The AGACNP is caring for a patient for which they are concer…
Questions
The AGACNP is cаring fоr а pаtient fоr which they are cоncerned is developing delirium. The AGACNP performs a bedside assessment using the Confusion Assessment Method for the ICU (CAM-ICU). Which of the following findings must be present to diagnose delirium using the CAM-ICU tool?
DRUG THERAPY OF HYPERTENSION 1) RAAS INHIBITORS (MOST IMPORTANT HTN SYSTEM TARGET) Blоcking RAAS → ↓ Angiоtensin II → ↓ vаsоconstriction + ↓ аldosterone ↓ Nа⁺/H₂O retention → ↓ volume ↓ sympathetic activity ↓ cardiac remodeling (HF benefit) A. ACE Inhibitors (ACEIs): Lisinopril, Enalapril, Captopril, Fosinopril, Benazepril MOA ACE inhibition → ↓ Angiotensin II ↑ Bradykinin → ↑ NO + PGI₂ → vasodilation Major physiologic effects ↓ SVR (vasodilation) ↓ aldosterone → ↓ Na⁺/H₂O retention Efferent arteriole dilation → ↓ intraglomerular pressure → ↓ proteinuria Uses (very high yield) First-line HTN (esp. DM, CKD) HFrEF (mortality benefit) Post-MI Proteinuric CKD Hypertensive urgency Adverse Effects (classic exam set) Dry cough (↑ bradykinin) Angioedema (dangerous) Hyperkalemia Hypotension (first dose) ↓ GFR in bilateral renal artery stenosis Teratogenic (fetal renal failure, oligohydramnios) Key interactions NSAIDs ↓ effect (↓ prostaglandins → afferent constriction) K⁺ supplements / K-sparing diuretics → severe hyperkalemia B. Angiotensin II Receptor Blockers (ARBs): Losartan, Valsartan, Candesartan, Telmisartan MOA Block AT1 receptor → inhibit Ang II actions directly Key differences vs ACEIs ❌ No bradykinin effect → NO cough ❌ No angioedema Uses ACEI intolerance (cough/angioedema) HTN, CKD, HFrEF AEs Hyperkalemia Hypotension Teratogenic Same renal risk in bilateral renal artery stenosis C. Renin Inhibitors: Aliskiren MOA Directly inhibits renin → ↓ Ang I → ↓ Ang II Uses Resistant HTN (limited clinical use) AEs Hyperkalemia Hypotension Renal dysfunction Avoid with ACEI/ARB (↑ renal + K⁺ toxicity) D. Aldosterone Receptor Antagonists (ARAs): Spironolactone, Eplerenone MOA Block aldosterone in collecting duct → ↓ Na⁺/H₂O retention + ↑ K⁺ retention Uses (VERY HIGH YIELD) Resistant HTN (key drug!) HFrEF (mortality benefit) Primary hyperaldosteronism Post-MI HF Hypokalemia Spironolactone: hirsutism, PCOS AEs Hyperkalemia (major) Metabolic acidosis Gynecomastia (spironolactone) Impotence, menstrual irregularities Contraindicated in pregnancy (spironolactone) 2) DIURETICS (↓ Na⁺ → ↓ volume + long-term ↓ SVR) A. Thiazides / Thiazide-like: Hydrochlorothiazide, Chlorthalidone, Indapamide MOA Block Na⁺/Cl⁻ cotransporter in DCT Uses (first-line HTN) Mild–moderate HTN Elderly Stroke prevention (very high yield) Calcium stone prevention (↓ urinary Ca²⁺) Nephrogenic DI AEs (“hyper” mnemonic) HyperGLUC: Hyperglycemia Hyperlipidemia Hyperuricemia (gout) Hypercalcemia Hypokalemia Hyponatremia Metabolic alkalosis B. Loop Diuretics: Furosemide, Bumetanide, Torsemide, Ethacrynic acid MOA Block Na⁺/K⁺/2Cl⁻ in thick ascending limb Uses HTN with CKD Pulmonary edema (HF) Edema (HF, liver, renal failure) Hypercalcemia (treatment) AEs (important distinctions) Ototoxicity Hypokalemia Hypocalcemia Hypomagnesemia Dehydration Interstitial nephritis Ethacrynic acid = safe in sulfa allergy C. K⁺-sparing diuretics 1. Aldosterone antagonist: Spironolactone, Eplerenone MOA Block aldosterone in collecting duct → ↓ Na⁺/H₂O retention + ↑ K⁺ retention Uses (VERY HIGH YIELD) Resistant HTN (key drug!) HFrEF (mortality benefit) Primary hyperaldosteronism Post-MI HF Hypokalemia Spironolactone: hirsutism, PCOS AEs Hyperkalemia (major) Metabolic acidosis Gynecomastia (spironolactone) Impotence, menstrual irregularities Contraindicated in pregnancy (spironolactone) 2. ENaC blockers: Amiloride, Triamterene MOA Block epithelial Na⁺ channels in collecting duct Uses Same as ARAs (adjunct HTN, hypokalemia prevention) AEs Hyperkalemia Amiloride: ↑ BUN Triamterene: Kidney stones Crystalluria AKI Megaloblastic anemia Question: A 68-year-old woman is started on a first-line antihypertensive medication. Two weeks later, she reports polyuria, weakness, and a gout flare. Laboratory findings include: Serum sodium: 131 mEq/L (ref: 135–145 mEq/L) Serum uric acid: elevated Which medication is most likely responsible?
DRUG THERAPY OF CORONARY ARTERY DISEASE β-Blоckers (BBs) Exаmples Selective β1 (cаrdiоselective): Metоprolol, Atenolol Non-selective β1 + β2: Proprаnolol Mixed β1, β2 + α1: Carvedilol Mechanism / Rationale β-blockers improve myocardial oxygen balance by: ↓ Myocardial O₂ demand ↓ Contractility ↓ Heart rate (↓ SA node automaticity) ↓ AV node conduction → ↓ HR ↑ Myocardial O₂ supply Prolong diastole → ↑ coronary perfusion time Uses Stable angina (prophylaxis + treatment) Acute coronary syndrome (ACS) if no contraindications: Avoid in shock, severe bradycardia, heart block, decompensated HF Often combined with nitrates → prevents reflex tachycardia Contraindications / Important cautions Prinzmetal (vasospastic) angina Non-selective β-blockers are contraindicated: Block β2 vasodilation → unopposed α1 vasoconstriction → coronary vasospasm → may precipitate MI Cocaine-associated chest pain Non-selective β-blockers worsen vasospasm: Cocaine ↑ catecholamines → unopposed α activity → severe vasoconstriction Organic Nitrates Examples Nitroglycerin (GTN) Isosorbide dinitrate Isosorbide mononitrate Mechanism / Rationale ↓ Myocardial O₂ demand Venodilation → ↓ preload Arterial dilation → ↓ afterload ↑ Myocardial O₂ supply Coronary vasodilation → ↑ blood flow Redistributes blood to ischemic regions Antiplatelet effect (transdermal NG) ↓ platelet aggregation via inhibition of GPIIb/IIIa binding Uses Acute angina relief: Sublingual nitroglycerin → relief in 2–5 min May repeat every 5 min up to 3 doses Chronic stable angina prophylaxis (long-acting forms) ACS with persistent chest pain Acute HTN emergencies, acute decompensated HF (IV nitroglycerin) Calcium Channel Blockers (CCBs) Mechanism / Rationale ↓ Myocardial O₂ demand ↓ preload and afterload (vasodilation) ↓ contractility (especially non-dihydropyridines) ↓ heart rate (↓ SA node) ↓ AV node conduction ↑ Myocardial O₂ supply Coronary vasodilation → improved perfusion Clinical Uses Stable angina (alternative or adjunct to β-blockers) Prinzmetal (vasospastic) angina (very important indication) Long-acting formulations preferred Short-acting nifedipine should be avoided alone (risk of reflex tachycardia) Combination therapy With β-blockers → prevents reflex tachycardia With nitrates → non-dihydropyridines help blunt tachycardia Ranolazin Mechanism / Rationale Acts specifically on ischemic myocardium: Inhibits late Na⁺ current during repolarization→ ↓ intracellular Na⁺→ ↓ Ca²⁺ overload (via Na⁺/Ca²⁺ exchanger)→ ↓ intracellular Ca²⁺ Net effects: Improves myocardial metabolism ↓ contractility → ↓ O₂ demand Antiarrhythmic effects (Class Id): ↓ automaticity ↓ early afterdepolarizations (EADs) Key advantage: does NOT significantly affect HR or BP Pharmacokinetics Oral administration Metabolized via CYP3A → significant drug interactions Renal excretion Uses Chronic stable angina (especially when HR/BP limit other drugs) Adjunct in refractory angina Some use in ventricular arrhythmias (off-label) Adverse Effects Common: Nausea Dizziness Headache Constipation Serious: QT interval prolongation → risk of torsades de pointes Contraindication Avoid with other QT-prolonging drugs Question: A 67-year-old woman with chronic stable angina remains symptomatic despite treatment with a β-blocker and a calcium channel blocker. Her blood pressure is 118/72 mmHg and heart rate is 64 bpm, limiting further dose escalation of her current medications. The decision is made to add ranolazine. Which of the following best describes the mechanism of action of this drug?