSRIs?
A: 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.

Q: What are benzodiazepines?
A: 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).

Q: What is a drug interaction?
A: 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.

Q: What is a synergistic drug interaction?
A: Synergism occurs when two drugs together produce an effect greater than the sum of their individual effects (1 + 1 > 2). Example: trimethoprim + sulfamethoxazole (co-trimoxazole) — both inhibit different steps in bacterial folate synthesis, producing superior antibacterial activity.

Q: What is an antagonistic drug interaction?
A: Antagonism occurs when one drug reduces or blocks the effect of another. Example: naloxone antagonizes morphine by competing for opioid receptors. Can be useful therapeutically (antidotes) or harmful (unintended reduction of drug efficacy).

Q: What is an adverse drug reaction (ADR)?
A: 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).

Q: What is a side effect vs an adverse effect?
A: 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.

Q: What is drug tolerance?
A: 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.

Q: What is drug dependence?
A: 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.

Q: What are the main dosage forms?
A: 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.

Q: What is the difference between a tablet and a capsule?
A: 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.

Q: What is an enteric-coated tablet?
A: 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.

Q: What is a sustained-release formulation?
A: Sustained-release (extended-release, SR, XR, ER) formulations are designed to release drug slowly over an extended period, reducing dosing frequency and maintaining stable blood levels. They should never be crushed or chewed as this can release the entire dose at once (dose dumping).

Q: What is OTC vs prescription drugs?
A: 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.

Q: What are controlled substances?
A: 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).

Q: What is a generic drug?
A: 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).

Q: What is bioequivalence?
A: 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.

Q: What are the phases of drug development?
A: 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).

Q: What is a Phase I clinical trial?
A: 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.

Q: What is a Phase III clinical trial?
A: 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.

Q: What is post-marketing surveillance (Phase IV)?
A: 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.

Q: What are corticosteroids?
A: 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.

Q: What are antihistamines?
A: 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.

Q: What are bronchodilators?
A: 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.

Q: What is metformin?
A: 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.

Q: What is insulin?
A: 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 (NPH), long-acting (glargine, 24h).

Q: What are antiepileptic drugs (AEDs)?
A: 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.

Q: What is the mechanism of aspirin?
A: 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.

Q: What are antifungal drugs?
A: 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).

Q: What are antiviral drugs?
A: 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.

Q: What are the main classes of antidepressants?
A: 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.

Q: What are antipsychotic drugs?
A: 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.

Q: What is a black box warning?
A: 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.

Q: What is the placebo effect?
A: 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.

Q: What is polypharmacy?
A: 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.

Q: What is a prodrug?
A: 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.

Q: What is pharmacogenomics?
A: 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.

Q: What are drug allergies?
A: 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.

Q: What is anaphylaxis?
A: 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.

Q: What are diuretics?
A: 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.

Q: What is the difference between bactericidal and bacteriostatic antibiotics?
A: 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.

Q: What is a drug's mechanism of action?
A: 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.

Q: What are the common drug suffixes and their drug classes?
A: Common suffixes: -olol (beta-blockers), -pril (ACE inhibitors), -sartan (ARBs), -statin (HMG-CoA reductase inhibitors), -prazole (PPIs), -dipine (CCBs), -cillin (penicillins), -mycin/-micin (macrolides/aminoglycosides), -azole (antifungals).

Q: What is the role of the FDA?
A: 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.

Q: What are laxatives and their types?
A: 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.

Q: What is the difference between narrow and wide therapeutic index drugs?
A: 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.

Q: What is tachyphylaxis?
A: 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).

Q: What are antiemetic drugs?
A: 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).

Q: What is the role of therapeutic drug monitoring (TDM)?
A: 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.