Pharm I: Hypertensive Meds.

Comprehensive vocabulary flashcards covering calcium channel blockers, adrenergic receptor agonists and antagonists, direct vasodilators, and nephron-targeted diuretics from lecture notes.

Dihydropyridine Calcium Channel Blockers

A class of calcium channel blockers that possess a greater affinity for vascular calcium channels than cardiac tissue, producing peripheral vasodilation and reductions in afterload and preload; commonly used first-line for uncomplicated hypertension.

Non-Dihydropyridine Calcium Channel Blockers

Calcium channel blockers, such as verapamil and diltiazem, that affect both vascular smooth muscle and cardiac muscle contraction, causing negative inotropic and chronotropic effects; generally avoided in heart failure.

Amlodipine

A widely used dihydropyridine calcium channel blocker frequently identified with peripheral edema as a common adverse effect that may lead to discontinuation.

Clevidipine

An intravenous dihydropyridine calcium channel blocker featuring a very short duration of action and rapid onset and offset, making it useful in acute clinical settings like hypertensive emergencies.

Simvastatin and Calcium Channel Blocker Interaction

A drug interaction in which concurrent administration of simvastatin with non-dihydropyridines (such as verapamil or diltiazem) increases the risk of skeletal muscle toxicity, myopathy, and rhabdomyolysis.

$\alpha_1$-Adrenoceptor Activation (Endogenous)

The physiological response occurring when an endogenous ligand binds the $\alpha_1$-adrenoceptor, resulting in vasoconstriction, increased peripheral resistance, and elevated blood pressure.

$\alpha_2$-Adrenoceptor Activation (Endogenous)

The physiological response occurring when an endogenous ligand binds the central $\alpha_2$-adrenoceptor, leading to inhibition of sympathetic outflow, decreased peripheral vascular resistance, and lowered blood pressure.

$\beta_1$-Adrenoceptor Activation (Endogenous)

The physiological response occurring when an endogenous ligand binds the $\beta_1$-adrenoceptor, resulting in increased heart rate (tachycardia), increased myocardial contractility (positive inotropic effect), and increased renin release.

$\beta_2$-Adrenoceptor Activation (Endogenous)

The physiological response occurring when an endogenous ligand binds the $\beta_2$-adrenoceptor, causing smooth muscle relaxation, bronchodilation, and peripheral vasodilation.

Intrinsic Sympathomimetic Activity (ISA)

A pharmacological property of partial agonist beta blockers that bind to beta receptors and competitively block endogenous catecholamines while exerting a weak, residual stimulant effect, resulting in less bradycardia.

Acebutolol and Pindolol

Two specific beta blockers characterized by possessing intrinsic sympathomimetic activity (acting as partial agonists rather than full antagonists).

Cardioselective $\beta_1$ Blockers

Beta blockers (such as metoprolol, atenolol, and bisoprolol) that preferentially inhibit $\beta_1$-receptors over $\beta_2$-receptors, reducing the risk of bronchoconstriction in patients with reactive airway disease.

Metoprolol Tartrate

The immediate-release salt form of metoprolol that requires twice-daily administration and should be taken with food.

Metoprolol Succinate

The extended-release formulation of metoprolol that is administered once daily and is clinically proven to reduce mortality in heart failure with reduced ejection fraction (HFrEF).

Esmolol

A short-acting intravenous cardioselective beta blocker with a rapid onset and short half-life, suited for acute clinical situations like diagnostic procedures, surgeries, or hypertensive emergencies.

Carvedilol

A non-selective beta blocker that also blocks vascular $\alpha_1$-receptors, providing dual cardiac depression and vasodilation; proven to reduce mortality in heart failure with reduced ejection fraction (HFrEF).

Labetalol

A combined $\alpha_1$- and non-selective $\beta$-receptor antagonist commonly utilized as a first-line drug for managing hypertension in pregnancy.

Beta-Blocker-Induced Hypoglycemic Unawareness

An adverse phenomenon occurring in diabetic patients taking beta blockers where sympathomimetic warning signs of hypoglycemia, notably tachycardia and tremors, are blunted or masked.

Beta-Blocker Rebound Tachycardia

A severe withdrawal response caused by chronic receptor upregulation that triggers acute tachycardia and elevated blood pressure if beta blocker therapy is abruptly discontinued without tapering.

$\alpha_1$-Receptor Antagonists

Antihypertensive agents that block vascular $\alpha_1$-receptors to reduce peripheral vascular resistance; often selected when hypertension co-occurs with benign prostatic hyperplasia (BPH).

First-Dose Syncope

A sudden severe postural hypotension and potential loss of consciousness following initial administration of $\alpha_1$-blockers, mitigated by starting at low doses and administering at bedtime.

Clonidine

A centrally acting $\alpha_2$-adrenoceptor agonist that reduces central sympathetic outflow; notoriously carries a severe risk of rebound hypertension if stopped abruptly.

Methyldopa

A centrally acting $\alpha_2$-adrenergic agonist considered a secondary preferred agent for treating hypertension during pregnancy.

Hydralazine

A direct arterial vasodilator that lowers afterload, frequently combined with a beta blocker and a diuretic to counter compensatory reflex tachycardia and fluid retention.

Sodium Nitroprusside

An intravenous direct arterial and venous vasodilator that increases nitric oxide and cyclic GMP ($\text{cGMP}$), indicated for acute hypertensive emergencies with a risk of cyanide toxicity.

Loop Diuretics

The most potent class of diuretics (e.g., furosemide, bumetanide) that inhibit the $Na^+/K^+/2Cl^-$ cotransporter in the thick ascending loop of Henle, where roughly $25\%$ of filtered sodium is reabsorbed.

Bumetanide

The most potent loop diuretic agent, frequently substituted when patients fail to achieve adequate diuresis on furosemide.

Ototoxicity

A documented adverse effect associated with loop diuretics, presenting as hearing impairment or ear damage, particularly when high intravenous doses are combined with aminoglycoside antibiotics.

Thiazide Diuretics

A first-line class of antihypertensives that inhibit sodium chloride cotransport in the distal convoluted tubule and reduce peripheral vascular resistance; unlike loop diuretics, they promote renal calcium reabsorption.

Chlorthalidone

A long-acting thiazide-like diuretic administered once daily, noted for high clinical efficacy in controlling blood pressure.

Hyperuricemia (Diuretic-Induced)

An elevation in serum uric acid resulting from loop and thiazide diuretics competing with uric acid for organic acid secretory pathways in the proximal convoluted tubule, potentially exacerbating gout.

Mineralocorticoid Receptor Antagonists (MRAs)

Potassium-sparing agents (spironolactone and eplerenone) that competitively block aldosterone receptors in the collecting tubules, decreasing sodium reabsorption and retaining potassium.

Triamterene and Amiloride

Potassium-sparing diuretics that directly inhibit epithelial sodium-potassium ion transport channels in the late distal tubule and collecting ducts without directly antagonizing the aldosterone receptor.