Cardiovascular Pharmacology Practice Flashcards

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Comprehensive practice flashcards reviewing cardiac pharmacology, mechanisms of action, side effects, contraindications, and nursing considerations based on NURS 3325 lecture materials.

Last updated 12:40 AM on 9/22/26
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50 Terms

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JNC-8 Hypertension Threshold (Age ≥ 60)

Blood pressure threshold defining hypertension in individuals aged 60 or older, set at SBP >150mmHg>150\,mmHg or DBP >90mmHg>90\,mmHg.

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

Blood pressure threshold defining hypertension in individuals aged under 60 and high-risk groups (CKD and DM), set at SBP >140mmHg>140\,mmHg or DBP >90mmHg>90\,mmHg.

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Alpha-2 Agonists

Central-acting antihypertensives (e.g., Clonidine, Methyldopa, Guanfacine) that stimulate alpha-2 receptors in the brain to decrease norepinephrine release, reducing sympathetic activity, heart rate, and blood pressure.

<p>Central-acting antihypertensives (e.g., Clonidine, Methyldopa, Guanfacine) that stimulate alpha-2 receptors in the brain to decrease norepinephrine release, reducing sympathetic activity, heart rate, and blood pressure.</p>
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Beta Blockers (-olol)

Cardiovascular medications (e.g., Propranolol, Metoprolol, Atenolol, Carvedilol, Bisoprolol) that block beta-1 receptors to lower heart rate, force of contraction, cardiac workload, and renal renin release.

<p>Cardiovascular medications (e.g., Propranolol, Metoprolol, Atenolol, Carvedilol, Bisoprolol) that block beta-1 receptors to lower heart rate, force of contraction, cardiac workload, and renal renin release.</p>
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Selective Beta-1 Blockers

Beta blockers (e.g., Atenolol, Metoprolol) that selectively target beta-1 receptors in the heart, making them generally safer for patients with asthma, COPD, or diabetes mellitus.

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Nonselective Beta Blockers

Beta blockers (e.g., Propranolol) that block both beta-1 and beta-2 receptors, which can cause bronchoconstriction and mask or delay recovery from hypoglycemia.

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ACE Inhibitors (-pril)

Antihypertensives (e.g., Lisinopril, Ramipril, Benazepril, Captopril, Enalapril) that block angiotensin-converting enzyme to prevent Angiotensin II formation, causing vasodilation and reduced aldosterone release.

<p>Antihypertensives (e.g., Lisinopril, Ramipril, Benazepril, Captopril, Enalapril) that block angiotensin-converting enzyme to prevent Angiotensin II formation, causing vasodilation and reduced aldosterone release.</p>
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Renin-Angiotensin-Aldosterone System (RAAS)

Endocrine cascade where renal renin converts liver angiotensinogen to Angiotensin I, which ACE converts primarily in lungs to Angiotensin II, promoting vasoconstriction and aldosterone-mediated sodium and water retention.

<p>Endocrine cascade where renal renin converts liver angiotensinogen to Angiotensin I, which ACE converts primarily in lungs to Angiotensin II, promoting vasoconstriction and aldosterone-mediated sodium and water retention.</p>
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Angioedema

A potentially life-threatening side effect of ACE inhibitors and ARBs characterized by rapid swelling of the face, lips, tongue, and throat that compromises the airway.

<p>A potentially life-threatening side effect of ACE inhibitors and ARBs characterized by rapid swelling of the face, lips, tongue, and throat that compromises the airway.</p>
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Angiotensin II Receptor Blockers (ARBs, -sartan)

Antihypertensives (e.g., Losartan, Irbesartan, Olmesartan, Valsartan, Telmisartan) that directly block Angiotensin II at AT1\text{AT}_1 receptors, lowering blood pressure and volume without causing ACE cough.

<p>Antihypertensives (e.g., Losartan, Irbesartan, Olmesartan, Valsartan, Telmisartan) that directly block Angiotensin II at $$\text{AT}_1$$ receptors, lowering blood pressure and volume without causing ACE cough.</p>
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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.

<p>Antihypertensives (e.g., Hydralazine, Minoxidil) that directly relax vascular smooth muscle to dilate arterioles, reducing systemic vascular resistance, afterload, and cardiac workload.</p>
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Calcium Channel Blockers (CCBs, -pine)

Cardiovascular drugs that block L-type calcium channels to inhibit calcium entry into cardiac and vascular smooth muscle cells, decreasing contraction and lowering blood pressure.

<p>Cardiovascular drugs that block L-type calcium channels to inhibit calcium entry into cardiac and vascular smooth muscle cells, decreasing contraction and lowering blood pressure.</p>
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Dihydropyridines

Subclass of calcium channel blockers (e.g., Amlodipine, Nifedipine, Nicardipine) that primarily target vascular smooth muscle to cause peripheral vasodilation and lower systemic vascular resistance.

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Non-Dihydropyridines

Subclass of calcium channel blockers (e.g., Diltiazem, Verapamil) that affect both the heart and blood vessels to decrease heart rate, AV node conduction, force of contraction, and blood pressure.

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Gingival Hyperplasia

Overgrowth of gum tissue around the teeth, recognized as a unique side effect of calcium channel blocker therapy that requires careful oral hygiene education.

<p>Overgrowth of gum tissue around the teeth, recognized as a unique side effect of calcium channel blocker therapy that requires careful oral hygiene education.</p>
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Loop Diuretics

Potent diuretics (e.g., Furosemide, Bumetanide, Torsemide) that block the Na+-K+-2Cl\text{Na}^+ \text{-K}^+ \text{-2Cl}^- cotransporter (NKCC2) in the thick ascending loop of Henle, leading to rapid water, sodium, chloride, and potassium excretion.

<p>Potent diuretics (e.g., Furosemide, Bumetanide, Torsemide) that block the $$\text{Na}^+ \text{-K}^+ \text{-2Cl}^-$$ cotransporter (NKCC2) in the thick ascending loop of Henle, leading to rapid water, sodium, chloride, and potassium excretion.</p>
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Ototoxicity

Adverse effect causing tinnitus or hearing loss associated with rapid intravenous administration of loop diuretics such as furosemide.

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Thiazide Diuretics

Diuretics (e.g., Hydrochlorothiazide, Chlorthalidone, Indapamide, Metolazone) that block the Na+/Cl\text{Na}^+/\text{Cl}^- cotransporter (NCC) in the distal convoluted tubule, producing moderate diuresis while enhancing calcium reabsorption.

<p>Diuretics (e.g., Hydrochlorothiazide, Chlorthalidone, Indapamide, Metolazone) that block the $$\text{Na}^+/\text{Cl}^-$$ cotransporter (NCC) in the distal convoluted tubule, producing moderate diuresis while enhancing calcium reabsorption.</p>
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Potassium-Sparing Diuretics

Diuretics (e.g., Spironolactone, Amiloride, Triamterene) acting in the late distal tubule and collecting duct to excrete sodium and water while retaining potassium in the blood.

<p>Diuretics (e.g., Spironolactone, Amiloride, Triamterene) acting in the late distal tubule and collecting duct to excrete sodium and water while retaining potassium in the blood.</p>
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Heart Failure

Complex clinical syndrome caused by functional or structural impairment that compromises the heart's ability to pump blood, reducing cardiac output and causing fluid back-up.

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Cardiac Glycosides (Digoxin)

Inotropic medication that blocks the Na+/K+\text{Na}^+/\text{K}^+ pump to increase intracellular calcium (strengthening contraction) and increases vagal activity to slow SA and AV node conduction (slowing heart rate).

<p>Inotropic medication that blocks the $$\text{Na}^+/\text{K}^+$$ pump to increase intracellular calcium (strengthening contraction) and increases vagal activity to slow SA and AV node conduction (slowing heart rate).</p>
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Digoxin Toxicity

Toxic state indicated by anorexia, nausea, vomiting, diarrhea, confusion, weakness, dysrhythmias, and characteristic blurred vision or yellow halos around lights.

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Stable vs. Unstable Angina

Stable angina is predictable chest pain triggered by stress/exertion and relieved by rest or nitroglycerin; unstable angina is unpredictable pain at rest or exertion representing a medical emergency.

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Nitrates (Nitroglycerin)

Antianginal medications (e.g., Sublingual or Topical Nitroglycerin, Isosorbide dinitrate, Isosorbide mononitrate) that release nitric oxide (NO) to dilate veins, reducing preload, cardiac workload, and myocardial oxygen demand.

<p>Antianginal medications (e.g., Sublingual or Topical Nitroglycerin, Isosorbide dinitrate, Isosorbide mononitrate) that release nitric oxide (NO) to dilate veins, reducing preload, cardiac workload, and myocardial oxygen demand.</p>
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Class III Antiarrhythmics (Amiodarone)

Potassium channel blocker that delays repolarization and prolongs the action potential, giving heart cells more time to reset between beats to control abnormal rhythms.

<p>Potassium channel blocker that delays repolarization and prolongs the action potential, giving heart cells more time to reset between beats to control abnormal rhythms.</p>
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Atropine

Anticholinergic drug that blocks muscarinic receptors to inhibit acetylcholine, removing parasympathetic inhibition to increase SA node firing, AV node conduction, and heart rate in bradycardia or asystole.

<p>Anticholinergic drug that blocks muscarinic receptors to inhibit acetylcholine, removing parasympathetic inhibition to increase SA node firing, AV node conduction, and heart rate in bradycardia or asystole.</p>
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Vasoactive Adrenergics

Sympathomimetic agents (e.g., Dobutamine, Dopamine, Epinephrine, Norepinephrine) that stimulate alpha and beta receptors to increase heart rate, contractility, vascular tone, and cardiac output.

<p>Sympathomimetic agents (e.g., Dobutamine, Dopamine, Epinephrine, Norepinephrine) that stimulate alpha and beta receptors to increase heart rate, contractility, vascular tone, and cardiac output.</p>
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Midodrine

Alpha-1 adrenergic agonist that constricts peripheral arteries and veins to raise systemic vascular resistance and venous return, used specifically for orthostatic hypotension.

<p>Alpha-1 adrenergic agonist that constricts peripheral arteries and veins to raise systemic vascular resistance and venous return, used specifically for orthostatic hypotension.</p>
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Supine Hypertension

Elevated blood pressure when lying down, a key side effect of midodrine managed by administering doses during waking hours and avoiding administration within 3 to 4 hours of bedtime.

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HMG-CoA Reductase Inhibitors (Statins)

Antilipemic drugs (e.g., Atorvastatin, Rosuvastatin, Simvastatin, Lovastatin, Pravastatin) that block liver HMG-CoA reductase to decrease cholesterol synthesis and increase hepatic clearance of LDL from blood.

<p>Antilipemic drugs (e.g., Atorvastatin, Rosuvastatin, Simvastatin, Lovastatin, Pravastatin) that block liver HMG-CoA reductase to decrease cholesterol synthesis and increase hepatic clearance of LDL from blood.</p>
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Rhabdomyolysis

Severe breakdown of skeletal muscle tissue that causes muscle cramps, myalgia, severe weakness, and dark urine, associated with statins, ezetimibe, or fibrate therapy.

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Selective Cholesterol Absorption Inhibitors (Ezetimibe)

Antilipemic agent (Zetia) that blocks the NPC1L1 transporter in the small intestine, decreasing cholesterol absorption so less reaches the liver and more LDL is cleared from blood.

<p>Antilipemic agent (Zetia) that blocks the NPC1L1 transporter in the small intestine, decreasing cholesterol absorption so less reaches the liver and more LDL is cleared from blood.</p>
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Bile Acid Sequestrants

Agents (e.g., Cholestyramine, Colestipol, Colesevelam) that trap bile acids in the intestine for stool excretion, prompting the liver to consume systemic cholesterol to synthesize new bile acids.

<p>Agents (e.g., Cholestyramine, Colestipol, Colesevelam) that trap bile acids in the intestine for stool excretion, prompting the liver to consume systemic cholesterol to synthesize new bile acids.</p>
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Niacin (Nicotinic Acid)

Lipid-lowering medication that reduces adipose fat breakdown and free fatty acid delivery to the liver, leading to reduced VLDL, LDL, and triglycerides, and increased HDL.

<p>Lipid-lowering medication that reduces adipose fat breakdown and free fatty acid delivery to the liver, leading to reduced VLDL, LDL, and triglycerides, and increased HDL.</p>
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Fibric Acid Derivatives (Fibrates)

Antilipemic drugs (e.g., Fenofibrate, Gemfibrozil) that activate PPAR-alpha to increase lipoprotein lipase (LPL) activity, accelerating triglyceride breakdown and elevating HDL.

<p>Antilipemic drugs (e.g., Fenofibrate, Gemfibrozil) that activate PPAR-alpha to increase lipoprotein lipase (LPL) activity, accelerating triglyceride breakdown and elevating HDL.</p>
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Anticoagulants Overview

Drug class that inhibits clotting factor action or synthesis to prevent clot formation and stop existing clots from growing, without dissolving pre-existing clots.

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Heparin

Parenteral anticoagulant that enhances antithrombin activity to block Factor Xa and Thrombin (Factor IIa), preventing fibrin formation and clot expansion.

<p>Parenteral anticoagulant that enhances antithrombin activity to block Factor Xa and Thrombin (Factor IIa), preventing fibrin formation and clot expansion.</p>
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Protamine Sulfate

The specific reversing antidote administered for unfractionated heparin and low molecular weight heparin (LMWH) toxicity or severe bleeding.

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Low Molecular Weight Heparin (LMWH)

Anticoagulants (e.g., Enoxaparin, Dalteparin) that bind antithrombin to primarily inhibit Factor Xa with less effect on Thrombin (Factor IIa), requiring no routine lab monitoring.

<p>Anticoagulants (e.g., Enoxaparin, Dalteparin) that bind antithrombin to primarily inhibit Factor Xa with less effect on Thrombin (Factor IIa), requiring no routine lab monitoring.</p>
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Warfarin

Anticoagulant that blocks vitamin K epoxide reductase in the liver to inhibit recycling of active vitamin K, decreasing clotting factors II, VII, IX, and X.

<p>Anticoagulant that blocks vitamin K epoxide reductase in the liver to inhibit recycling of active vitamin K, decreasing clotting factors II, VII, IX, and X.</p>
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Vitamin K

The specific reversing antidote administered for warfarin toxicity or excessively elevated INR levels (>3>3).

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Factor Xa Inhibitors (-xaban)

Anticoagulants (e.g., Apixaban, Rivaroxaban, Edoxaban) that directly block Factor Xa, inhibiting conversion of prothrombin to thrombin and fibrinogen to fibrin.

<p>Anticoagulants (e.g., Apixaban, Rivaroxaban, Edoxaban) that directly block Factor Xa, inhibiting conversion of prothrombin to thrombin and fibrinogen to fibrin.</p>
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Andexanet Alfa

The specific reversal agent designed for managing severe bleeding caused by Factor Xa inhibitors like apixaban and rivaroxaban.

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Direct Thrombin Inhibitors

Anticoagulants (e.g., Dabigatran, Argatroban, Bivalirudin) that directly block Thrombin (Factor IIa) to inhibit fibrin formation and clot expansion.

<p>Anticoagulants (e.g., Dabigatran, Argatroban, Bivalirudin) that directly block Thrombin (Factor IIa) to inhibit fibrin formation and clot expansion.</p>
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Antiplatelet Drugs

Medications that inhibit platelet activation, aggregation, or clumping to prevent arterial thrombosis in high-risk cardiovascular patients.

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Aspirin

Antiplatelet drug that inhibits COX-1 enzyme in platelets, reducing Thromboxane A2\text{A}_2 synthesis and preventing platelet clumping.

<p>Antiplatelet drug that inhibits COX-1 enzyme in platelets, reducing Thromboxane $$\text{A}_2$$ synthesis and preventing platelet clumping.</p>
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ADP Receptor Inhibitors

Antiplatelet drugs (e.g., Clopidogrel, Prasugrel, Ticagrelor) that block P2Y12\text{P2Y}_{12} ADP receptors on platelets to prevent ADP signaling and platelet clumping.

<p>Antiplatelet drugs (e.g., Clopidogrel, Prasugrel, Ticagrelor) that block $$\text{P2Y}_{12}$$ ADP receptors on platelets to prevent ADP signaling and platelet clumping.</p>
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Thrombolytics Overview

High-risk medication class that actively dissolves existing thrombi by activating the fibrinolytic system, unlike anticoagulants or antiplatelet agents.

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Alteplase (tPA)

Thrombolytic drug that activates plasminogen to plasmin, which breaks down fibrin to dissolve pre-existing blood clots.

<p>Thrombolytic drug that activates plasminogen to plasmin, which breaks down fibrin to dissolve pre-existing blood clots.</p>
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Six Rights of Safe Medication Administration

Fundamental nursing safety standard ensuring right patient, right medication, right dose, right route, right time, and right documentation.