Summary NURS 330 Pharmacology Final Exam Blueprint | Complete 100% updated 2025/26.

NURS 330 Pharmacology Final Exam Blueprint | Complete 100% updated 2025/26. HTN BP classification, when to initiate pharmacotherapy, BP targets ● BP Classification ○ Normal: Systolic BP (SBP) 120 mmHg and Diastolic BP (DBP) 80 mmHg ○ Elevated (Prehypertension): SBP 120–129 mmHg and DBP 80 mmHg ○ Hypertension Stage 1: SBP 130–139 mmHg or DBP 80–89 mmHg ○ Hypertension Stage 2: SBP ≥ 140 mmHg or DBP ≥ 90 mmHg ○ Hypertensive Crisis: SBP 180 mmHg or DBP 120 mmHg ● When to Initiate Pharmacotherapy ○ Expect the Question to Ask: ■ A 45 year old patient has a BP of 135/88 mmHg with CKD. Would you initiate hypertension pharmacotherapy? → YES ■ A 48 year old patient presents with BP of 137/86, no comorbidities, and ASCVD risk is 10%. Would you initiate pharmacotherapy? → NO ○ Stage 1 Hypertension: If history of cardiovascular disease, has a 10-year atherosclerotic cardiovascular disease risk of 10% or more, or falls into one of the special populations (DM, CKD, age 65 or older). Otherwise, lifestyle modifications first. Begin with 1 pharmaceutical agent ○ Stage 2 Hypertension: Pharmacotherapy is generally started immediately. Begin with 2 pharmaceutical agents ○ High-Risk Populations: Patients with diabetes, chronic kidney disease, or heart failure. ● BP Targets 130/80 mmHg for most adults, especially those with diabetes or CKD. Compelling indications & appropriate drugs for each - Monotherapy Appropriate for Stage 1 Hypertension: - ACE-inhibitors & ARBs → first line therapy - ACEI → “-pril” → lisinopril, enalapril, ramipril - ARB → “-sartan” → valsartan, losartan, olmesartan - CCBs - CCB → “-dipine” → amlodipine, nifedipine - ***verapamil and diltiazem are also CCBs, but they are nondihydropyridines*** - Thiazides - Thiazides → “-thiazide” → hydrochlorothiazide, chlorothiazide - Algorithm for Compelling Indications: - HTN & HF or Stable Ischemic Heart Disease (e.g. heart attack or angina) → ACE-inhibitor & beta blocker - HTN & DM or CKD → ACEs & ARBs - HTN & stroke → ACE-inhibitors & thiazides - Expect the Question to Ask: Patient presents with stage 1 hypertension & HF with preserved ejection fraction. What is the most appropriate first line treatment? - CCBs - Thiazides - Beta blockers w ACE - Spironolactone 1. Heart Failure: Preferred: ACEIs, ARBs, Beta-blockers, Diuretics 2. CKD: ACEIs or ARBs→ reduce proteinuria and prevent progression of kidney damage. 3. Post-myocardial infarction: Beta-blockers, ACEIs/ARBs, Aldosterone antagonists. 4. Stroke Prevention: Thiazide diuretics, ACEIs, or a combination of both. 5. Diabetes Mellitus: ACEIs or ARBs to protect kidney function. ACE inhibitors: Drugs, mechanism of action, ADE ● Examples: Lisinopril, Enalapril, Ramipril, Captopril ● Mechanism of Action: Inhibit angiotensin-converting enzyme, which prevents the conversion of angiotensin I to angiotensin II. ○ Angiotensin II is a potent vasoconstrictor, and its inhibition leads to vasodilation, reduced aldosterone release, and decreased blood pressure. ○ Less water retention (d/t reduced aldosterone release) ● Adverse Drug Effects (ADE): ○ Cough (due to increased bradykinin) ○ Hyperkalemia (due to reduced aldosterone) ○ Angioedema (rare but severe) ○ Hypotension (especially after the first dose) ○ Renal impairment (monitor renal function) ● Notes from the Review: ○ Contraindicated in pregnancy & renal artery stenosis (can cause CKD) ○ Monitor serum K Calcium Channel Blockers: Drugs & mechanism of action ● Dihydropyridines: Amlodipine, Nifedipine ● Non-dihydropyridines: Verapamil, Diltiazem ● Mechanism of Action: ○ Dihydropyridines: Block calcium channels in vascular & arterial smooth muscle, causing vasodilation and reduced blood pressure; works in peripheral vessels ■ Primarily cause vasodilation, thus are more useful in hypertension. ■ Risk for edema ○ Non-dihydropyridines: In addition to vasodilation, these drugs also inhibit calcium influx in the heart, reducing heart rate and contractility, which can be useful for arrhythmias and angina; works in both peripheral vessels and myocardial tissues ■ Used in hypertension, angina, and arrhythmias (e.g., atrial fibrillation, rapid ventricular response). ■ Risk for bradycardia (can cause AV node block) Thiazide diuretics vs. loop diuretics (moa, side effects, electrolyte disruptions) ● Thiazide Diuretics: ○ Drugs: Hydrochlorothiazide (HCTZ), Chlorthalidone, Indapamide ○ Mechanism of Action: Inhibit sodium reabsorption in the distal convoluted tubule, leading to water excretion and decreased blood volume. ■ Reduced fluid volume → decrease in BP ○ Electrolyte Disruptions: HypOkalemia, HypOnatremia, HypERcalcemia, HypERglycemia ○ Side Effects: Dizziness, weakness, muscle cramps (due to potassium loss) ● Loop Diuretics: ○ Drugs: Furosemide, Bumetanide, Torsemide ○ Mechanism of Action: Inhibit sodium and chloride reabsorption in the loop of Henle, leading to significant diuresis. ○ Electrolyte Disruptions: HypOkalemia, HypOnatremia, HypOcalcemia, HypOmagnesemia ○ Side Effects: Dehydration, Ototoxicity (especially at high doses), Hypotension ● Notes from the Review: ○ Know the differentiating sites (DCT vs Loop of Henle) ○ Both can cause hypOkalemia ○ Thiazides are usually first line therapy ■ Can't use in patients with renal impairment (requires proper renal perfusion to reach DCT) ○ Loop diuretics usually indicated in instances with fluid retention Alpha-1 blockers: drugs, moa, dual indications ● Drugs: Prazosin, Terazosin, Doxazosin ● Mechanism of Action: work by blocking alpha-1 adrenergic receptors in smooth muscles, leading to vasodilation and reduced peripheral vascular resistance. ● Dual Indications: ○ Hypertension: Reduce systemic vascular resistance and lower BP. ○ Benign Prostatic Hyperplasia: Relax smooth muscle in the bladder neck and prostate, improving urine flow. .......................................................Continued