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Intro to pharm

Cardiovascular pharm

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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