NURS 5334-PHARM: Advanced Pharmacology Study Guide

NURS 5334-PHARM: Advanced Pharmacology Study Guide Unit 1: Foundational Principles of Pharmacology 1. Define pharmacokinetics and list its four primary processes. ANSWER Pharmacokinetics is what the body does to a drug. Its four primary processes are Absorption, Distribution, Metabolism, and Excretion (ADME). 2. What is the first-pass effect, and how does it affect oral drug bioavailability? ANSWER The first-pass effect is the extensive hepatic metabolism of a drug before it reaches systemic circulation. It significantly reduces the bioavailability of orally administered drugs, often requiring higher oral doses or alternative routes. 3. Differentiate between a drug's potency and its efficacy. ANSWER Potency refers to the amount of drug needed to produce a given effect (e.g., a lower ED50 means higher potency). Efficacy refers to the maximum therapeutic response a drug can produce, regardless of dose. 4. Explain the concept of therapeutic index (TI) and its clinical significance. ANSWER The Therapeutic Index (TI) is the ratio of a drug's toxic dose (TD50 or LD50) to its effective dose (ED50). A low TI (e.g., digoxin, warfarin) indicates a narrow margin of safety, requiring close monitoring. A high TI (e.g., penicillin) is generally safer. 5. What is the role of cytochrome P450 enzymes in drug metabolism, and why are genetic polymorphisms important? ANSWER Cytochrome P450 (CYP) enzymes are the major catalysts for Phase I drug metabolism. Genetic polymorphisms can create "poor metabolizers" or "ultra-rapid metabolizers," leading to dangerously high or subtherapeutic drug levels, respectively, with standard dosing. Unit 2: Autonomic and Cardiovascular Pharmacology 6. A patient prescribed a non-selective beta-blocker (propranolol) for hypertension must be cautioned about which acute side effect if they have a history of asthma? ANSWER They must be cautioned about bronchoconstriction. Non-selective betablockers inhibit β2-receptors in the lungs, which can precipitate severe asthma attacks. 7. What is the mechanism of action and primary use of ACE inhibitors (e.g., lisinopril)? ANSWER ACE inhibitors block the conversion of angiotensin I to angiotensin II, reducing vasoconstriction and aldosterone secretion. They are first-line for hypertension, heart failure, and diabetic nephropathy. 8. Why is monitoring for a persistent dry cough important in patients on ACE inhibitors? ANSWER A dry cough is a common side effect (up to 20% of patients) due to accumulation of bradykinin. While not dangerous, it often necessitates switching to an ARB (Angiotensin II Receptor Blocker). 9. Describe the "dihydropyridine" vs. "non-dihydropyridine" classification of calcium channel blockers and their differing primary uses. ANSWER Dihydropyridines (e.g., amlodipine, nifedipine) act primarily on vascular smooth muscle, causing vasodilation; used for hypertension. Non-dihydropyridines (e.g., diltiazem, verapamil) act on the heart and vessels, slowing AV conduction; used for arrhythmias and angina. 10. What is the mechanism of action of spironolactone, and why must serum potassium be monitored? ANSWER Spironolactone is a potassium-sparing diuretic that acts as an aldosterone antagonist in the distal tubule. It reduces sodium reabsorption while inhibiting potassium excretion, posing a significant risk for hyperkalemia. 11. What is the primary life-threatening toxicity of digoxin, and what are its early symptoms? ANSWER The primary toxicity is lethal arrhythmias. Early symptoms include anorexia, nausea, vomiting, confusion, and visual disturbances (yellow/green halos). 12. When initiating statin therapy (e.g., atorvastatin), what two baseline labs are essential, and what is the primary patient education point regarding side effects? ANSWER Obtain baseline liver function tests (LFTs) and a lipid panel. Educate the patient to report unexplained muscle pain, tenderness, or weakness immediately, as this could indicate myopathy/rhabdomyolysis. Unit 3: Central Nervous System Pharmacology 13. Differentiate between the mechanism of action of SSRIs (e.g., sertraline) and SNRIs (e.g., venlafaxine). ANSWER SSRIs selectively inhibit the reuptake of serotonin. SNRIs inhibit the reuptake of both serotonin and norepinephrine, which may provide broader efficacy for some patients. 14. What is "black box warning" associated with all antidepressants in children, adolescents, and young adults? ANSWER Antidepressants carry a black box warning for an increased risk of suicidal thinking and behavior (suicidality) in patients aged 24 and younger, especially during the initial weeks of treatment. 15. Why must MAOIs (e.g., phenelzine) not be combined with SSRIs or foods high in tyramine? ANSWER MAOIs irreversibly inhibit monoamine oxidase. Combining them with serotonergic drugs can cause serotonin syndrome. Combining them with tyramine-rich foods (aged cheeses, cured meats) can cause a hypertensive crisis due to potent vasoconstriction. 16. Describe the mechanism of benzodiazepines (e.g., lorazepam) and the critical safety consideration for long-term use. ANSWER Benzodiazepines potentiate the effect of GABA, the brain's main inhibitory neurotransmitter. Long-term use leads to tolerance, dependence, and a severe, potentially life-threatening withdrawal syndrome. 17. What is the primary advantage of second-generation ("atypical") antipsychotics (e.g., risperidone) over first-generation agents? ANSWER They have a significantly lower risk of causing extrapyramidal symptoms (EPS) like dystonia and tardive dyskinesia. However, they carry a higher metabolic risk (weight gain, diabetes, dyslipidemia). 18. What is the "opioid triad" of toxicity, and what is the specific antidote? ANSWER The opioid toxicity triad is: 1) Pinpoint pupils (miosis), 2) Respiratory depression, 3) Unconsciousness (coma). The specific antidote is naloxone. 19. For a patient with neuropathic pain, why might an antidepressant (e.g., duloxetine) or an anticonvulsant (e.g., gabapentin) be preferred over a traditional opioid? ANSWER Neuropathic pain involves aberrant signaling in the nervous system. Duloxetine (SNRI) and gabapentin (alpha-2-delta ligand) modulate this specific pain signaling pathway more effectively and with fewer risks (e.g., addiction, tolerance) than opioids, which are generally less effective for pure neuropathic pain. Unit 4: Endocrine and Antimicrobial Pharmacology 20. Describe the stepwise pharmacologic management for Type 2 Diabetes, per current guidelines. ANSWER First line is lifestyle modification + metformin. Second line involves adding an agent based on patient comorbidities: SGLT2 inhibitor (e.g., empagliflozin) for heart/kidney disease, or GLP-1 agonist (e.g., semaglutide) for cardiovascular benefit/weight loss. Insulin is added if goals are not met.