INI CET Pharmacology Flashcards

24 sample cards from the Pharmacology deck

Sampled from the end of the deck, so these are different cards from the ones shown on the syllabus page.

1. What is serotonin syndrome and its key features?

   Serotonin syndrome results from excess serotonergic activity (e.g., SSRI + MAOI). Triad: neuromuscular excitation (clonus, hyperreflexia), autonomic instability (hyperthermia, tachycardia), and altered mental status. Treat with cyproheptadine and supportive care.

2. Why must MAOIs be combined cautiously, and what is the tyramine reaction?

   MAOIs with tyramine-rich foods (aged cheese, wine) cause a hypertensive crisis because unmetabolized tyramine releases stored catecholamines. MAOIs also risk serotonin syndrome with serotonergic drugs.

3. What is the mechanism of NSAIDs and the difference between COX-1 and COX-2 inhibition?

   NSAIDs inhibit cyclooxygenase, reducing prostaglandin synthesis (analgesia, anti-inflammatory, antipyretic). COX-1 is constitutive (gastric protection, platelets); COX-2 is inducible (inflammation). Selective COX-2 inhibitors (celecoxib) spare the GI tract but increase cardiovascular risk.

4. What is the mechanism and antidote for acetaminophen (paracetamol) overdose?

   Overdose depletes glutathione, allowing toxic NAPQI to accumulate and cause hepatocellular necrosis. Antidote: N-acetylcysteine, which replenishes glutathione.

5. What is the mechanism of opioid analgesics and how is overdose treated?

   Opioids agonize mu (and kappa/delta) receptors (Gi-coupled), inhibiting pain transmission. Overdose causes the triad of CNS depression, respiratory depression, and miosis (pinpoint pupils). Antidote: naloxone (opioid antagonist).

6. What is the mechanism of buspirone and why is it preferred for chronic anxiety?

   Buspirone is a 5-HT1A partial agonist. It lacks sedation, dependence, and abuse potential and does not potentiate alcohol, but has a slow onset (1-2 weeks), so it is not for acute anxiety.

7. State the formulas for cardiac output, mean arterial pressure, and stroke volume.

   Cardiac Output (CO) = Heart Rate x Stroke Volume. Mean Arterial Pressure (MAP) = CO x Total Peripheral Resistance; MAP = DBP + 1/3(Pulse Pressure). Stroke Volume = End-Diastolic Volume - End-Systolic Volume.

8. Describe the cardiac action potential phases and the ion movements.

   Phase 0: rapid depolarization (Na+ influx). Phase 1: early repolarization (transient K+ out, Na+ closes). Phase 2: plateau (Ca2+ influx balances K+ efflux). Phase 3: repolarization (K+ efflux). Phase 4: resting potential (K+); pacemakers have funny Na+ current.

9. Classify antiarrhythmic drugs (Vaughan-Williams) with the target of each class.

   Class I: Na+ channel blockers (Ia quinidine, Ib lidocaine, Ic flecainide). Class II: beta-blockers. Class III: K+ channel blockers (amiodarone, sotalol). Class IV: Ca2+ channel blockers (verapamil, diltiazem).

10. How does the RAAS regulate blood pressure?

    Low BP/Na+ stimulates renin (from juxtaglomerular cells), which converts angiotensinogen to angiotensin I; ACE converts it to angiotensin II (vasoconstriction, aldosterone release causing Na+/water retention), raising BP. ADH also contributes.

11. What is the mechanism of thyroid hormone synthesis and where do antithyroid drugs act?

    Iodide is trapped, oxidized by thyroid peroxidase, organified onto thyroglobulin, and coupled to form T3/T4. Thioamides (propylthiouracil, methimazole) inhibit thyroid peroxidase; PTU also blocks peripheral T4-to-T3 conversion.

12. What are the major effects and adverse effects of glucocorticoids?

    Glucocorticoids are anti-inflammatory/immunosuppressive (inhibit phospholipase A2 via lipocortin, decrease cytokines). Adverse effects: Cushingoid features, osteoporosis, hyperglycemia, immunosuppression, adrenal suppression, peptic ulcers, and mood changes.

13. Compare the mechanisms of sulfonylureas, biguanides (metformin), and DPP-4 inhibitors.

    Sulfonylureas (glipizide) close K-ATP channels to stimulate insulin secretion (risk: hypoglycemia). Metformin decreases hepatic gluconeogenesis and increases insulin sensitivity (no hypoglycemia; risk: lactic acidosis). DPP-4 inhibitors (-gliptins) increase incretin (GLP-1) levels.

14. Differentiate rapid, short, intermediate, and long-acting insulin preparations.

    Rapid-acting: lispro, aspart, glulisine (onset ~15 min). Short-acting: regular insulin. Intermediate: NPH. Long-acting: glargine, detemir, degludec (peakless, basal coverage).

15. What are the principles of antimicrobial therapy regarding bactericidal vs bacteriostatic and concentration vs time-dependent killing?

    Bactericidal drugs kill bacteria (beta-lactams, aminoglycosides, fluoroquinolones); bacteriostatic inhibit growth (tetracyclines, macrolides, sulfonamides). Concentration-dependent killing: aminoglycosides, fluoroquinolones. Time-dependent: beta-lactams, vancomycin.

16. List the main mechanisms of antibiotic action by drug class.

    Cell wall synthesis: beta-lactams, vancomycin. Protein synthesis (30S): aminoglycosides, tetracyclines; (50S): macrolides, clindamycin, chloramphenicol, linezolid. DNA gyrase: fluoroquinolones. Folate synthesis: sulfonamides, trimethoprim. RNA polymerase: rifampin.

17. What are the main mechanisms of antimicrobial resistance?

    Enzymatic drug inactivation (beta-lactamases, aminoglycoside-modifying enzymes), target modification (altered PBPs in MRSA, ribosomal methylation), decreased uptake/increased efflux pumps, and bypass of metabolic pathways. Resistance spreads via plasmids/transposons.

18. What cell-cycle concept underlies cancer chemotherapy, and how do cell-cycle specific vs non-specific drugs differ?

    Tumor cells are killed by first-order (log) kill kinetics. Cell-cycle-specific drugs act on a particular phase (e.g., antimetabolites in S phase, vinca alkaloids/taxanes in M phase). Cell-cycle-non-specific drugs (alkylating agents, anthracyclines) act in any phase, including G0.

19. Match these anticancer drugs to mechanism: methotrexate, vincristine, cisplatin, doxorubicin, 5-fluorouracil.

    Methotrexate: dihydrofolate reductase inhibitor (antimetabolite). Vincristine: inhibits microtubule assembly (M phase). Cisplatin: crosslinks DNA (alkylating-like). Doxorubicin: intercalates DNA and inhibits topoisomerase II (cardiotoxic). 5-FU: thymidylate synthase inhibitor.

20. Give examples of hormonal therapy for breast and prostate cancer.

    Breast cancer (ER-positive): tamoxifen (SERM), aromatase inhibitors (anastrozole, letrozole). Prostate cancer: GnRH agonists (leuprolide), GnRH antagonists, anti-androgens (flutamide, bicalutamide).

21. What are the principal mechanisms of cellular toxicity (mechanisms of toxicity)?

    Oxidative stress (reactive oxygen species/free radicals), covalent binding to macromolecules, lipid peroxidation, depletion of glutathione/ATP, disruption of calcium homeostasis, mitochondrial dysfunction, and immune-mediated injury leading to apoptosis or necrosis.

22. What factors affect the toxicity of a substance?

    Dose and duration of exposure, route of exposure, the chemical's properties, age, sex, genetics (pharmacogenetics), nutritional/health status, presence of other chemicals (additive/synergistic interactions), and species differences.

23. What is toxicokinetics and how does it differ from pharmacokinetics?

    Toxicokinetics applies pharmacokinetic principles (ADME) to toxic exposure levels, often where elimination becomes saturated (zero-order) and metabolism may generate reactive metabolites. It quantifies systemic exposure to relate dose to toxic effect in safety assessment.

24. What is the difference between additive, synergistic, and antagonistic drug interactions?

    Additive: combined effect equals the sum (1+1=2). Synergistic/potentiation: combined effect greater than the sum (1+1>2). Antagonistic: one drug reduces or blocks the effect of another (1+1<2), used therapeutically in antidotes.

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