Cardiovascular System Medications

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Vocabulary practice flashcards covering cardiovascular pharmacology drug classes, mechanisms of action, drug examples, side effects, and key nursing considerations.

38 Terms

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JNC-8 Hypertension Definition (Age ≥60\ge 60)

Systolic blood pressure (SBP) >150 mmHg> 150\,\text{mmHg} or diastolic blood pressure (DBP) >90 mmHg> 90\,\text{mmHg}.

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JNC-8 Hypertension Definition (Age <60< 60 & High-Risk Groups)

Systolic blood pressure (SBP) >140 mmHg> 140\,\text{mmHg} or diastolic blood pressure (DBP) >90 mmHg> 90\,\text{mmHg} in individuals aged under 60 or high-risk groups with chronic kidney disease (CKD) or diabetes mellitus (DM).

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Alpha-2 Agonists

Antihypertensive agents (e.g., Clonidine, Methyldopa, Guanfacine) that stimulate central alpha-2 receptors to decrease norepinephrine release, reducing sympathetic activity, heart rate, and blood pressure.

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Beta-1 Blockade

Inhibition of β1\beta_1 receptors in the heart and kidneys, resulting in decreased heart rate, reduced force of contraction, decreased cardiac workload, lowered renin release, and reduced blood pressure.

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Beta-2 Blockade

Inhibition of β2\beta_2 receptors causing bronchoconstriction in the lungs, masked symptoms of hypoglycemia, and delayed recovery from hypoglycemia.

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ACE Inhibitors

Antihypertensive drugs ending in '-pril' (e.g., Lisinopril, Ramipril, Benazepril, Captopril, Enalapril) that block angiotensin-converting enzyme, stopping Angiotensin I conversion to Angiotensin II to promote vasodilation and decrease aldosterone release.

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ACE Cough

A persistent dry cough occurring as a common side effect of ACE inhibitor administration due to altered bradykinin metabolism in the lungs.

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<p>Angioedema</p>

Angioedema

A rapid, severe, and potentially life-threatening swelling of the dermis and submucosal tissue (commonly affecting lips, tongue, and face) associated with ACE inhibitors and ARBs.

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Angiotensin II Receptor Blockers (ARBs)

Antihypertensive drugs ending in '-sartan' (e.g., Losartan, Irbesartan, Olmesartan, Valsartan, Telmisartan) that selectively block Angiotensin II from binding to AT1\text{AT}_1 receptors, causing blood vessel relaxation and reduced fluid retention.

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Direct-Acting Vasodilators

Antihypertensives (e.g., Hydralazine, Minoxidil) that directly relax vascular smooth muscle to dilate arterioles, reducing systemic vascular resistance, afterload, and cardiac workload.

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Dihydropyridine Calcium Channel Blockers

Calcium channel blockers ending in '-pine' (e.g., Amlodipine, Nifedipine, Nicardipine) that primarily target vascular smooth muscle to produce vasodilation and lower systemic vascular resistance.

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Non-Dihydropyridine Calcium Channel Blockers

Calcium channel blockers (e.g., Diltiazem, Verapamil) that act on both vascular smooth muscle and heart cells, decreasing heart rate, AV node conduction, myocardial force of contraction, and blood pressure.

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<p>Gingival Hyperplasia</p>

Gingival Hyperplasia

An overgrowth of gum tissue around the teeth that serves as a notable side effect of calcium channel blocker therapy, requiring strict oral hygiene.

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Loop Diuretics

Potassium-wasting diuretics (e.g., Furosemide, Bumetanide, Torsemide) that block the Na+−K+−2Cl−\text{Na}^+-\text{K}^+-2\text{Cl}^- cotransporter (NKCC2) in the thick ascending loop of Henle, producing potent diuresis.

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Thiazide Diuretics

Potassium-wasting diuretics (e.g., Hydrochlorothiazide, Chlorthalidone, Indapamide) that block the Na+/Cl−\text{Na}^+/\text{Cl}^- cotransporter (NCC) in the distal convoluted tubule and increase calcium reabsorption.

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Potassium-Sparing Diuretics

Diuretics that promote mild diuresis while retaining potassium in the blood, acting either as aldosterone antagonists (Spironolactone, Eplerenone) or ENaC sodium channel blockers (Amiloride, Triamterene).

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Digoxin

A cardiac glycoside that inhibits the Na+/K+\text{Na}^+/\text{K}^+ pump to increase intracellular Ca2+\text{Ca}^{2+} (enhancing myocardial contraction strength) and increases vagal tone to slow SA and AV node conduction.

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Digibind

The specific antidote medication administered for Digoxin toxicity.

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Nitrates

Antianginal medications (e.g., Nitroglycerin, Isosorbide dinitrate, Isosorbide mononitrate) that release nitric oxide (NO) to relax vascular smooth muscle, reducing venous return (preload) and myocardial oxygen demand.

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Class III Antiarrhythmics

Potassium channel blockers (e.g., Amiodarone) that prolong cardiac repolarization, giving heart cells more time to reset between beats to control abnormal rhythms.

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Atropine

An anticholinergic agent that blocks muscarinic receptors to remove parasympathetic suppression on the heart, increasing SA node firing, AV node conduction, and heart rate.

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Vasoactive Adrenergics

Medications (e.g., Dobutamine, Dopamine, Epinephrine, Norepinephrine) that stimulate adrenergic receptors to raise heart rate, force of contraction, cardiac output, and systemic blood pressure.

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Midodrine

An α1\alpha_1-adrenergic agonist that causes constriction of peripheral arterioles and veins to increase systemic vascular resistance and treat orthostatic hypotension.

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Statins (HMG-CoA Reductase Inhibitors)

Antilipemic drugs ending in '-statin' (e.g., Atorvastatin, Lovastatin, Pravastatin, Rosuvastatin, Simvastatin) that block HMG-CoA reductase in the liver to decrease cholesterol synthesis and increase hepatic LDL clearance.

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Rhabdomyolysis

A grave adverse effect characterized by skeletal muscle breakdown and myalgia, associated with statins and cholesterol absorption inhibitors.

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Ezetimibe

A selective cholesterol absorption inhibitor that blocks the NPC1L1 transporter in the brush border of the small intestine, lowering LDL delivery to the liver.

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Bile Acid Sequestrants

Antilipemic agents (e.g., Cholestyramine, Colestipol, Colesevelam) that bind bile acids in the intestine for fecal elimination, forcing the liver to consume circulating cholesterol to synthesize new bile acids.

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Niacin

Nicotinic acid antilipemic therapy that reduces adipose tissue lipolysis, decreasing free fatty acid delivery to the liver and lowering liver synthesis of VLDL, triglycerides, and LDL.

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Fibric Acid Derivatives (Fibrates)

Antilipemic drugs (e.g., Fenofibrate, Gemfibrozil) that activate PPAR−α\text{PPAR}-\alpha receptors to increase lipoprotein lipase (LPL) activity, rapidly breaking down triglyceride-rich particles.

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Heparin

An anticoagulant that enhances antithrombin activity to inhibit Factor Xa and Thrombin (Factor IIa), preventing new clot growth without dissolving existing clots; monitored by PTT.

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Protamine Sulfate

The therapeutic antidote utilized to reverse the anticoagulant effects of Heparin and Low Molecular Weight Heparin.

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Low Molecular Weight Heparin (LMWH)

Anticoagulants such as Enoxaparin and Dalteparin that bind antithrombin to selectively inhibit Factor Xa over Thrombin, supplied in prefilled syringes with an intact air bubble.

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Warfarin

An oral anticoagulant that inhibits vitamin K epoxide reductase in the liver, depleting active vitamin K and clotting factors II, VII, IX, and X; monitored routinely by PT/INR.

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Factor Xa Inhibitors

Oral anticoagulants ending in '-xaban' (e.g., Apixaban, Rivaroxaban, Edoxaban) that directly block Factor Xa to inhibit prothrombin-to-thrombin conversion; reversed by Andexanet alfa.

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Direct-Acting Thrombin Inhibitors

Anticoagulants (e.g., Dabigatran, Argatroban, Bivalirudin) that directly bind and block Thrombin (Factor IIa) to halt fibrinogen conversion into fibrin.

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Aspirin

An antiplatelet agent that irreversibly inhibits cyclooxygenase-1 (COX-1), decreasing Thromboxane A2A_2 levels and preventing arterial platelet aggregation.

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ADP Receptor Inhibitors

Antiplatelet agents (e.g., Clopidogrel, Prasugrel, Ticagrelor) that block P2Y12P2Y_{12} ADP receptors on platelets to inhibit ADP signaling and reduce platelet activation.

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Alteplase (tPA)

A thrombolytic agent that converts plasminogen into active plasmin, which directly degrades fibrin meshwork to dissolve pre-existing blood clots.