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Intro to pharm
Cardiovascular pharm
| Question | Answer |
|---|---|
| What is the approximate distribution of the 5L of blood in the body? | 9% pulmonary; 7% heart; 84% systemic (64% veins) |
| What are some characteristics of blood flow? | resistance declines in order for blood to flow; increase in pressure maintains flow; pressure falls as blood moves; blood returns to the heart by help of venous pump |
| What are some characteristics of cardiac output? | 5L/min; CO= stroke volume + heart rate |
| How is stroke volume determined? | contractility; preload; afterload |
| What is preload? | force of venous return, increase in preload increases stroke volume |
| What is afterload? | arterial pressure; increase in afterload decreases stroke volume |
| What is starling's relationship? | the ventricular contraction is proportional to the muscle fiber length; as fiber length increases, contractile force increases; more blood brought into healthy heart, more blood pumped out; venous return increases, cardiac output increases; venous return |
| What are some characteristics of arterial pressure? | AP= peripheral resistance x cardiac output; regulated by the autonomic nervous system (rapid steady-state control), renin-angiotensin aldosterone system (hours/days), and the kidneys (long term) |
| How is peripheral resistance regulated? | constriction/dilation of arterioles |
| What are some characteristics of angiotensin? | angiotensin I = little activity; angiotensin II = high activity (increase BP & release aldosterone); angiotensin III = moderate activity |
| What are some characteristics of angiotensin II? | renin catalyzes angiotensin to angiotensin I (BP, blood volume, renal perfusion); ACE catalyzes angiotensin I to antiotensin II (ACE: angiotensin-converting enzyme; abundant especially in lungs) |
| What turns on the RAAS (renin-angiotensin aldosterone system)? | factors that lower BP; turning on raises blood pressure by vasoconstriction & retention of sodium & water |
| What are some uses for ACE inhibitors? | hypertension, heart failure, myocardial infarction, diabetic nephropathy, prevention of MI/stroke/death in patients at high cardiac risk |
| What are some examples of ACE inhibitors used for myocardial infarction? | captopril (capoten), lisinopril (prinivil), trandolapril (mavik) |
| What is an example of an ACE inhibitor used for diabetic neuropathy? | captopril (capoten) |
| What are some characteristics of ACE inhibitors? | do not interfere with cardiac reflexes; no lethargy, weakness, or sexual dysfunction; reduce risk of cardio mortality caused by hypertension; reduce levels of angiotensin II; increase levels of bradykinin |
| What are some adverse effects of ACE inhibitors? | first-dose hypotension (diuretics enhance); cough; hyperkalemia; renal failure (contraindicated); fetal injury |
| What are some characteristics of angiotensin II receptor blockers (ARBs)? | used for hypertension, heart failure (valsartan/diovan), diabetic neuropathy (irbesartan/avapro & losartan/cozaar), blocking action of angiotensin II (dilation of arterioles & veins; decrease aldosterone); suffix -sartan |
| What are some adverse effects of angiotensin II receptor blockers (ARBs)? | fetal harm, renal failure |
| What is an example drug for selective aldosterone receptor blockers? | eplerenone (inspra): only for hypertension, excretion of sodium and water, adverse effect: hyperkalemia |
| Where is calcium critical in the body? | vascular smooth muscle and heart |
| What are some characteristics of the VSM? | regulate contraction (calcium blocked= dilation) |
| What impact does calcium blockage have on the heart? | decreases contraction |
| What is the role of the SA node in the heart? | pacemaker activity; decrease calcium = decrease heart rate |
| What is the role of the AV node in the heart? | excitability of cells; decrease calcium = decrease velocity of conduction |
| What receptors are coupled to calcium channels? | beta one receptors; beta blockers have the same effects as calcium channel blockers (decrease contractility, decrease heart rate, suppress conduction) |
| What is the location of action for the calcium channel blocker family: dihydropyridines (nifedipine/adalat)? | arterioles |
| What is the location of action for the calcium channel blocker family: verapamil (calan)/diltiazem (cardizem)? | arterioles & heart |
| What are some uses for verapamil & diltiazem? | angina pectoris, hypertension, cardiac dysrhythmias, migraines |
| What are the hemodynamic effects of verapamil & diltiazem? | direct: reduce AV conduction, reduce heart rate; overall dilation; indirect: NE release & increase heart rate |
| What are some adverse effects of verapamil & diltiazem? | constipation, swelling of ankles & feet, exacerbation of cardiac failure, increase digoxin toxicity, beta blockers have additive effects (possibility of cardiosuppression) |
| What are some uses for Nifedipine? | angina pectoris, hypertension |
| What are the hemodynamic effects of Nifedipine? | direct: blocks channels in VSM = dilation; indirect: NE released & increases heart rate; overall lowers BP, increases heart rate, increases contractile force |
| What are some adverse effects of Nifedipine? | swelling of ankles/feet, reflex tachycardia (does not exacerbate heart failure) |
| What are some characteristics of vasodilators? | arterioles-decrease afterload; veins-decrease preload; arterioles & veins; used for hypertension + angina pectoris + heart failure + Myocardial infarction |
| What are some adverse effects of vasodilators? | postural hypotension, reflex tachycardia, expansion of blood volume |
| What are some characteristics/uses for the vasodilator: hydralazine (apresoline)? | dilate arterioles, used for hypertension, hypertensive crisis, heart failure |
| What are some adverse effects of the vasodilator hydralazine (apresoline)? | reflex tachycardia, increase blood volume, systemic lupus-like syndrome, minimal hypotension |
| What are some characteristics of the vasodilator minoxidil (loniten)? | dilates arterioles, used for severe hypotension & hair growth (rogaine); adverse effects are reflex tachycardia, sodium & water retention, hypertrichosis |
| What are some characteristics of the vasodilator sodium nitroprusside (nitropres)? | dilate arterioles/veins; used for hypertensive emergencies; adverse effects include excessive hypotension, cyanide poisoning, thiocyanate toxicity |
| What are the consequences of chronic hypertension? | morbidity, heart disease, kidney disease, stroke |
| What are some lifestyle modifications that can be made to alter hypertension? | weight loss, sodium restriction, alcohol restriction, exercise (aerobic x10), smoking cessation, potassium and calcium maintenance |
| What are the primary determinants of arterial blood pressure? | cardiac output x peripheral resistance |
| What is cardiac output determined by? | heart rate, contractility, blood volume, venous return |
| What determines peripheral resistance? | arteriolar constriction |
| What are some sites of action for hyptertensive medications? | 1. brainstem: clonidine, methyldopa 2. sympathetic ganglia: mecamylamine 3. adrenergic terminals: guanethidine, reserpine 4. Cardiac beta one receptors: propranolol, metoprolol, other beta blockers 5. vascular alpha one receptors: prazosin, terazosin |
| What are the effects of clonidine, which works at the brainstem? | suppression of sympathetic outflow decreases sympathetic stimulation at the heart and blood vessels |
| What are the efects of trimethaphan, which works at the sympathetic ganglia? | ganglionic blockade reduces sympathetic stimulation of the heart and blood vessels |
| What are the effects of guanethidine, which works at the adrenergic nerve terminals? | reduced norepinephrine release decreases sympathetic stimulation of the heart and blood vessels |
| What are the effects of propranolol, which works at the cardiac beta one receptors? | beta one blockade decreases heart rate and myocardial contractility |
| What are the effects of prazosin, which works at the vascular alpha one receptors? | alpha one blockade causes vasodilation |
| What are the effects of hydralazine, which works at the vascular smooth muscle? | relaxation of vascular smooth muscle causes vasodilation |
| What are the effects of chlorothiazide, which works at the renal tubules? | promotion of diuresis results in decreased blood volume |
| What are the effects of propanolol, which works at beta one receptors on juxtaglomerular cells? | beta one blockade suppresses renin release, resulting in vasodilation secondary to reduced production of angiotensin II and prevention of aldosterone-mediated volume expansion |
| What are the effects of captopril, which works on angiotensin-converting enzyme (ACE)? | inhibition of ACE decreases formation of angiotensin II and thereby prevents vasoconstriction & aldosterone-mediated volume expansion |
| What are the effects of losartan, which works on angiotensin II receptors? | blockade of angiotensin II receptors prevents angiotensin-mediated vasoconstriction and aldosterone-mediated volume expansion |
| What are the effects of eplerenone, which works on aldosterone receptors? | blockade of aldosterone receptors in the kidney promotes excretion of sodium and water, and thereby reduces blood volume |
| What are some thiazides and related diuretics used for chronic hypertension? | bendrofluinethiazide, benzthiazide, chlorothiazide, chlorthalidone, cyclothiazide, hydrochlorothiazide, hydrofumethiazide, indapamide, metolazone, polythiazide, quinethazone, trichlormethiazide |
| What are some loop diuretics used to treat chronic hypertension? | furosemide, ethacrynic acid, bumetanide, torsemide |
| What are some potassium-sparing diuretics used to treat chronic hypertension? | spironolactone, triamterene, amiloride |
| What are some beta blockers used to treat chronic hypertension? | acebutolol (has ISA), atenolol, betaxolol, bisoprolol, carteolol (has ISA), metoprolol, nadolol, penbutolol (has ISA), pindolol (has ISA), propranolol, timolol (ISA= intrinsic sympathomimetic activity) |
| What are some alpha one blockers used to treat chronic hypertension? | doxazosin, prazosin, terazosin |
| What are some alpha/beta blockers used to treat chronic hypertension? | carvedilol, labetalol |
| What are some centrally acting alpha2 agonists used to treat chronic hypertension? | clonidine, methyldopa, guanabenz, guanfacine |
| What are some adrenergic neuron blockers used to treat chronic chronic hypertension? | guanethidine, guanadrel, reserpine |
| What are some ACE inhibitors used to treat chronic hypertension? | benazepril, captopril, enalapril, fosinopril, lisinopril, moexipril, quinapril, ramipril, trandolapril |
| What are some aldosterone receptor blockers used to treat chronic hypertension? | eplerenone, spironolactone |
| What are some angiotensin II receptor blockers used to treat chronic hypertension? | candesartan, eprosartan, irbesartan, losartan, olmesartan, valsartan |
| What are some calcium channel blockers? | amlodipine, diltiazem (non-DHP), felodipine, isradipine, nifedipine, nicardipine, nimodipine, nisoldipine, verapamil (non-DHP) |
| What are some direct-acting vasodilators? | hydralazine, minoxidil |
| What are the characteristics of heart failure? | characterized by reduced cardiac output, fluid retention, and ventricular dysfunction (dilation, wall thickness, sphere shape) |
| What are the compensatory responses? | compensating for reduced cardiac output, more damage, 1. cardiac dilation 2. activation of the sympathetic nervous system 3. activation of the renin-angiotensin-aldosterone system 4. retention of water and increased blood volume |
| What are the classifications for heart failure? | class I: no limitation class II: slight limitation class III: marked limitation class IV: symptoms occur at rest (exercise training improves clinical status) |
| What are the types of drugs used for heart failure? | ACE inhibitors (dilate arterioles/veins, reduce aldosterone), diuretics (decrease overload volume) |
| What are some characteristics of digoxin (lanoxin)? | cardiac glycoside, positive inotropic action (increases force of contraction/CO, inhibits Na+/K+ ATPase, calcium accumulation, facilitates interaction of myosin/actin), K+ interference |
| What are the therapeutic effects of digoxin (lanoxin)? | increase contractility, increase urine production, reduces heart rate, afterload, and venous pressure, decrease heart size (does NOT prolong life) |
| What are some adverse effects of digoxin (lanoxin)? | dysrhythmias, nausea/vomiting, fatigue, visual disturbances (blurred/yellow vision), drug interactions (diuretics-K+ loss, ACE inhibitors-K+ increase, quinidine, verapamil) |
| What are some characteristics of spiranolactone (aldactone)? | potassium-sparing diuretic, aldosterone-receptor blocker (aldosterone promotes remodeling: fibrosis, rise in heart failure), ACE inhibitors decreases formation (spironolactone blocks action), Adverse effects= gynecomastia, hyperkalemia |
| What are some characteristics of dysrhythmias? | abnormality in rhythm of heartbeat, tachydysrhythmia (increase), bradydysrhythmia (decrease), drugs can also cause dysrhythmias |
| What are some characteristics of impulse conduction in the heart? | atria/ventricles coordinated, SA node is pacemaker, AV node delays for blood filling, His-Purkinje system-rapid activity spread |
| What are some characteristics of cardiac action potentials? | relate to ion movement (depolarized or polarized), fast or slow action potentials |
| What are some characteristics of fast action potentials in the cardiac system? | His-purkinje & atrial/ventricular muscle, Phase O: influx of sodium; phase 1: repolarization phase 2: calcium enters; phase 3: exit of potassium; phase 4: automaticity |
| What are some characteristics of slow action potentials? | SA & AV node, phase 0: slow influx of calcium; phase 1, 2, 3: not significant; phase 4: not well understood |
| What occurs during the P wave of an EKG? | depolarization in the atria (contraction) |
| What occurs during the QRS wave of an EKG? | depolarization in the ventricles (contraction, widens if slow) |
| What occurs during the T wave of an EKG? | repolarization of the ventricles |
| What occurs during the PR interval of an EKG? | time between P wave & QRS (lengthen= delay in AV node conduction, common med side effect) |
| What occurs during the QT interval of an EKG? | time between QRS and T wave |
| What occurs during the ST segment of an EKG? | end of QRS and beginning of T wave |
| How are dysrhythmias generated? | disturbances of automaticity, or conduction |
| What are the locations for dysrhythmias generated due to disturbances of automaticity? | cells in SA node, AV node, or His-Purkinje |
| What are some dysrhythmias generated due to disturbances of conduction? | AV block (first degree-delayed impulse conduction, second degree-some impulses pass, third degree-none pass), reentry (cycle of repetitive cardiac stimulation) |
| What are class I antidysrhythmic drugs? | sodium channel blockers (examples IA: quinidine, procainamide/pronestyl, disopyramide/norpace)(examples IB: lidocaine/xylocaine, phenytoin/dilantin, mexiletine/mexitil, tocainide/tonocard) (examples IC: flecainide/tambocor, propafenone/rythmol; other: mor |
| What are class II antidysrhythmic drugs? | beta-blockers (examples: propranolol/inerdal, acebutolol/sectral, esmolol/brevibloc) |
| What are class III antidysrhythmic drugs? | potassium channel blockers-delay repolarization (examples: amiodarone/cordarone/pacerone, dofetilide/tikosyn, bretylium, sotalol/betapace) |
| What are class IV antidysrhythmic drugs? | calcium channel blockers |
| What are some proarrythmic drug effects? | drugs worsen dysrhythmia & generate new cases; doubled rate of mortality (esp class I); severe situations; benefits must be clear; prolong QT interval |
| supraventricular dysrhythmias | areas of heart above ventricle (atria, SA node, AV node); not especially harmful; class II & IV; sustained supraventricular tachycardia; atrial flutter; atrial fib |
| ventricular dysrhythmias | significant disruption; class I & III; sustained ventricular tachycardia, ventricular fib, ventricular premature beats, Digoxin-induced ventricular dysrhythmias, Torsades de Pointes |
| treatment of dysrhythmias | termination of dysrhythmias, long-term suppression with drugs, implantable defibrillator |
| sodium channel blockers | class I, decrease conduction in atria, ventricles & His-purkinje system |
| quinidine | class IA sodium channel blocker (similar to anesthetics); heart: delays repolarization, EKG: widens QRS/prolongs QT, Use: ventricular dysrhythmias, Side effects: GI, arterial embolism, prodysrhythmia, hypotension; Drug interaction: digoxin |
| lidocaine | class IB sodium channel blocker; heart: accelerates repolarization; EKG: none; Use: ventricular dysrhythmias; side effects: drowsiness, confusion, prodysrhythmias |
| Propranolol | class II: beta blocker; effects B1 & B2 receptors, Heart: decreased velocity of conduction (also blocks calcium channels); EKG: prolonged PR interval; Use: supraventricular & ventricular premature beats; Side effects: heart failure, hypotension, bronchosp |
| Bretylium | class III potassium channel blockers; short-term therapy; heart: delay repolarization; EKG: prolongs QT interval; side effects: hypotension; use: ventricular dysrhythmias |
| Amiodarone | class III potassium channel blockers; heart: delay repolarization; EKG: QRS widening, PR/QT lengthening; side effects: lung damage, visual impairment, prodysrhythmias; use: ventricular and supraventricular; Drug interactions: quinidine, procainamide, digo |
| Verapamil & Diltiazem | class IV calcium channel blocker; heart: decreases velocity of conduction; EKG: prolong QT interval; side effects: hypotension, bradycardia, heart failure; use: supraventricular; drug interactions: digoxin, beta blockers |
| VLDL | triglycerides; probably contribute to atherosclerosis |
| LDL | cholesterol (bad); definately contribute to atherosclerosis <100 optimal |
| HDL | protect against atherosclerosis, cholesterol (good) ~50 |
| HMG-CoA reductase inhibitors (statins) | decrease LDL; increase HDL; decrease TG; inhibits enzyme needed for cholesterol synthesis; side effects: hepatoxicity, myopathy, fetal malformations; atorvastatin, simvastatin |
| Nicotinic Acid | decrease LDL, increase HDL, decrease TG, decreases VLDL (LDL are byproducts of VLDL), side effects: itching, GI, hepatoxic, gouty arthritis, Niaspan, niacor |
| Bile-acid sequestrants | decreases LDL, increases HDL, NO change TG, cholesterol is required to produce bile-acid--liver cells increase LDL receptors therby increasing LDL uptake; side effects: constipation; cholestyramine, colesevelam |
| fibric acid | little/no effect on LDL; increases HDL; lowers TG; accelerate clearance of VLDL therby reducing TG; side effects: gallstones, myopathy, hepatoxic; gemfibrozil |
| Nitroglycerin | organic nitrate, stable angina-decrease oxygen demand; variant angina-increases oxygen supply; side effects: headache, orthostatic hypertension, reflex tachycardia; drug interactions: sildenafil; tolerance |
| Beta blockers | stable angina-decreases oxygen demand; not used for variant angina; side effects: bradycardia, bronchoconstriction; Propanolol, metoprolol |
| Calcium channel blockers | stable angina-decrease oxygen demand; variant angina-increase oxygen supply; side effects: hypotension, reflex tachycardia; Verapamil & Diltiazem |
| reducing risk factors for angina | stop smoking, lower cholesterol, lower BP, diabetic management, decrease obesity, increase physical activity |
| coagulation | produces fibrin to reinforce plug, fibrin produced through clotting factors, vitamin K required for clotting factor synthesis |
| Heparin (unfractionated) | helps antithrombin inactivate clotting factors, suppresses formation of fibrin, use: pregnancy/surgery/MI; side effects: hemorrhage, allergies, thrombocytopenia; MW: 3000-30000daltons; lab monitoring |
| Low molecular weight heparin | used for DVT following hip/knee replacement; side effects: hemorrhage/thrombocytopenia; MW: 1,000-9,000daltons; no lab monitoring; Enoxaprin, Dalteparin |
| Warfarin | oral anticoagulant, antagonist of vitamin K, use prophylaxis of thrombosis; side effects: hemorrhage/teratogenesis; Drug interactions: heparin, asprin, acetaminophen, prothrombin time (PT) |
| Asprin | inhibits COX needed to synthesize thromboxane |
| adenosine receptor antagonist | inhibit ADP-simulated aggregation, Ticlopidine, Clopidogrel |
| glycoprotein IIb/IIa receptor antagonist | block final step of aggregation, Abciximab, tirofibam |
| streptokinase | thrombolytic drug, remove thrombi, binds to plasminogen to form plasmin, which digests fibrin, use: MI & DVT |
| Alteplase | tPA, tissue plasminogen activaor, recomb DNA technology, side effects: intracranial bleeding |
| drug therapy for MI | reperfusion, morphine, antiplatelet drugs, anticoagulants, nitroglycerin, beta-adrenergic blocking agents, ACE inhibitors |
| Complications of MI | ventricular dysrhythmias, cardiogenic shock, CHF, Cardiac rupture, pericarditis |
| secondary prevention for MI | reduce risk factors, exercise, drug therapy |
Created by:
mpost51
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