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119 Cards in this Set
- Front
- Back
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What is the problem with alpha-2 agonists?
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CNS depression, rebound phenomenon, low BP
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What are the alpha-2 agonists? What is their main action?
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Clonidine, A-methyl DOPA. Antihypertensives, decrease SANS activity
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What is the Nictotinic anatgonist (Ganglionic blocker), action? And side effect
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Mecamylamine. Decrease SANS vasodilation- therapeautic. Decrease PANS (dry mouth and skin, mydriasis, cycloplegia, constipation)-unwanted side effects
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What drugs cause NT depletion? Which is more harmful?
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reserpine, guanethidine, decrease NE concentration. Problem is that Reserpine causes CNS depression because it can cross BBB
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What are the beta-1 and beta-2 nonselective antagonists? What is their main action
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Propranolol, Timolol, Nadolol. Antuarrhytmic, Antianginal, HTN
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What are the beta-1 cardioselective anatagonists? What is their main action?
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Atenolol, Metoprolol, Acebutolol. Antihypertensive
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What is the problem with beta blockers?
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Cardiac depression, rebound phenomenon, CNS depression
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What drugs cause a First dose effect?
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alpha blockers, angiotensin blockers or synthesis blockers, ACEI or ARBs
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What is the problem with alpha blockers?
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This is the postural precipitous drop in BP on starting the drug or increasing a dose (hypotension upon standing)
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What are the alpha blockers?
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Prazosin, Doxazosin, terazosin, Tamulosin, Alfuzosin, Phentolamine, Phenoxybenzamine
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What are the vasodilators? And their problems?
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Hydralazine, Minoxidil, Diazoxide (affect smooth muscle ion transport), Nitroprusside- NO donor. Causes hypotension, reflexive tachycardia, angina pectoris, MI
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What are the Ca channel blockers? And problems
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Nifedipine (-dipines) Verapamil and Diltiazem (useful against arrythmias). Causes hypotension, reflexive tachycardia and cardiac depression.
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What are the duiretics?
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Loops= Furosemide, Ethacrynic acid. Thiazides= hydrochlorothiazide (causes hypokalemia and alkalosis). K-sparing= spironolactone, amiloride, triamterene,
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What are the ACE inhibitors? And problems
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Captopril, Lisinopril- direct acting. Enalapril- prodrugs. Problems- cough, angiodema (bradykinin), vasodilation, hyperkalemia
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What are the angiotensin 2 antagonists (ARB) and what is the advantage?
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Losartan, Valsartan. Advantage- no cough, no angiodema, because no bradykinin
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What are the strategies for therapy in CHF?
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Cardiotonics- digitalis (Ca), Dobutamine (beta 1), inamrinone (cAMP)
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What are the class 1 antiarrhythmics?
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Na channel blockers. Elevate threshold for depolarization, slow impulse conduction. Ia- quinidine, procainamide. Ib- lidocaine. Ic- flecainide
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What are the class 2 antiarrhytmics?
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Beta blockers, Propanolol. Resist NE and E contributions to SA node
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What are the class 3 antiarrhytmics?
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K channel blockers, Amiodarone and sotaolol. delay repolarization in phase 3 and prolonging phase 2 and the action potential.
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What are the class 4 antiarrhytmics?
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Ca channel blockers, Verapamil, Diltiazem. Suppress AV nide and stop it.
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What is coronary steel syndrome?
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When nitrates are given, some act directly on NO donors -> cGMP -> vasodilation -> some req mt enzymes that synthesize or reduce NO
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What is the mechanism of action for vasodilators?
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Cause activation of K channels, interfere with Ca channel function, promote NO synthesis in vascular endothelium, domantion of NO to the vascular smooth muscle
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What is the mechanism of action for Hydralazine? And its side effects
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Acts at the arteriole and produces powerful vasodilation, dramatic drop in PVR and BP. Side effects are vascular: headache, flushing. Dizziness, hypotension, tachycardia, angina pectoris--LUPUS LIKE SYMPTOMS
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What is the mechanism of action of minoxidil? And side effects
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Vasodilation by opening K channels and blocking Ca channels. SE- HYPERTRICHOSIS, hypotension, SANS and angiotensin 2 compensation
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What is minoxidil used in combination with?
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A diuretic and beta-blocker to reduce risk of reflexive tachy, palpitations, angina and edema
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What is the mechanism of action of diazoxide? And SE
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restricted to IV use. SE- hypotension, RT, angina, myocardial ischemia, HYPERGLYCEMIA, water retention
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What is the mechanism of action of sodium nitroprusside?
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Unstable, short acting. It is a NO donoe, decreases preload and afterload.
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What is the mechanism of action of Ca channel blockers
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Reduce workload
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What are the 'dipines' and their moa. What are they used in conjuction with?
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Nifedipine, nitrendipine, amlodipine, nicardipine, act only on the arteriole not on cardiac nodal tissue. Used with beta-blockers because patients with coronary artery disease may get anginal pain or MI during SANS reflex
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What are the moa of Verapamil and dilitiazem?
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Resist SANS because of Ca blockade at SA and AV node. They are also ANTIARRYTHMIC
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What are the alpha-2 agonists? What is their main action?
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Clonidine, A-methyl DOPA. Antihypertensives
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Which blockade would HR not increase?
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Ganglionic blockade
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What is Alpha blocker toxicity?
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Loss of TPR- hypotension, congestion, first dose effect. Reflexive tachycardia, high HR. urinary incontinence, GI hyperactivity, miosis
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What is the antihypertensive drug combination for beta blocker vs increased HR and renin
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Metoprolol and hydrochlorothiazide
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What is the antihypertensive drug combination for decreased SANS, vasodilation and CO
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clonidine and chlorothalidone
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What is the antihypertensive drug combination for decreased SANS, decreased volume and CO
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reserpine and hydrochlorothiazide
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What is the antihypertensive drug combination to avoid hypokalemia
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amiloride and hydrochlorothiazide
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What is the antihypertensive drug combination to decrease TPR, cardiac response, A2-aldo
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verapamil and enalapril
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What is the antihypertensive drug combination for decreased TPR and CO, fluid retetion. Tox of decreased BP, inc HR and dizziness
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Prazosin and polythiazide
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What is classical/typical angina induced by?
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exercise, eating, cold stress. Can be caused by loss of cornary perfusion pressure, vasodilators
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How do potent vasodilators cause angina?
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by Coronary steal and sympathetic reflex (hypotension and tachycardia)
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What are the problems with nifedipine
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typical angina pectoris, hypotension, reflexive tachy, increase HR via SANS, cause coronary steal. Best used with a beta blocker. Can be tolerated if the patient does not have an underlying CAD and can tolerate exercise
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What is the MOA of nitrates?
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drug metabolism releases NO, activating guanylyl cyclase, cGMP, dephosphorylating active MLC, smooth muscle relaxation
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Nitrates
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Nitroglycerin, isosorbide dinitrate, amyl nitrite
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What drug combinations that is good for angina and prevent nifedipine reflex tachycardia
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Nifedipine and beta blockers
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What drug combinations are two mechanisms to reduce heart work
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Ca channel blockers and nitrates
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What is the mechanism of action of diuretics?
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Nephron Na recovery is blocked by a diuretic drug and H2O follows it out. When Na leaves the tubule the osmotic pressure goes up then H2O goes down the concentration gradient and is reabsorbed. Duiretics block all of this
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What works on the thick ascending loop?
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Loop diuretics; ethacrynic acid, furosemide, bumetanide
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What works on the distal convoluted tubule?
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thiazide and related drugs: hydrochlorothiazide
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What works on the collecting tubule?
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K-sparing- amiloride, triamterene, spironlactone (aldosterone antagonists)
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What is the MOA of hydrochlorothiazides?
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Blocks Na/Cl transporter at the distal convoluted tubule. Na is eliminated and H2O follows it
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What are the side effects of hydrochlorothiazide?
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Hyperuricemia (b/c thiazides compete with uric acid for secretion), hypokalemia, metabolic alkalosis, hyperglycemia (impaired pancreatic insulin release)
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What is the MOA of ethacrynic acid and furosemide?
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Block NaCl reabsorption in the thick ascending limb of the loop of henle by blocking Na/K/2Cl transporter. By blocking transporter, bring more K in and Na stays in the urine
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What is the MOA of Potassium Sparing Diuretics: Sprionolactone and triamterene?
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competitive antagonist at the aldosterone receptor (spironolactone) or block Na influx at the luminal membrane (triamterene) in the principal cells of the late distal/collecting tubule
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What are the potassium sparing diuretics used in combination with to prevent K loss
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combination with thiazide
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what are the side effects of spironolactone and triamterene
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hyperkalemia and gynecomastia
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when is spironolactone used over triamterene?
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when renin-angiotensin aldosterone is high
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When is renin released?
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renal artery BP is low, plasma Na is low, SANS activates B-1 receptors
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How does ACE lead to vasoconstriction?
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is a PDP (peptidyl dipeptidase) aka kinase 2, enzyme that converts bradykinin, a powerful vasodilator to inactive fragments
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What are the different actions of bradykinin?
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1-Vasodilator, powerful endogenous substance. Decreasing arterial resistance and increased venous capicitance (decrease TPR and CO = dec BP). 2-Proinflammatory, pain swelling and angiodema. 3-bronchoconstrictor- may induce airway irritability, cough, airway obstruction
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What are the direct-acting ACE inhibitors?
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Captopril and lisinopril
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What are the prodrug ACE inhibitors?
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Enalapril, ramipril, quinapril, benazepril, fosinopril
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What are the side effects of ACE inhibitors?
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hypotension, first dose phenomenon, acute renal failure, hyperkalemia, cough, resp irritability, angiodema
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Bradykinin side effects
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cough, airway irrtability, angiodema
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Ang 2 Receptor antagonists (ARBS) or (Sartans) and MOA
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Block At-1 receptor at arterioles, adrenal cortex and SANS elements. Irbesartan, Candesartan, Losartan, Valsartan
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What are the advantages of ARBs
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designed to avoid side effects caused by bradykinin, no cough or bronchoconstriction, no angiodema, used as alternative to ACEIs
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Name the drug, potentiates antithrombin 3, may cause bleeding, stopped by protamine
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heparin
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Name the drug. Oral anticoagulant, blocks clotting factor synthesis by inhibiting recycling of vitamin K. may cause bleeding
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Warfarin
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What are the fibrinolytics?
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Streptokinase and altepase
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MOA of ticlopidine, clopidogrel
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block ADP receptor in platelets
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Name the drug, class 3 increases APD and ERP. Controls arrythymias and ventricular extra systoles
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amiodarone
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Class 1b Na channel blocker, post MI, control of arrythymias and ventricular extra systoles
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Lidocaine
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Name the drug for pulmonary congestion due to acute heart failure, rapid reduction of ECF volume, less pulmonary vol/pressure
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Furosemide
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Name the drug for pulmonary congestion due to acute heart failure, pain relief during MI
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morphine
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Name the drug for pulmonary congestion due to acute heart failure, bronchodilation, vasodilation, cardiac stimulation due to phosphodiesterase inhibition (inc cAMP)
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aminophylline
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What drigs increase left ventricle contractile force for RVF by adding volume?
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dopamine, dobutamine, inamirnone, milrinone
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What can suppress DADs and EADs
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beta blockers, Ca channel blockers, lidocaine, or amiodarone
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Drugs of Class 1A antiarrhythmic
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quinidine, procainamide, disopyramide
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Drugs of class 1B antiarrhythimic
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lidocaine and pheytoin
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Drugs of class 1C antiarrhythmic
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felcainide, encainide, moricizine
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Drugs of class 2 antiarrthytmic
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propanolol, and the cardioselectives: acebutolol, metoprolol, atenolol, esmolol
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Drugs of class 3 antiarrhythmic
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amiodarone, bretylium, sotalol, ibutilide
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Drugs of class 4 antiarrhythmic
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verapamil, diltiazem
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What is a special antiarrhythmic drug
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adenosine and digoxin
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What is the MOA of a class 1 antiarrythmic
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blocks Na channel, decreases V, conduction velocity and increases fibrillation threshold, increases ERP
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What are the side effects of procainimide?
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Slow acetylation- Lupus, fast acetylation- Torsades de Pointes
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What drug can suppress digoxin ventricular arrhythmias without aggrevating dig-related AV node depression
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Phenytoin, increases AV nodal impulse conduction
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What are the tenacious sodium channel blockers that were revealed to be dangerous by the CAST trial?
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Flecainide, encainide, moricizine
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What is the consequence of blocking K?
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It delays repolarization, extends AP longer APD is a longer ERP (effective refractory period)
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Amiodarone?
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K channel blocker, class 3. It is both alpha and beta blocker, low BP, low HR, vasodilation. It imitates class 1,2,3,4 and has a long half life.
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What are the side effects of amiodarone?
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cardiac depression, pulmonary fibrosis, liver damage, optic nerve, cornea halos, and blue skin…smurf skin!
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What is a common side effect of the class 3 antiarrythymics?
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Torsades de pointes because they increase APD duration, onset of EAD
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what is the MOA of a class 3 antiarrythymic?
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decrease SA node heart rate, decrease AV nide conduction. Decreases EADs and DADs
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What are the side effects of a class 3 antiarrythmic?
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bradycardia, asystole, AV depression, AV block, vasodilation, hyoptension and constipation
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what is the MOA of digoxin?
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invokes muscarinic Ach effect, can depress AV node to protect the ventricle during atrial events
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What is digoxin toxicity?
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V extra systoles, V tach, AV depression, AV block
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What are the 4 AV nodal depressants?
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Digoxin, Adenosine, Verapamil, Propanolol
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Why is lidocaine special?
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short acting, few or no side effects, used for supression of extra systoles in MI or post-MI ischemic hearts
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What drugs are used in CHF?
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Diuretics, ACEi, ARBs, Vasodilators, Beta-blockers, Digitalis, Cardiotonics, Recombinant BNP
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MOA of diuretics for CHF?
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Hydrochlorothiazide, Inadapmide, ethacrynic acid, furosemide. Decreases ECF, blood volume, venous return, vasodilate. Causes hyokalemia. Spirnolactone, Amiloride and triameterene prevent hyokalemia
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MOA of ACEi on CHF?
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decrease afterload, blood volume and cardiac remodeling
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MOA of hydralazine in CHF?
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decreases afterload
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What is the MOA of digitalis?
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Blocks Na/K ATPase, improves Ca availability in cardiac cells
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What are the adverse effects of digitalis?
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Increase automaticity causing ventricular extrasystoles (v tach and v fib). AV nodal depression
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What drug can aggrevate digitalis induced AV depression?
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Beta blockers, Ca blockers and adenosine
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What are the CHF Cardiotonics?
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Beta1 agonists- Dobutamine, NE, Epi, Isoproterenol. Phosphodiesterase inhibitors- inamrinone, milirinone
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What is the MOA of Recombinant BNP?
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increases cGMP, relax smooth muscle.
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What combination is most common in CHF patients?
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Diuretics and ACEi
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What conditions would you use loops? K sparing?
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loops- renal disease and CHF. K sparing- primary or secondary hyperaldosteronism
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What are the side effect of loops?
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hypokalemia, hypovalemia, hyperuricemia, hyperglycemia, hypocalcemia
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Name the beta 2 agonists that are inhaled, early short-term benefit, oral dose longer action
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Albuterol and Metaproterenol, Terbutaline
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Name the beta 2 agaonists that are delayed, long-term action, 12-24 hr/inhalation
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Salmeterol, Formeterol
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What are the adenosine antagonists
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Methylxanthines Theophylline and Aminophylline
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What are the nonselective beta adrenergic agonists?
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ephedrine, epinephrine, isoproterenol
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what are the side effects associated with using beta agonists in asthma?
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tachycardia, palpitations, sk muscle tremor, hyperglycemia
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What are the mast cell stabilizers?
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cromolyn sodium, nedocromil
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Which are the antiinflammatory corticosteroid drugs?
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Corticosteroids Beclomethasone and Triamcinolone (inhaled, relatively safe); Prednisone (oral, Cushingoid toxicity); Methylprednisolone (iv, emergency, safe for short-term)
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Name the anti-muscarinic asthma med?
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ipratropium bromide
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What drug is used before b-2 agonists in the treatment of COPD?
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ipratropium bromide
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