Unit 4 Drugs Flashcards

Question

Quinapril (Accupril)

Answer 1

(antihypertensives, angina, inotropic) * Class: long-acting ACE inhibitor (vasodilators) * (-pril = ACE inhibitor) * Mechanism: Blocks endothelial ACE from converting angiotensin I to angiotensin II (potent vasoconstrictor); as a side effect, also prevents breakdown of bradykinin (potent vasodilator) * Therapeutics: * Angina: Reduces incidence of future CAD events in patients at risk for/ with vascular disease * Antihypertensive and Inotropic: * 1st-line for CHF * left ventricular hypertrophy * post-MI (prevents left ventricular remodeling) * Important Side Effects: Dry cough, angioedema, hyperkalemia, hypotension, decreased renal function * Other Side Effects: * Miscellaneous: * Long-acting * Contraindicated in: * pregnancy * **renal artery stenosis** * hyperkalemia * prior angioedema (no ARB allowed, either) * Caution in renal failure * **May reduce risk of diabetes**

Answer 2

(antihypertensives, angina, inotropic) * Class: long-acting ACE inhibitor (vasodilators) * (-pril = ACE inhibitor) * Mechanism: Blocks endothelial ACE from converting angiotensin I to angiotensin II (potent vasoconstrictor); as a side effect, also prevents breakdown of bradykinin (potent vasodilator) * Therapeutics: * Angina: Reduces incidence of future CAD events in patients at risk for/ with vascular disease * Antihypertensive and Inotropic: * 1st-line for CHF * left ventricular hypertrophy * post-MI (prevents left ventricular remodeling) * Important Side Effects: Dry cough, angioedema, hyperkalemia, hypotension, inhibits renal autoregulation * Other Side Effects: * Miscellaneous: * Long-acting; * Contraindicated in: * pregnancy * **renal artery stenosis** * hyperkalemia * prior Angioedema (no ARB allowed, either); * Caution in renal failure * **May reduce risk of diabetes**

Answer 3

(antihypertensives, angina, inotropic) * Class ACE inhibitor (vasodilators) * (-pril = ACE inhibitor) * Mechanism: Blocks endothelial ACE from converting angiotensin I to angiotensin II (potent vasoconstrictor); as a side effect, also prevents breakdown of bradykinin (potent vasodilator) * Therapeutics: * Angina: Reduces incidence of future CAD events in patients at risk for/ with vascular disease * Antihypertensive & Inotropic: * 1st-line for CHF * left ventricular hypertrophy * post-MI (prevents left ventricular remodeling) * Important Side Effects: Dry cough, angioedema, hyperkalemia, hypotension, decreased renal function * Other Side Effects: * Miscellaneous: * Metabolized to enalaprilat, a more active metabolite * Contraindicated in: * pregnancy * **renal artery stenosis** * hyperkalemia * prior angioedema (no ARB allowed, either) * Caution in renal failure * **May reduce risk of diabetes**

Answer 4

(antihypertensive, inotropic) * Class: Angiotensin II Recepter Blocker (ARB) * (-sartan) * Mechanism: * Competitively inhibits binding of angiotensin II to type 1 angiotensin II receptors (AT1) in vascular endothelium * stimulates vascular smooth muscle contraction * dilates arteries and veins * promotes renal excretion of Na+ and water * inhibits cardiac and vascular remodeling * Therapeutics: * Used in place of an ACE-I when cough is an issue * To decrease peripheral vascular resistance w/little change in HR or CO; same uses as ACE-I (CHF, LV hypertrophy, post MI to prevent LV remodeling) * Important Side Effects: * Angioedema * hyperkalemia * hypotension * decreased renal function * **dry cough less frequent than with ACE-I** * Other Side Effects: * Miscellaneous: * Contraindicated in: * pregnancy * **renal artery stenosis** * hyperkalemia * prior angioedema (no ACE-i allowed, either) * caution in renal failure

Answer 5

(antihypertensive, inotropic) * Class: Angiotensin II Recepter Blocker (ARB) * (-sartan) * Mechanism: Competitively inhibits binding of angiotensin II to type 1 angiotensin II receptors (AT1) in vascular endothelium * stimulates vascular smooth muscle contraction * dilates arteries and veins * promotes renal excretion of Na+ and water * inhibits cardiac and vascular remodeling * Therapeutics: * Used in place of an ACE-I when cough is an issue * To decrease peripheral vascular resistance w/little change in HR or CO; same uses as ACE-I (CHF, LV hypertrophy, post MI to prevent LV remodeling) * Important Side Effects: * Angioedema * hyperkalemia * hypotension * decreased renal function * **dry cough less frequent than with ACE-I** * Other Side Effects: * Miscellaneous: * Contraindicated in: * pregnancy * **renal artery stenosis** * hyperkalemia * prior angioedema (no ACE-i allowed, either) * caution in renal failure

Answer 6

(antihypertensive, inotropic) * Class: Angiotensin II Recepter Blocker (ARB) * (-sartan) * Mechanism: Competitively inhibits binding of angiotensin II to type 1 angiotensin II receptors (AT1) in vascular endothelium * stimulates vascular smooth muscle contraction * dilates arteries and veins * promotes renal excretion of Na+ and water * inhibits cardiac and vascular remodeling * Therapeutics: * Used in place of an ACE-I when cough is an issue * To decrease peripheral vascular resistance w/little change in HR or CO; same uses as ACE-I (CHF, LV hypertrophy, post MI to prevent LV remodeling) * Important Side Effects: * Angioedema * hyperkalemia * hypotension * decreased renal function * **dry cough less frequent than with ACE-I** * Other Side Effects: * Miscellaneous: * Contraindicated in: * pregnancy * **renal artery stenosis** * hyperkalemia * prior angioedema (no ACE-i allowed, either) * caution in renal failure

Answer 7

(inotropic) * Class: Angiotensin II Recepter Blocker (ARB) * (-sartan) * Mechanism: Competitively inhibits binding of angiotensin II to type 1 angiotensin II receptors (AT1) in vascular endothelium * stimulates vascular smooth muscle contraction * dilates arteries and veins * promotes renal excretion of Na+ and water * inhibits cardiac and vascular remodeling * Therapeutics: Used in place of an ACEI when cough is an issue * Important Side Effects: Angioedema, hyperkalemia, hypotension, decresed GFR * Other Side Effects: * Miscellaneous:

Answer 8

(inotropic) * Class: Angiotensin Receptor Blocker (ARB) * Mechanism: Blocks type 1 angiotensin II receptors (stimulates vascular smooth muscle contraction, dilates arteries and veins, promotes renal excretion of Na and water, inhibits cardiac & vascular remodeling) * Therapeutics: Used in place of an ACEI when cough is an issue * Important Side Effects: Angioedema, hyperkalemia, hypotension, decresed GFR * Other Side Effects: * Miscellaneous:

Answer 9

(inotropic) * Class: Angiotensin II Recepter Blocker (ARB) * (-sartan) * Mechanism: Competitively inhibits binding of angiotensin II to type 1 angiotensin II receptors (AT1) in vascular endothelium * stimulates vascular smooth muscle contraction * dilates arteries and veins * promotes renal excretion of Na+ and water * inhibits cardiac and vascular remodeling * Therapeutics: Used in place of an ACE-I when cough is an issue * Important Side Effects: Angioedema, hyperkalemia, hypotension, decresed GFR * Other Side Effects: * Miscellaneous:

Answer 10

(antihyertensives) * Class: Renin inhibitor (**"****iren"**--\>**"inhibits renin"**) * Mechanism: inhibits renin * Therapeutics: Not very effective * Important Side Effects: * Other Side Effects: * Miscellaneous:

Answer 11

(antihypertensives, angina, anti-arrhythmic) * Class: Calcium channel blockers - non-dihydropyridine; * Class IV anti-arrhythmic * Mechanism: * Interact with L-type voltage gated plasma membrane Ca channel --\> decreased calcium entry into vascular smooth muscle cell, preventing contraction * **causes:** * **decreased contractility** * **decreased firing rate of aberrant pacemaker sites** * **and decreased conduction velocity** * **prolongs repolarization in SA node and AV node (--\> decreases HR)** * less vasodilation than the dihydropyridines * **act on heart** (in contrast to dihydropyr) * Anti-arrhythmic: Blockade of L-type calcium channels: slow SA & AV node activity; prolong AV refractoriness * Therapeutics: * Hypertension * anti-anginal (chronotropic effects --\> decreased myocardial oxygen demand) * Anti-arrhythmic: Prevent or terminate reentrant SVTs * **used in pts w/ chronic kidney disease** * Important Side Effects: * Leg edema * bradycardia * **AV nodal blockade** * hypotension * dizziness * **_worsening heart failure (negative inotrope)_** * Other Side Effects: * Constipation (most common) * headache * flushing * Increased serum digoxin levels * Miscellaneous: * Contraindicated in: * overt decompensated systolic heart failure * bradycardia * sinus node dysfunction * high-degree AV block * WPW

Answer 12

(antihypertensives, angina, anti-arrhythmic) * Class: Calcium channel blockers - non-dihydropyridine; * Class IV anti-arrhythmic * Mechanism: * Interact with L-type voltage gated plasma membrane Ca channel --\> decreased calcium entry into vascular smooth muscle cell, preventing contraction * **causes:** * **decreased contractility** * **decreased firing rate of aberrant pacemaker sites** * **and decreased conduction velocity** * **prolongs repolarization in SA node and AV node (--\> decreases HR)** * less vasodilation than the dihydropyridines * **act on heart** (in contrast to dihydropyr); verapamil = ventricle * Anti-arrhythmic: Blockade of L-type calcium channels: slow SA & AV node activity; prolong AV refractoriness * Therapeutics: * Hypertension * anti-anginal (chronotropic effects --\> decreased myocardial oxygen demand) * Anti-arrhythmic: Prevent / terminate reentrant SVTs * **used in pts w/ chronic kidney disease** * Important Side Effects: * Leg edema * bradycardia * **AV nodal blockade** * hypotension * dizziness * **_worsening heart failure (negative inotrope)_** * Other Side Effects: * Constipation (most common) * headache * flushing * Increased serum digoxin levels * Miscellaneous: * Contraindicated in: * overt decompensated systolic heart failure * bradycardia * sinus node dysfunction * high-degree AV block * WPW

Answer 13

(antihypertensives, angina, anti-arrhythmic) * Class: Calcium channel blocker - 1st generation dihydropyridine; Class IV anti-arrhythmic * dihydropyridine CCB = -dipine * Mechanism: * Interact with L-type voltage gated plasma membrane Ca channel --\> decreased calcium entry into vascular smooth muscle cell, preventing contraction * **causes dilation of epicardial coronary arteries and arteriolar resistance arteries** * less heart-specific activity * **act on vascular smooth muscle** (**vasoselective**, but less than 2nd gen) * anti-arrhythmic: Blockade of L-type calcium channels: slow SA & AV node activity; prolong AV refractoriness * Therapeutics: * HTN * Raynaud's * angina (3rd choice drug b/c cause reflex tachycardia and may worsen angina by increasing myocardial O2 demand) * Antiarrhythmic: prevent or terminate reentrant SVTs * Important Side Effects: * Leg edema (more than 2nd generation) * heart failure * reflex tachycardia (more than 2nd gen) *[lipophilic agents gain entry to brain and depress vasomotor center, causing vasodilation and rapidly dropping BP; this decreases effective stoke vol and causes more reflex sympathetic activation (Increse HR, leading to adverse CV effects) to try to maintain CO; long-acting agents are less lipophilic, and will cause less sympathetic activation and initial fall in BP]* * Anti-arrhythmic: Hypotension, bradycardia, dizziness * Other Side Effects: * Constipation (most common) * headache * flushing * Increased serum digoxin levels * Miscellaneous: * Contraindicated in: * overt decompensated systolic heart failure * bradycardia * sinus node dysfunction * WPW * no benefit in preserving renal function

Answer 14

(antihypertensives, angina, anti-arrhythmic) * Class: Calcium channel blocker - 2nd generation dihydropyridine; Class IV anti-arrhythmic * dihydropyridine CCB = -dipine * Mechanism: * Interact with L-type voltage gated plasma membrane Ca channel --\> decreased calcium entry into vascular smooth muscle cell, preventing contraction * **causes dilation of epicardial coronary arteries and arteriolar resistance arteries** * less heart-specific activity * **act on vascular smooth muscle** (**vasoselective**, and more than 1st gen) * anti-arrhythmic: Blockade of L-type calcium channels: slow SA & AV node activity; prolong AV refractoriness * Therapeutics: * HTN * Raynaud's * **1st line agent for coronary vasospasm** * angina (3rd choice drug b/c cause reflex tachycardia and may worsen angina by increasing myocardial O2 demand) * Antiarrhythmic: prevent or terminate reentrant SVTs * Important Side Effects: * Leg edema (less than 1st generation) * heart failure * reflex tachycardia (less than 1st gen) *[lipophilic agents gain entry to brain and depress vasomotor center, causing vasodilation and rapidly dropping BP; this decreases effective stoke vol and causes more reflex sympathetic activation (Increse HR, leading to adverse CV effects) to try to maintain CO; long-acting agents are less lipophilic, and will cause less sympathetic activation and initial fall in BP]* * Anti-arrhythmic: Hypotension, bradycardia, dizziness * Other Side Effects: * Constipation (most common) * headache * flushing * Increased serum digoxin levels * Miscellaneous: * Contraindicated in: * overt decompensated systolic heart failure * bradycardia * sinus node dysfunction * WPW * no benefit in preserving renal function

Answer 15

(angina) * Class: Calcium channel blocker - 2nd generation dihydropyridine * dihydropyridine CCB = -dipine * Mechanism: * Interact with L-type voltage gated plasma membrane Ca channel --\> decreased calcium entry into vascular smooth muscle cell, preventing contraction * **causes dilation of epicardial coronary arteries and arteriolar resistance arteries** * less heart-specific activity * **act on vascular smooth muscle** (**vasoselective**, and more than 1st gen) * Therapeutics: * **1st line agent for coronary vasospasm** * angina (3rd choice drug) * Raynaud's * Important Side Effects: * Leg edema (less than 1st generation) * heart failure * reflex tachycardia (less than 1st gen) * Other Side Effects: * Constipation (most common) * headache * flushing * Miscellaneous: * Contraindicated in: * overt decompensated heart failure * bradycardia * sinus node dysfunction

Answer 16

(angina) * Class: Calcium channel blocker - 2nd generation dihydropyridine * dihydropyridine CCB = -dipine * Mechanism: * Interact with L-type voltage gated plasma membrane Ca channel --\> decreased calcium entry into vascular smooth muscle cell, preventing contraction * **causes dilation of epicardial coronary arteries and arteriolar resistance arteries** * less heart-specific activity * **act on vascular smooth muscle** (**vasoselective**, and more than 1st gen) * Therapeutics: * 1**st line agent for coronary vasospasm** * angina (3rd choice drug) * Raynaud's * Important Side Effects: * Leg edema (less than 1st generation) * heart failure, * reflex tachycardia (less than 1st gen) * Other Side Effects: * Constipation (most common) * headache * flushing * Miscellaneous: * Contraindicated in: * overt decompensated heart failure * bradycardia * sinus node dysfunction

Answer 17

(antihypertensives, anti-arrhythmic) * Class: Nonselective β-blocker, Class II anti-arrhythmic * Mechanism: blocks β1 and β2 receptors * **Reduces cardiac output (primary reason for BP lowering)** * Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxta glomerular cells) * Reduces norepinephrine release from neurons * Decreases sympathetic tone (in vessels) * Overall you should expect very modest BP improvement from BB’s * _Anti-arrhythmic:_ Decreases SA & AV node activity (phase 4 depolarization) * Therapeutics: * HTN? * Control of ventricular rate in atrial fibrillation/flutter * long-term suppression of SVTs * PVCs * Important Side Effects: * Bronchospasm * bradycardia (negative chronotrope) * CHF (negative ionotrope) * masking of hypoglycemia symptoms * Heart block * hypotension * Other Side Effects: * Decreased exercise capacity * depression (crosses BBB) * worsening symptoms of peripheral vascular disease * Anti-arrhythmic: Contraindicated in WPW * **_Contraindicated in asthma_** * **_Contrindicated in HF_** * Miscellaneous:

Answer 18

(antihypertensive, angina, inotropic, anti-arrhythmic) * Class: β1-selective blocker; Class II anti-arrhythmics * Mechanism: * Antihypertensive: Moderately selective β1 blockade * **Reduces cardiac output (primary reason for BP lowering)** * Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxtaglomerular cells) * Reduces norepinephrine release from neurons * Decreases sympathetic tone (in vessels) * Overall you should expect very modest BP improvement from BB’s * _Angina:_ Decrease contractility and HR (reduced myocardial O₂ demand) * Inotropic (HF): Blocks high circulating levels of catecholamines * _Anti-arrhythmic:_ Decreases SA & AV node activity (phase 4 depolarization) * Therapeutics: * hypertension? * Angina: * Prevent MIs * prevent sudden cardiac death * increase survival post-MI (if patients suddenly stop, really bad!) * Inotropic: **_Dramatically decreases mortality in CHF patients (sustained release aka metoprolol succinate)_** * Anti-arrhythmic: * Control of ventricular rate in atrial fibrillation/flutter * long-term suppression of SVTs * PVCs * Important Side Effects: * Less likely to have bronchospasm, hypoglycemic awareness, and depression * Fatigue, worsening claudication, impotence (so men don't take) * Heart block, hypotension, bradycardia * **Contraindicated in asthma** * Other Side Effects: decreased exercise tolerance, lethargy, insomnia * Anti-arrhythmic: Contraindicated in WPW * Miscellaneous: * Angina: * Contraindicated in: * severe bradycardia * high degree AV block * sick sinus syndrome * unstable LV failure; * relative contraindication in: * asthma * severe depression * peripheral vascular disease * Inotropic: Should be started at very low dose and slowly ratchet up; do not stop suddenly

Answer 19

(antihypertensive, angina) * Class: β1-selective blocker * Mechanism: * Antihypertensive: Moderately selective β1 blockade * **Reduces cardiac output (primary reason for BP lowering)** * Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxtaglomerular cells) * Reduces norepinephrine release from neurons * Decreases sympathetic tone (in vessels) * Overall you should expect very modest BP improvement from BB’s * Angina: Decrease contractility and HR (reduced myocardial O₂ demand) * Therapeutics: * hypertension? * Angina: * Prevent MIs * prevent sudden cardiac death * increase survival post-MI (if patients suddenly stop, really bad!) * Important Side Effects: * Less likely to have bronchospasm, hypoglycemic awareness, and depression * Fatigue, worsening claudication, impotence (so men don't take) * **Contraindicated in asthma** * Other Side Effects: Decreased exercise tolerance, lethargy, insomnia * Miscellaneous: * Angina: * Contraindicated in: * severe bradycardia * high degree AV block * sick sinus syndrome * unstable LV failure * relative contraindication in: * asthma * severe depression * peripheral vascular disease

Answer 20

(antihypertensives) * Class: β1-selective blocker * Mechanism: Moderately selective β1 blockade * **Reduces cardiac output (primary reason for BP lowering)** * Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxta glomerular cells) * Reduces norepinephrine release from neurons * Decreases sympathetic tone (in vessels) * Overall you should expect very modest BP improvement from BB’s * Therapeutics: * Important Side Effects: Less likely to have bronchospasm, hypoglycemic awareness, and depression * **Contraindicated in asthma** * Other Side Effects: * Miscellaneous: **Longer-acting than other beta-blockers**

Answer 21

(antihypertensive, angina, inotropic) * Class: β1-selective blocker * Mechanism: * Antihypertensive: Moderately selective β1 blockade * **Reduces cardiac output (primary reason for BP lowering)** * Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxtaglomerular cells) * Reduces norepinephrine release from neurons * Decreases sympathetic tone (in vessels) * Overall you should expect very modest BP improvement from BB’s * Angina: Decrease contractility and HR (reduced myocardial O₂ demand) * Inotropic: Blocks high circulating levels of catecholamines * Therapeutics: * hypertension? * Angina: * Prevent MIs * prevent sudden cardiac death * increase survival post-MI (if patients suddenly stop, really bad!) * Inotropic: **_Dramatically decreases mortality in CHF patients_** * Important Side Effects: * Less likely to have bronchospasm, hypoglycemic awareness, and depression * Fatigue, worsening claudication, impotence (so men don't take) * **Contraindicated in asthma** * Other Side Effects: Decreased exercise tolerance, lethargy, insomnia * Miscellaneous: * **Longer-acting than other beta-blockers** * Angina: * Contraindicated in: * severe bradycardia * high degree AV block * sick sinus syndrome * unstable LV failure * relative contraindication in: * asthma * severe depression * peripheral vascular disease * Inotropic: Should be started at very low dose and slowly ratchet up; do not stop suddenly

Answer 22

(antihypertensives, anti-arrhythmic) * Class: β1-selective blocker; Class II anti-arrhythmic * Mechanism: * **Reduces cardiac output (primary reason for BP lowering)** * Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxta glomerular cells) * Reduces norepinephrine release from neurons * Decreases sympathetic tone (in vessels) * Overall you should expect very modest BP improvement from BB’s - Anti-arrhythmic: Decreases SA & AV node activity (phase 4 depolarization) * Therapeutics: * HTN: **AV nodal blockade in unstable patients** * Anti-arrhythmic: * Control of ventricular rate in atrial fibrillation/flutter * long-term suppression of SVTs * PVCs * Important Side Effects: * Heart block * hypotension * bronchospasm * bradycardia * **Contraindicated in asthma** * Other Side Effects: Contraindicated in WPW * Miscellaneous: **Short half-life (makes it unique; used IV)**

Answer 23

(antihypertensives) * Class: Combined αβ blocker * Mechanism: β1 blockade with vasodilatory effects * **Reduces cardiac output (primary reason for BP lowering)** * Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxta glomerular cells) * Reduces norepinephrine release from neurons * Decreases sympathetic tone (in vessels) * Overall you should expect very modest BP improvement from BB’s * Therapeutics: **Hypertensive urgency** * Important Side Effects: **Contraindicated in asthma** * Other Side Effects: * Miscellaneous:

Answer 24

(antihypertensives, inotropic, anti-arrhythmic) * Class: Combined αβ blocker; Class II anti-arrhythmic * 3rd generation β-blocker * Mechanism: * Antihypertensive: **β1 blockade with vasodilatory effects** * **Reduces cardiac output (primary reason for BP lowering)** * Inhibits renin release (by blocking binding of catecholamines to B1 receptors on juxta glomerular cells) * Reduces norepinephrine release from neurons * Decreases sympathetic tone (in vessels) * Overall you should expect very modest BP improvement from BB’s * **decrease afterload** * Inotropic (HF): **Blocks high circulating levels of catecholamines** * Anti-arrhythmic: Decreases SA & AV node activity (phase 4 depolarization) * Therapeutics: * Antihypertensives: **Acute coronary syndrome, CHF** * Inotropic: \*_**Dramatically decreases mortality in CHF patients\***_ * Anti-arrhythmic: * Control of ventricular rate in atrial fibrillation/flutter * long-term suppression of SVTs * PVCs * Important Side Effects: * Heart block * hypotension * bronchospasm * bradycardia * **Contraindicated in asthma** * Other Side Effects: Contraindicated in WPW * Miscellaneous: * Inotropic: Should be started at very low dose and slowly ratchet up; do not stop suddenly

Answer 25

(antihypertensives) * Class: α1-adrenergic receptor antagonist (α1-blocker) * (-zosin) * Mechanism: Blocks post-synaptic α1-adrenergic receptor on vascular smooth muscle * decrease peripheral resistance by dilating arterioles & veins * Therapeutics: * BPH * second-tier meds for HTN (use when other condition around, not for isolated hypertension) * b/c compared to thiazides, ACE-Is, & CCBs, this class os drug is more likely to cause cardiac complications * Important Side Effects: * Orthostatic hypotension * fluid retention * worsening angina (secondary to reflex tachycardia) * Other Side Effects: * Miscellaneous:

Answer 26

(antihypertensives) * Class: α1-adrenergic receptor antagonist (α1-blocker) * (-zosin) * Mechanism: Blocks post-synaptic α1-adrenergic receptor antagonist on vascular smooth muscle * decrease peripheral resistance by dilating arterioles & veins * Therapeutics: * BPH * second-tier meds (use when other condition around, not for isolated hypertension) * b/c compared to thiazides, ACE-Is, & CCBs, this class os drug is more likely to cause cardiac complications * Important Side Effects: * Orthostatic hypotension * fluid retention * worsening angina (secondary to reflex tachycardia) * Other Side Effects: * Miscellaneous:

Answer 27

(antihypertensives) * Class: Central α2-agonist (central-acting sympathoplegic) * Mechanism: Stimulation of central α2a adrenergic receptors --\> reduction in sympathetic outflow from vasomotor systems in brainstem; inhibition of renin release (secondary to decreased sympathetic tone) * Therapeutics: * Important Side Effects: Rebound HTN if abruptly stopped; moderate orthostatic hypotension * Other Side Effects: Sedation, dry mouth, fatigue, depression * Miscellaneous: clonidine is the only one routinely used

Answer 28

(antihypertensives) * Class: Central α2-agonist (central-acting sympathoplegic) * Mechanism: Stimulation of central α2a adrenergic receptors --\> reduction in sympathetic outflow from vasomotor systems in brainstem; inhibition of renin release (secondary to decreased sympathetic tone) * Therapeutics: **Hypertension of pregnancy (only)** * Important Side Effects: Rebound HTN if abruptly stopped; moderate orthostatic hypotension * Other Side Effects: Sedation, dry mouth, fatigue, depression * Miscellaneous: * Takes place of dopa, so less NE (also, methyl-NE activates α2)

Answer 29

(antihypertensives) * Class: Ganglion blocking agent (adrenergic neuron blocking agent) * Mechanism: blocks transport of NE, DA, & 5HT into storage granules in PNS & CNS --\> less neurotransmitter available when nerves are stimulated * Therapeutics: Decrease cardiac output and systemic vascular resistance * Important Side Effects: * Sedation, mental depression, Parkinsonism symptoms * Other Side Effects: * Miscellaneous: not used

Answer 30

(antihypertensives) * Class: Direct (vasodilators) * Mechanism: Relax smooth muscle of peripheral arterioles * Therapeutics: Hypertensive urgency; patients with BOTH advanced CHF and hypertension * Important Side Effects: Drug-induced lupus * Other Side Effects: reflex tachycardia * Miscellaneous: Serves as an antioxidant, preventing oxidation of NO

Answer 31

(antihypertensives) * Class: Direct (vasodilators) * Mechanism: Relax smooth muscle of peripheral arterioles * Therapeutics: Refractory hypertension; hair loss * Important Side Effects: Pericardial effusion; hirsutism * Other Side Effects: reflex tachycardia * Miscellaneous: Smooth muscle relaxation by opening cardiovascular ATP-sensitive potassium channels

Answer 32

(hypolipidemics) * Class: Nicotinic acid * Mechanism: Reduction of liver triglyceride synthesis, leading to less hepatic VLDL (thus, LDL) production; decreases lipolysis in adipose tissue, leading to lowered FFA transport to liver (thus, less triglycerides); reduced hepatic clearance of ApoAI (raising HDL) * Therapeutics: Best agent to increase HDL (30-40%); as good as fibrates and statins at lowering triglycerides (35-45%); lowers LDL (20-30%); hypertriglyceridemia and low HDL * Important Side Effects: Flushing, pruritis of face and upper trunk, rashes, acanthosis nigricans (hyperpigmentation) * Other Side Effects: Hepatotoxicity, hyperuricemia, hyperglycemia; dyspepsia/reactivation of peptic ulcer disease; rarely, toxic ambylopia, tachyarrhythmias, a-fib (in elderly) and myopathy * Miscellaneous: Water soluble B vitamin complex at [low]; hypolipidemic at [high]; side effects limit compliance (\<50% eligible patients follow on it); contraindicated in DM and gout patients; prevent flushing and pruritus with ASA

Answer 33

(hypolipidemics) * Class: Fibric Acid Derivatives (Fibrates) * Mechanism: Unknown; may interact w/peroxisome proliferator-activated receptor (esp. PPARα) to stimulate LPL synthesis (enhance TG-rich lipoprotein clearance); inhibit apoC III expression (enhance VLDL clearance); stimulation of apoAI and apoAII (increase HDL) * Therapeutics: Marked reduction in VLDL (thus, triglycerides); variable and small effect on LDL; small increase in HDL (10%); severe hypertriglyceridemia * Important Side Effects: Potentiate oral anticoagulants (displace from albumin), increase bile lithogenicity; myositis flu-like syndrome in 5%, other effects in 10% (not serious) * Other Side Effects: * Miscellaneous: Combination w/statin inadvisable due to higher myositis risk

Answer 34

(hypolipidemics) * Class: Fibric Acid Derivatives (Fibrates) * Mechanism: Unknown; may interact w/peroxisome proliferator-activated receptor (esp. PPARα) to stimulate LPL synthesis (enhance TG-rich lipoprotein clearance); inhibit apoC III expression (enhance VLDL clearance); stimulation of apoAI and apoAII (increase HDL) * Therapeutics: Marked reduction in VLDL (thus, triglycerides); variable and small effect on LDL; small increase in HDL (10%); severe hypertriglyceridemia * Important Side Effects: Potentiate oral anticoagulants (displace from albumin), increase bile lithogenicity (less than clofibrate); myositis flu-like syndrome in 5%, other effects in 10% (not serious) * Other Side Effects: * Miscellaneous: Combination w/statin inadvisable due to higher myositis risk

Answer 35

(hypolipidemics) * Class: Fibric Acid Derivatives (Fibrates) * Mechanism: Unknown; may interact w/peroxisome proliferator-activated receptor (esp. PPARα) to stimulate LPL synthesis (enhance TG-rich lipoprotein clearance); inhibit apoC III expression (enhance VLDL clearance); stimulation of apoAI and apoAII (increase HDL) * Therapeutics: Marked reduction in VLDL (thus, triglycerides); variable and small effect on LDL; small increase in HDL (10%); severe hypertriglyceridemia * Important Side Effects: Potentiate oral anticoagulants (displace from albumin), increase bile lithogenicity (less than clofibrate); myositis flu-like syndrome in 5%, other effects in 10% (not serious) * Other Side Effects: * Miscellaneous: Combination w/statin inadvisable due to higher myositis risk

Answer 36

(hypolipidemics) * Class: Bile acid sequestrants * Mechanism: Very positively charged resins binds negative charged bile acids, inhibiting reabsorption and increasing cholesterol loss; leads to increase in LDL receptors in liver (to make more cholesterol), decreasing LDL in blood * Therapeutics: Decrease LDL (25%), but slight increase (5%) in TG and HDL * Important Side Effects: Very safe (only hypolipidemic indicated for children) because not systematically absorbed; impairs fat soluble vitamin absorption, binds other drugs (e.g., cardiac glycosides, coumarins) * Other Side Effects: Bloating, dyspepsia, constipation, gritty/unpleasant taste * Miscellaneous: Standard treatment in combo w/statin; contraindicated in hypertriglyceridemia

Answer 37

(hypolipidemics) * Class: Bile acid sequestrants * Mechanism: Very positively charged resins binds negative charged bile acids, inhibiting reabsorption and increasing cholesterol loss; leads to increase in LDL receptors in liver (to make more cholesterol), decreasing LDL in blood * Therapeutics: Decrease LDL (25%), but slight increase (5%) in TG and HDL * Important Side Effects: Very safe (only hypolipidemic indicated for children) because not systematically absorbed; impairs fat soluble vitamin absorption, binds other drugs (e.g., cardiac glycosides, coumarins) * Other Side Effects: Bloating, dyspepsia, constipation, gritty/unpleasant taste * Miscellaneous: Standard treatment in combo w/statin; contraindicated in hypertriglyceridemia

Answer 38

(hypolipidemics) * Class: Bile acid sequestrants * Mechanism: Very positively charged resins binds negative charged bile acids, inhibiting reabsorption and increasing cholesterol loss; leads to increase in LDL receptors in liver (to make more cholesterol), decreasing LDL in blood * Therapeutics: Decrease LDL (25%), but slight increase (5%) in TG and HDL * Important Side Effects: Very safe (only hypolipidemic indicated for children) because not systematically absorbed; impairs fat soluble vitamin absorption, binds other drugs (e.g., cardiac glycosides, coumarins) * Other Side Effects: Bloating, dyspepsia, constipation, gritty/unpleasant taste * Miscellaneous: Standard treatment in combo w/statin; contraindicated in hypertriglyceridemia

Answer 39

(hypolipidemics) * Class: HMG-CoA reductase Inhibitors (-statins) * Mechanism: Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG * Therapeutics: Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%) * Important Side Effects: Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking) * Other Side Effects: * Miscellaneous: Lactone prodrug (modified in liver to hydroxy acid form); must be taken in evening; Advicor = niacin + lovastatin

Answer 40

(hypolipidemics) * Class: HMG-CoA reductase Inhibitors (-statins) * Mechanism: Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG * Therapeutics: Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%) * Important Side Effects: Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking) * Other Side Effects: * Miscellaneous: Lactone prodrug (modified in liver to hydroxy acid form); must be taken in evening; Vytorin = ezetemibe + simvastatin

Answer 41

(hypolipidemics) * Class: HMG-CoA reductase Inhibitors (-statins) * Mechanism: Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG * Therapeutics: Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%) * Important Side Effects: Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking) * Other Side Effects: * Miscellaneous: Must be taken in evening

Answer 42

(hypolipidemics) * Class: HMG-CoA reductase Inhibitors (-statins) * Mechanism: Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG * Therapeutics: Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%) * Important Side Effects: Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking) * Other Side Effects: * Miscellaneous: Must be taken in evening

Answer 43

(hypolipidemics) * Class: HMG-CoA reductase Inhibitors (-statins) * Mechanism: Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG * Therapeutics: Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%) * Important Side Effects: Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking) * Other Side Effects: * Miscellaneous: Due to longer half-life, can be taken anytime per day

Answer 44

(hypolipidemics) * Class: HMG-CoA reductase Inhibitors (-statins) * Mechanism: Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG * Therapeutics: Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%) * Important Side Effects: Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking) * Other Side Effects: * Miscellaneous: Due to longer half-life, can be taken anytime per day

Answer 45

(hypolipidemics) * Class: HMG-CoA reductase Inhibitors (-statins) * Mechanism: Inhibits HMG-CoA reductase formation of mevalonate; leads to activation of SREBP, a membrane-bound transcription factor that increases LDL-R synthesis and lessens degradation; reduction in cholesterol decreases VLDL synthesis, lowering TG * Therapeutics: Reduce LDL (20-55%) and TG (25%), while increasing HDL (5-10%); treatment of dyslipidemia (reduces fatal & nonfatal CHD, strokes; total mortality reduction is 20%) * Important Side Effects: Very few; hepatic dysfunction in 1% (serious hepatotoxicity rare); myopathy/rhabdomyolysis (reduced if factors inhibiting statin catabolism lacking) * Other Side Effects: * Miscellaneous: Due to longer half-life, can be taken anytime per day

Answer 46

(hypolipidemics) * Class: Inhibits enterocyte absorption of cholesterol in intestine * Mechanism: Decreases LDL-C alone (15-20%) or in combination w/statin (60%) * Therapeutics: Inhibits cholesterol absorption by enterocytes in jejunum (70% in mice), leading to less cholesterol in chylomicrons; reduction in chylomicron remnant cholesterol delivery to liver; may also decrease atherogenesis directly (remnants very atherogenic) * Important Side Effects: None (rare allergies) * Other Side Effects: * Miscellaneous: Long-term decrease in endpoints not seen yet (questionable effectiveness)

Answer 47

(hypolipidemics) * Class: PCSK9 inhibitors * Mechanism: Inhibits an endopeptidase (PCSK9) responsible for LDL-R degradation, resulting in higher numbers of LDL-Rs on hepatocytes * Therapeutics: 2nd line therapy for hypercholesterolemia not controlled by diet and statins * Important Side Effects: Injection site reactions; flu-like symptoms; nose and throat irritation; muscle pain; diarrhea * Other Side Effects: * Miscellaneous:

Answer 48

(hypolipidemics) * Class: PCSK9 inhibitors * Mechanism: Inhibits an endopeptidase (PCSK9) responsible for LDL-R degradation, resulting in higher numbers of LDL-Rs on hepatocytes * Therapeutics: 2nd line therapy for hypercholesterolemia not controlled by diet and statins * Important Side Effects: Injection site reactions; flu-like symptoms; nose and throat irritation; muscle pain; diarrhea * Other Side Effects: * Miscellaneous:

Answer 49

(angina) * Class: NSAID - Antiplatelet agent * Mechanism: Irreversible inhibition of COX (thus no TxA2 synthesis), so blocks platelet aggregation * Therapeutics: Reduction in adverse events (MI, CVA, death); for those w/stable angina, unstable angina, acute MI, prophylaxis * Important Side Effects: * Other Side Effects: * Miscellaneous: Low-doses; if you're allergic, you'll get asthma

Answer 50

(angina) * Class: Thienopyridine antiplatelet agent * Mechanism: Inhibits platelet aggregation by ADP; reduces blood viscosity by decreasing plasma fibrinogen and increasing RBC deformability * Therapeutics: Aspirin alternative * Important Side Effects: Neutropenia and, rarely, TTP * Other Side Effects: * Miscellaneous: Not really used anymore

Answer 51

(angina) * Class: Thienopyridine antiplatelet agent * Mechanism: Selectively and irreversibly inhibits ADP binding to P2Y12 (blocks ADP-dependent activation of glycoprotein IIb/IIIa complex) * Therapeutics: Great antithrombotic; standard of care w/ stent * Important Side Effects: Bleeding * Other Side Effects: * Miscellaneous: No surgical or dental procedures if patient taking this

Answer 52

(angina) * Class: Thienopyridine antiplatelet agent * Mechanism: Irreversibly binds P2Y12 receptor (G protein-coupled chemoreceptor for ADP) * Therapeutics: Reduce thrombotic events in those w/percutaneous coronary intervention (e.g., stent) * Important Side Effects: Massive bleeding risk * Other Side Effects: * Miscellaneous: Drug is limited to patients under 75 in age, greater than 60 Kg in weight, and no history of stroke or TIA.

Answer 53

(angina) * Class: Adenosine-like antiplatelet agent * Mechanism: Reversibly blocks ADP receptors * Therapeutics: Great antithrombic * Important Side Effects: Bleeding * Other Side Effects: * Miscellaneous: Requires bid dosing

Answer 54

(angina) * Class: Pyrimido-pyrimidine antiplatelet agent * Mechanism: Increases platelet intracellular cAMP (inhibits phosphodiesterase 5, activates adenylate cyclase, inhibits uptake of adenosine from vascular endothelium and RBCs) * Therapeutics: Decrease peripheral vascular disease (as an adjunct); stress test of heart * Important Side Effects: Vasodilation of coronary arteries can enhance exercise-induced ischemia (because it elevates extracellular adenosine levels) * Other Side Effects: * Miscellaneous:

Answer 55

(angina) * Class: Quinoline antiplatelet agent * Mechanism: Inhibits cellular phosphodiesterase & so raises intracellular cAMP * Therapeutics: Treatment for claudication with peripheral vascular disease * Important Side Effects: Vasodilation * Other Side Effects: * Miscellaneous: Contraindicated in heart failure

Answer 56

(angina, inotropic) * Class: long-acting ACE inhibitor (vasodilators) * Mechanism: Blocks endothelial ACE from converting angiotensin I to angiotensin II (potent vasoconstrictor); as a side effect, also prevents breakdown of bradykinin (potent vasodilator) * Therapeutics: * Angina & Inotropic: 1st-line for CHF; post-MI (prevents left ventricular remodeling); Reduces incidence of future CAD events in patients at risk for/ with vascular disease * Important Side Effects: Dry cough, angioedema, hyperkalemia, hypotension, inhibits renal autoregulation * Other Side Effects: * Miscellaneous: * Long-acting; * Contraindicated in pregnancy, renal artery stenosis, hyperkalemia, and prior Angioedema (no ARB allowed, either); * Caution in renal failure;

Answer 57

(angina) * Class: Vasodilator * Mechanism: Endothelium independent vasodilator; endothelial effects (inhibits platelet aggregation, inhibits leukocyte-endothelial interactions (anti-inflammatory)) * Therapeutics: For acute episodes; long-acting formulations are for those already on other drugs and still can't control angina * Important Side Effects: Tolerance w/chronic use (need nitrate free periods of 8-12 hours), headaches, hypotension, activation of Bezold-Jarisch reflex (causes bradycardia) * Other Side Effects: Decrease preload * Miscellaneous: Contraindicated in hypertrophic cardiomyopathy, severe aortic stenosis, significant hypotension, use of phosphodiesterase inhibitors

Answer 58

(angina) * Class: Vasodilator * Mechanism: Endothelium independent vasodilator; endothelial effects (inhibits platelet aggregation, inhibits leukocyte-endothelial interactions (anti-inflammatory)) * Therapeutics: For acute episodes; long-acting formulations are for those already on other drugs and still can't control angina * Important Side Effects: Tolerance w/chronic use (need nitrate free periods of 8-12 hours), headaches, hypotension, activation of Bezold-Jarisch reflex (causes bradycardia) * Other Side Effects: Decrease preload * Miscellaneous: Contraindicated in hypertrophic cardiomyopathy, severe aortic stenosis, significant hypotension, use of phosphodiesterase inhibitors

Answer 59

(inotropic, anti-arrhythmic) * Class: Cardiac glycoside, anti-arrhythmic * Mechanism: Inhibits Na/K/ATPase (increases contractility d/t more Ca); increases vagal activity to heart (reduces SA firing rate, slows conduction through AV node) * Therapeutics: Improves LV function, decreases neurohormonal activation, increases vagal tone, normalizes arterial baroreceptors; decreases hospitalizations in CHF (no mortality benefit); - anti-arrhythmic: Atrial fibrillation/flutter, chronic SVT, HF * Important Side Effects: Very narrow therapeutic-toxic window (mostly arrhythmias) - anti-arrhythmic: Nausea, cognitive dysfunction, blurred or yellow vision * Other Side Effects: May cause DAD arrhythmias * Miscellaneous: Eliminated in kidneys, so dose according to renal function

Answer 60

(inotropic) * Class: β1 receptor agonist * Mechanism: Positive inotrope and chronotrope * Therapeutics: Acutely decompensated patients (about half will die after 6 months) * Important Side Effects: Quick acting, but can develop tachyphylaxis after 48 hours * Other Side Effects: * Miscellaneous: No NE release; given IV

Answer 61

(inotropic) * Class: Phosphodiesterase IIIa inhibitor * Mechanism: Inhibits cAMP breakdown * Therapeutics: Acute setting of heart failure; short-term only * Important Side Effects: Increased hypotensive and atrial arrhythmia events acutely. 2 month mortality nearly 50% higher than placebo * Other Side Effects: * Miscellaneous: Given IV, depends on renal clearance, no tolerance after 72 hours

Answer 62

(asthma) * Class: Bronchodilator - short-acting β2 agonist) * Mechanism: Relax bronchial smooth muscle, inhibit mediator release (mast cells, basophils), increase mucociliary clearance, suppression of microvascular permeability * Therapeutics: Prevent or reduce exercise-induced bronhospasms; mild asthma & acute exacerbations * Important Side Effects: Musculoskeletal tremor, Tachycardia, hyperglycemia, hypokalemia, hypomagnesemia * Other Side Effects: Tolerance with chronic use, Prolonged QTc, lactic acidosis, paradoxical bronchospasm * Miscellaneous: 5 minutes to take action, 4-6 hours duration; nebulizer delivers more, but greater side effects. Note: Levalbuterol is R-isomer of albuterol.

Answer 63

(asthma) * Class: Bronchodilator - short-acting β2 agonist) * Mechanism: Relax bronchial smooth muscle, inhibit mediator release (mast cells, basophils), increase mucociliary clearance, suppression of microvascular permeability * Therapeutics: Prevent or reduce exercise-induced bronhospasms; mild asthma & acute exacerbations * Important Side Effects: Musculoskeletal tremor, Tachycardia, hyperglycemia, hypokalemia, hypomagnesemia * Other Side Effects: Tolerance with chronic use, Prolonged QTc, lactic acidosis, paradoxical bronchospasm * Miscellaneous: 5 minutes to take action, 4-6 hours duration; nebulizer delivers more, but greater side effects. Note: Levalbuterol is R-isomer of albuterol.

Answer 64

(asthma) * Class: Bronchodilator - short-acting β2 agonist) * Mechanism: Relax bronchial smooth muscle, inhibit mediator release (mast cells, basophils), increase mucociliary clearance, suppression of microvascular permeability * Therapeutics: Prevent or reduce exercise-induced bronhospasms; mild asthma & acute exacerbations * Important Side Effects: Musculoskeletal tremor, Tachycardia, hyperglycemia, hypokalemia, hypomagnesemia * Other Side Effects: Tolerance with chronic use, Prolonged QTc, lactic acidosis, paradoxical bronchospasm * Miscellaneous: 5 minutes to take action, 4-6 hours duration; nebulizer delivers more, but greater side effects. Note: Levalbuterol is R-isomer of albuterol.

Answer 65

(asthma) * Class: Bronchodilator - short-acting β2 agonist) * Mechanism: Relax bronchial smooth muscle, inhibit mediator release (mast cells, basophils), increase mucociliary clearance, suppression of microvascular permeability * Therapeutics: Prevent or reduce exercise-induced bronhospasms; mild asthma & acute exacerbations * Important Side Effects: Musculoskeletal tremor, Tachycardia, hyperglycemia, hypokalemia, hypomagnesemia * Other Side Effects: Tolerance with chronic use, Prolonged QTc, lactic acidosis, paradoxical bronchospasm * Miscellaneous: 5 minutes to take action, 4-6 hours duration; nebulizer delivers more, but greater side effects. Note: Levalbuterol is R-isomer of albuterol.

Answer 66

(asthma) * Class: Bronchodilator - long-acting β2 agonist * Mechanism: Relax bronchial smooth muscle, inhibit mediator release (mast cells, basophils), increase mucociliary clearance, suppression of microvascular permeability * Therapeutics: used for long-term control of asthma symptoms (always in comination with inhaled steroids) * Important Side Effects: Musculoskeletal tremor, Tachycardia, hyperglycemia, hypokalemia, hypomagnesemia * Other Side Effects: Tolerance with chronic use, Prolonged QTc, lactic acidosis, paradoxical bronchospasm * Miscellaneous: 10-15 minutes to take action, 6-12 hours (max) of duration; nebulizer delivers more, but greater side effects; oral is least effective (requires more dose --\> side effects); can be used night symptoms, but not ideal

Answer 67

(asthma) * Class: Bronchodilator - long-acting β2 agonist * Mechanism: Relax bronchial smooth muscle, inhibit mediator release (mast cells, basophils), increase mucociliary clearance, suppression of microvascular permeability * Therapeutics: used for long-term control of asthma symptoms (always in comination with inhaled steroids) * Important Side Effects: Musculoskeletal tremor, Tachycardia, hyperglycemia, hypokalemia, hypomagnesemia * Other Side Effects: Tolerance with chronic use, Prolonged QTc, lactic acidosis, paradoxical bronchospasm * Miscellaneous: 10-15 minutes to take action, 6-12 hours (max) of duration; nebulizer delivers more, but greater side effects; oral is least effective (requires more dose --\> side effects); can be used night symptoms, but not ideal

Answer 68

(asthma) * Class: Bronchodilator - long-acting β2 agonist * Mechanism: Relax bronchial smooth muscle, inhibit mediator release (mast cells, basophils), increase mucociliary clearance, suppression of microvascular permeability * Therapeutics: used for long-term control of asthma symptoms (always in comination with inhaled steroids) * Important Side Effects: Musculoskeletal tremor, Tachycardia, hyperglycemia, hypokalemia, hypomagnesemia * Other Side Effects: Tolerance with chronic use, Prolonged QTc, lactic acidosis, paradoxical bronchospasm * Miscellaneous: 10-15 minutes to take action, 6-12 hours (max) of duration; nebulizer delivers more, but greater side effects; oral is least effective (requires more dose --\> side effects); can be used night symptoms, but not ideal

Answer 69

(asthma) * Class: Bronchodilator (Methylxanthine) * Mechanism: Phosphodiesterase inhibition and enhanced signalling via increased cAMP and cGMP; relax bronchial smooth muscle * Therapeutics: Reduce inflammation and bronchospasm in moderate to severe asthma, night symptoms * Important Side Effects: CNS stimulation or seizures, tachycardia/arrythmias, anorexia, nausea * Other Side Effects: * Miscellaneous: Low therapeutic index! Metabolized by liver; cimetidine and quinoline increase blood levels

Answer 70

(asthma) * Class: Bronchodilator (Methylxanthine) * Mechanism: Phosphodiesterase inhibition and enhanced signalling via increased cAMP and cGMP; relax bronchial smooth muscle * Therapeutics: Reduce inflammation and bronchospasm in moderate to severe asthma, night symptoms * Important Side Effects: CNS stimulation or seizures, tachycardia/arrythmias, anorexia, nausea * Other Side Effects: * Miscellaneous: Low therapeutic index! Metabolized by liver; cimetidine and quinoline increase blood levels

Answer 71

(asthma) * Class: Bronchodilator (Methylxanthine) * Mechanism: Phosphodiesterase inhibition and enhanced signalling via increased cAMP and cGMP; relax bronchial smooth muscle * Therapeutics: Reduce inflammation and bronchospasm in moderate to severe asthma, night symptoms * Important Side Effects: CNS stimulation or seizures, tachycardia/arrythmias, anorexia, nausea * Other Side Effects: * Miscellaneous: Low therapeutic index! Metabolized by liver; cimetidine and quinoline increase blood levels

Answer 72

(asthma) * Class: Methylxanthine * Mechanism: Selective PDE4 inhibitor; more of an anti-inflammatory agent than bronchodilator * Therapeutics: COPD * Important Side Effects: CNS stimulation or seizures, tachycardia/arrythmias, anorexia, nausea * Other Side Effects: * Miscellaneous:

Answer 73

(asthma) * Class: Quarternary amine antimuscarinic * Mechanism: Blocks vagal pathways and decreases vagal tone to bronchial smooth muscle; also blocks the reflex bronchoconstriction caused by inhaled irritants * Therapeutics: First-line agent for chronic COPD; status asthmaticus (w/ nebulized β2-agonists); no role in chronic stable asthma * Important Side Effects: Typical antimuscarinic effects; acute angle glaucoma; paradoxical bronchospasm * Other Side Effects: * Miscellaneous: Note: tiotropium has anti-inflammatory properties and decreases mucus secretion.

Answer 74

(asthma) * Class: Quarternary amine antimuscarinic * Mechanism: Blocks vagal pathways and decreases vagal tone to bronchial smooth muscle; also blocks the reflex bronchoconstriction caused by inhaled irritants * Therapeutics: First-line agent for chronic COPD; status asthmaticus (w/ nebulized β2-agonists); no role in chronic stable asthma * Important Side Effects: Typical antimuscarinic effects; acute angle glaucoma; paradoxical bronchospasm * Other Side Effects: * Miscellaneous: Note: tiotropium has anti-inflammatory properties and decreases mucus secretion.

Answer 75

(asthma) * Class: Quarternary amine antimuscarinic * Mechanism: Blocks vagal pathways and decreases vagal tone to bronchial smooth muscle; also blocks the reflex bronchoconstriction caused by inhaled irritants * Therapeutics: First-line agent for chronic COPD; status asthmaticus (w/ nebulized β2-agonists); no role in chronic stable asthma * Important Side Effects: Typical antimuscarinic effects; acute angle glaucoma; paradoxical bronchospasm * Other Side Effects: * Miscellaneous: Note: tiotropium has anti-inflammatory properties and decreases mucus secretion.

Answer 76

(asthma) * Class: Quarternary amine antimuscarinic * Mechanism: Blocks vagal pathways and decreases vagal tone to bronchial smooth muscle; also blocks the reflex bronchoconstriction caused by inhaled irritants * Therapeutics: Functionally similar to tiotropium * Important Side Effects: Less systemic & CNS side effects than other antimuscarinics due to extremely short circulation half-life. * Other Side Effects: * Miscellaneous:

Answer 77

(asthma) * Class: Corticosteroid - anti-inflammatory agent * Mechanism: Anti-inflammatory effects: inhibition of growth factor secretion, inhibition of arachidonic acid metabolites and platelet activation factor, inhibition of leukocyte accumulation, decreased vascular permeability, inhibition of neuropeptide-mediated responses, inhibition of mucous glycoprotein secretion * Therapeutics: Cornerstone treatment of persistent asthma; beneficial comination with beta-2 agonist; limited role in COPD * Important Side Effects: Inhaled has thrush, hoarseness, dry cough, mild adrenal suppression (higher doses); oral has mood-swings, increased appetite, and suppression of adrenocorticotropic hormone secretion (Cushing's Syndrome) * Other Side Effects: * Miscellaneous:

Answer 78

(asthma) * Class: Corticosteroid - anti-inflammatory agent * Mechanism: Anti-inflammatory effects: inhibition of growth factor secretion, inhibition of arachidonic acid metabolites and platelet activation factor, inhibition of leukocyte accumulation, decreased vascular permeability, inhibition of neuropeptide-mediated responses, inhibition of mucous glycoprotein secretion * Therapeutics: Cornerstone treatment of persistent asthma; beneficial comination with beta-2 agonist; limited role in COPD * Important Side Effects: Inhaled has thrush, hoarseness, dry cough, mild adrenal suppression (higher doses); oral has mood-swings, increased appetite, and suppression of adrenocorticotropic hormone secretion (Cushing's Syndrome) * Other Side Effects: * Miscellaneous:

Answer 79

(asthma) * Class: Corticosteroid - anti-inflammatory agent * Mechanism: Anti-inflammatory effects: inhibition of growth factor secretion, inhibition of arachidonic acid metabolites and platelet activation factor, inhibition of leukocyte accumulation, decreased vascular permeability, inhibition of neuropeptide-mediated responses, inhibition of mucous glycoprotein secretion * Therapeutics: Cornerstone treatment of persistent asthma; beneficial comination with beta-2 agonist; limited role in COPD * Important Side Effects: Inhaled has thrush, hoarseness, dry cough, mild adrenal suppression (higher doses); oral has mood-swings, increased appetite, and suppression of adrenocorticotropic hormone secretion (Cushing's Syndrome) * Other Side Effects: * Miscellaneous:

Answer 80

(asthma) * Class: Corticosteroid - anti-inflammatory agent * Mechanism: Same as other corticosteroids, but is a prodrug and only activated by airway esterase. * Therapeutics: Cornerstone treatment of persistent asthma; beneficial comination with beta-2 agonist; limited role in COPD * Important Side Effects: Less side effects than other corticosteroids (on site activation required) * Other Side Effects: * Miscellaneous:

Answer 81

(asthma) * Class: Anti-inflammatory agent * Mechanism: Prevent mast cell degranulation and mediator release from mast cells * Therapeutics: Prophylaxis for inhibiting both early and late phase reactions; best results in mild and allergic asthma * Important Side Effects: Minimal local side effect (cough & throat irritation) * Other Side Effects: * Miscellaneous:

Answer 82

(asthma) * Class: Anti-inflammatory agent * Mechanism: Prevent mast cell degranulation and mediator release from mast cells * Therapeutics: Prophylaxis for inhibiting both early and late phase reactions; best results in mild and allergic asthma * Important Side Effects: Minimal local side effect (cough & throat irritation) * Other Side Effects: * Miscellaneous:

Answer 83

(asthma) * Class: Leukotriene inhibitor * Mechanism: Leukotriene receptor antagonist * Therapeutics: Add-on therapy in mild persistent asthma; aspirin-induced asthma; prophylaxis for exercise-induced bronchospasm * Important Side Effects: Well tolerated * Other Side Effects: * Miscellaneous: Must monitor liver function test.

Answer 84

(asthma) * Class: Leukotriene inhibitor * Mechanism: Leukotriene receptor antagonist * Therapeutics: Add-on therapy in mild persistent asthma; aspirin-induced asthma; prophylaxis for exercise-induced bronchospasm * Important Side Effects: Well tolerated * Other Side Effects: * Miscellaneous: Must monitor liver function test.

Answer 85

(asthma) * Class: Leukotriene inhibitor * Mechanism: Leukotriene receptor antagonist * Therapeutics: Add-on therapy in mild persistent asthma; aspirin-induced asthma; prophylaxis for exercise-induced bronchospasm * Important Side Effects: Well tolerated * Other Side Effects: * Miscellaneous: Must monitor liver function test.

Answer 86

(asthma) * Class: Leukotriene inhibitor * Mechanism: Inhibits 5-lipoxygenase and blocks leukotriene synthesis * Therapeutics: Add-on therapy in mild persistent asthma; aspirin-induced asthma; prophylaxis for exercise-induced bronchospasm * Important Side Effects: Liver toxicity * Other Side Effects: * Miscellaneous:

Answer 87

(asthma) * Class: Anti-IgE mAB * Mechanism: Blocks IgE function. * Therapeutics: Poorly controlled severe asthma * Important Side Effects: * Other Side Effects: * Miscellaneous: Administered by subQ injection every 3 weeks

Answer 88

(anti-arrhythmics) * Class: Class IA anti-arrhythmics * Mechanism: Block inward potassium rectifying channel (slow rate) at normal concentrations; blocks sodium channels (fast rate) at high concentrations * Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia * Important Side Effects: QT prolongation; TdP arrhythmias; heart block; hypotension; lupus-like syndrome * Other Side Effects: GI symptoms; cinchonism, hepatitis, & thrombocytopenia w/ quinidine; anticholinergic effects w/ disopyramise * Miscellaneous:

Answer 89

(anti-arrhythmics) * Class: Class IA anti-arrhythmics * Mechanism: Block inward potassium rectifying channel (slow rate) at normal concentrations; blocks sodium channels (fast rate) at high concentrations * Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia * Important Side Effects: QT prolongation; TdP arrhythmias; heart block; hypotension; lupus-like syndrome * Other Side Effects: GI symptoms; cinchonism, hepatitis, & thrombocytopenia w/ quinidine; anticholinergic effects w/ disopyramise * Miscellaneous:

Answer 90

(anti-arrhythmics) * Class: Class IA anti-arrhythmics * Mechanism: Block inward potassium rectifying channel (slow rate) at normal concentrations; blocks sodium channels (fast rate) at high concentrations * Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia * Important Side Effects: QT prolongation; TdP arrhythmias; heart block; hypotension; lupus-like syndrome * Other Side Effects: GI symptoms; cinchonism, hepatitis, & thrombocytopenia w/ quinidine; anticholinergic effects w/ disopyramise * Miscellaneous:

Answer 91

(anti-arrhythmics) * Class: Class IB anti-arrhythmics * Mechanism: Block sodium channels in inactivated state mostly; no action on atrial tissue * Therapeutics: Digitalis toxicity * Important Side Effects: Tremor; nausea; seizures; local anesthetic action * Other Side Effects: GI toxicity w/ mexiletine * Miscellaneous:

Answer 92

(anti-arrhythmics) * Class: Class IB anti-arrhythmics * Mechanism: Block sodium channels in inactivated state mostly; no action on atrial tissue * Therapeutics: Digitalis toxicity * Important Side Effects: Tremor; nausea; seizures; local anesthetic action * Other Side Effects: GI toxicity w/ mexiletine * Miscellaneous:

Answer 93

(anti-arrhythmics) * Class: Class IC anti-arrhythmics * Mechanism: Sodium channel blockers (most potent in class I), acting as negative ionotrope * Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia * Important Side Effects: Worsened heart failure, proarrhythmia in ischemic tissue, increased mortality * Other Side Effects: Blurred vision w/ flecainide; sinus bradycardia & brochospasm w/ propafenone * Miscellaneous:

Answer 94

(anti-arrhythmics) * Class: Class IC anti-arrhythmics * Mechanism: Sodium channel blockers (most potent in class I), acting as negative ionotrope * Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia * Important Side Effects: Worsened heart failure, proarrhythmia in ischemic tissue, increased mortality * Other Side Effects: Blurred vision w/ flecainide; sinus bradycardia & brochospasm w/ propafenone * Miscellaneous:

Answer 95

(anti-arrhythmics) * Class: Class IC anti-arrhythmics * Mechanism: Sodium channel blockers (most potent in class I), acting as negative ionotrope * Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia * Important Side Effects: Worsened heart failure, proarrhythmia in ischemic tissue, increased mortality

Answer 96

(anti-arrhythmics) * Class: Class II anti-arrhythmics - beta blockers (selective) * Mechanism: Blocks beta-adrenergic receptors; decrease SA, AV node activity (phase 4 depolarization) * Therapeutics: Control of ventricular rate in atrial fibrillation/flutter; long-term suppression of SVTs; PVCs * Important Side Effects: Heart block; hypotension, brochospasm; bradycardia * Other Side Effects: Contraindicated in WPW * Miscellaneous: Decreases mortality in CHF.

Answer 97

(anti-arrhythmics) * Class: Class III anti-arrhythmics * Mechanism: K channel blockade = prolongs refractoriness * Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia * Important Side Effects: Torsades de Pointes; QT prolongation, bradycardia; pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction, hypotension, brochospasm * Other Side Effects: Photosensitivity (blue-gray skin; numerous drug interactions; N & V w/ dronedarone * Miscellaneous:

Answer 98

(anti-arrhythmics) * Class: Class III anti-arrhythmics * Mechanism: K channel blockade = prolongs refractoriness * Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia * Important Side Effects: Torsades de Pointes; QT prolongation, bradycardia; pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction, hypotension, brochospasm * Other Side Effects: Photosensitivity (blue-gray skin; numerous drug interactions; N & V w/ dronedarone * Miscellaneous:

Answer 99

(anti-arrhythmics) * Class: Class III anti-arrhythmics * Mechanism: K channel blockade = prolongs refractoriness * Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia * Important Side Effects: Torsades de Pointes; QT prolongation, bradycardia; pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction, hypotension, brochospasm * Other Side Effects: Photosensitivity (blue-gray skin; numerous drug interactions; N & V w/ dronedarone * Miscellaneous:

Answer 100

(anti-arrhythmics) * Class: Class III anti-arrhythmics * Mechanism: K channel blockade = prolongs refractoriness * Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia * Important Side Effects: Torsades de Pointes; QT prolongation, bradycardia; pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction, hypotension, brochospasm * Other Side Effects: Photosensitivity (blue-gray skin; numerous drug interactions; N & V w/ dronedarone * Miscellaneous:

Answer 101

(anti-arrhythmics) * Class: Class III anti-arrhythmics * Mechanism: K channel blockade = prolongs refractoriness * Therapeutics: Atrial fibrillation/flutter, paroxsymal supraventricular tachycardia, ventricular tachycardia * Important Side Effects: Torsades de Pointes; QT prolongation, bradycardia; pulmonary fibrosis, peripheral neuropathy, hepatic dysfunction, hypotension, brochospasm * Other Side Effects: Photosensitivity (blue-gray skin; numerous drug interactions; N & V w/ dronedarone * Miscellaneous:

Answer 102

* Class: Anti-arrhythmic * Mechanism: Adenosine receptors in atrium, sinus node, AV node; activates K current, shortening AP, hyperpolarizing tissue, and slowing down automaticity and AV conduction * Therapeutics: AF, paroxsymal supraventricular tachycardia * Important Side Effects: Sedation, dyspnea, hypotension * Other Side Effects: * Miscellaneous:

Answer 103

* Class: Anti-arrhythmic * Mechanism: * Therapeutics: Prevents recurrent TdP and some digitalis-induced arrhythmias * Important Side Effects: * Other Side Effects: * Miscellaneous: Alternative to amiodarone for shock-refractory cardiac arrest.