NURS 306 Study Guide Exam #2

Calcium channel blockers (-pine)

Smooth muscle relaxation by preventing calcium from entering cells and connecting to receptors → prevents contraction of muscles.

Calcium channel blockers effect on coronary arteries

Relaxation of smooth muscle surrounding heart causes coronary arteries to dilate → increase blood flow to heart and increase oxygen supply.

Cardiac glycosides - Digoxin

Increase myocardial contraction → increases cardiac output and improves circulation.

Digoxin effect on heart rate

Decreases HR and conduction through the AV node.

Digoxin mechanism

Reversibly inhibits sodium-potassium ATPase in cell membrane of cardiomyocytes, causing Ca to build up in cardiomyocytes to allow muscle fibers to contract more efficiently → increase in force of contraction and cardiac output.

Antianginals

Reduction of venous tone → decrease workload of heart and promotes vasodilation.

Antianginals effect on vascular smooth muscle

Acts directly on vascular smooth muscle and causes relaxation and dilation of vessels.

Antianginals effect on venous return

Decrease venous return to the heart, lowers wall tension (preload).

Coagulation Modifiers

Includes oral anticoagulants, heparin, low molecular weight heparin, and antiplatelets.

Heparin

Parenteral anticoagulant that prevents the formation of fibrin.

Low molecular weight heparin

Prevent conversion of fibrinogen to fibrin (final step in clotting process).

Warfarin

Prolongs clotting time by interfering with the synthesis of vitamin K-dependent clotting factors and depletes vitamin K reserves.

Vitamin K and clotting factors

Clotting factors, like prothrombin, require active form of vitamin K to make them.

Rivaroxaban

Selectively inhibits coagulation factor Xa in clotting cascade, which prevents prothrombin from converting to thrombin.

Dabigatran

Inhibits thrombin that is free in blood or bound to clot, stops conversion of fibrinogen into fibrin.

Antiplatelets

Prevent clot formation by preventing platelet aggregation before clotting cascade occurs.

Antiplatelets effect

Decrease platelet aggregation and inhibit thrombus formation.

Aspirin

An antiplatelet that prevents clot formation.

P2Y12 adenosine diphosphate (ADP) receptor blockers

Inhibit binding of ADP to platelet P2Y12 receptor → inhibits platelet aggregation.

Glycoprotein (GP) IIb/IIIa receptor blockers

Prevent platelet aggregation by blocking GP IIb/IIIa receptors.

Thrombolytics

"Lyse" or dissolve a currently existing clot.

Angiotensin II receptor blockers (ARBs) (-sartan)

Block angiotensin II from binding to receptors in blood vessels.

Angiotensin II effect on aldosterone

Prevents angiotensin II from stimulating aldosterone release, vasoconstriction of arterioles and veins, and renal system.

Vasoconstriction of renal system

Preventing vasoconstriction of renal system would make you pee a lot → less fluids.

Angiotensin converting enzyme (ACE) inhibitors

Inhibit enzyme that converts angiotensin I to angiotensin II.

Angiotensin II

A vasoconstrictor that causes aldosterone release.

Aldosterone

Retains fluids by suppressing urination; suppressing this means decreasing Na and water retention by the kidneys while sparing K from excretion.

Angiotensin Receptor-Neprilysin Inhibitors (ARNi)

Combination of valsartan (ARB) and sacubitril (neprilysin inhibitor) - Enestro.

Valsartan

Has normal functions of ARB.

Sacubitril

Inhibits neprilysin.

Neprilysin

An enzyme that breaks down several peptides that are beneficial for cardiac functions.

Beneficial peptides

Peptides that reduce blood volume and pressure while dilating the blood vessels.

Adrenergic drugs

Include Alpha1 blockers, beta blockers, and combination alpha and beta blockers.

Alpha2 receptor agonist

Centrally acting adrenergic drugs that stimulate alpha2 adrenergic receptors, reducing sympathetic nervous system activity and norepinephrine production, leading to reduced blood pressure.

Alpha1 receptor blockers

Block alpha1-adrenergic receptors, which are stimulated by norepinephrine and increase BP; when blocked, BP is decreased and blood vessels are dilated.

Beta receptor blockers

Block beta1 receptors, reducing heart rate.

Renin

Reduction in secretion of renin to prevent angiotensin II.

First generation beta blockers

Non-selective blockers that block beta1 and beta2 receptors.

Second generation beta blockers

Cardioselective blockers that have limited blockade of beta1 receptors.

Third generation beta blockers

Vasodilating blockers that create vasodilation and produce nonselective or cardioselective beta blockade.

Combination alpha1 and beta receptor blockers

Beta1 receptor blockade reduces HR, alpha1 receptor blockade promotes vasodilation.

Ivabradine

SA node modulator that inhibits f-channels within SA node, resulting in reduced heart rate.

Loop diuretics

Act primarily along thick ascending limb of the loop of Henle, blocking chloride and sodium resorption.

Thiazide and Thiazide-Like diuretics

Considered equivalent in their effects, primarily acting on the distal convoluted tubule to inhibit resorption of Na, K, and Cl.

Potassium-sparing diuretics

Aldosterone-inhibiting diuretics that block aldosterone receptors, causing sodium and water to be excreted while retaining potassium.

Osmotic diuretics

Contain a nonabsorbable solute called mannitol, which increases osmotic pressure in glomerular filtrate.

Carbonic Anhydrase Inhibitors (CAIs)

Inhibit activity of the enzyme carbonic anhydrase in the kidneys, leading to reduced formation of hydrogen and bicarbonate.

Eplerenone

Selective aldosterone blocker that inhibits aldosterone action at receptor sites in the kidney, heart, blood vessels, and brain.

Bosentan

Endothelin receptor blocker that reduces blood pressure by blocking the action of endothelin hormone.

Verapamil

Calcium channel blocker associated with angioedema, hyperkalemia, and fetal harm (black box warning).

Digoxin

Cardiac glycoside with a long half-life, easy to accumulate to toxic levels, and a very narrow therapeutic range.

Nitroglycerin

Vasodilator that can cause circulatory collapse, paradoxical bradycardia, paresthesia, and peripheral edema.

Furosemide

Loop diuretic with a black box warning for fluid and electrolyte loss and potential ototoxicity.

Heparin

Coagulation modifier associated with spinal/epidural hematoma, heparin-induced thrombocytopenia, and osteoporosis.

Valsartan

ARB with a black box warning for fetal toxicity and potential decreased renal function.

Hydralazine

Vasodilator that requires extreme caution with associated syncope.

Metoprolol

Beta blocker with a black box warning against abrupt withdrawal, which can exacerbate angina and precipitate an MI.

Propranolol

Beta blocker with a black box warning against abrupt withdrawal, which can exacerbate angina and precipitate an MI.

Ivabradine

SA node modulator associated with atrial fibrillation, bradycardia, and conduction disturbances.

Hydrochlorothiazide

Thiazide diuretic that can cause electrolyte imbalance, specifically hypokalemia and hypercalcemia.

Enalapril

ACE inhibitor associated with angioedema, hyperkalemia, fetal harm (black box warning), first dose hypotension, and decreased renal function.

Valsartan/sacubitril

ARNi with a black box warning for fetal harm and associated with angioedema, hyperkalemia, and renal function deterioration.

Amlodipine

Calcium channel blocker.

Propranolol

Beta blocker.

Losartan

ARBs.

Lisinopril

ACE inhibitor.

Hydrochlorothiazide

Thiazide diuretic.

Enoxaparin

Low molecular weight heparin.

Isosorbide dinitrate

Antianginal, subclass: Nitrates.

Clopidogrel

Antiplatelet, subclass: P2Y12 adenosine diphosphate (ADP) receptor blockers.

Clonidine

Adrenergic drug, subclass: Alpha2 receptor agonist - centrally acting adrenergic drug.

Doxazosin

Adrenergic drug, subclass: Alpha-adrenergic-blocking drug or alpha blocker, specifically Alpha1 receptor blocker.