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46 Cards in this Set
- Front
- Back
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intrinsic factors affecting CO, SV and stroke work
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control of intracellular calcium levels (affecting contractility)
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catecholamine affects in heart failure
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exacerbate myocardial ischemia
calcium overload of myocardial tissue energy deprivation free radical production arrhythmias cell death impaired beta receptor responsiveness |
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extrinsic factors affecting CO, SV and stroke work
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preload
afterload |
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pharmacological approach to treating CHF (7)
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positive inotropes
vasodilators inodilators receptor agonist inotropes/vasodilators 3rd gen beta adrenergic antagonists diuretics ACEI |
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3 compensatory mech of failing heart
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hypertrophy
increase sympathetic activity activate renin-angiotensin system |
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Digoxin mechanism of action
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positive inotropy
prolongs refractory period in AV node Decreased conduction through SA and AV nodes |
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What is the mechanism of action of cardiac glycosides?
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disrupts ('poisons') the Na-K-ATP-ase pump
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CHF pt response to digitalis
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decreased HR
decreased SVR decreased heart size decreased LVEDV and pressure decreased pulmonary congestion improved renal function |
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How is digoxin eliminated?
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in the urine, unchanged
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How is digitoxin eliminated?
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extensively metabolized in the liver and excreted in the feces
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phosphodiesterase inhibitors
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amrinone
milrinone they increase the intracellular conc of cAMP |
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shorter acting?
digoxin or digitalis |
digoxin
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central acting alpha 2 antihypertensives
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clonidine
guanabenz guanfacine methyldopa act at the vasomotor center; stim alpha 2 receptors; inhibit NE release; decreases sympthatetic outflow & ***leaves parasympathetic activity predominating |
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adrenergic neuron blocking antihypertensives
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reserpine
guanethidine guanadrel |
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anti-HTN alpha 1 blockers
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prazocin
terazocin doxazocin indoramine tamsulocin |
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What is first "dose" effect and which drug(s) exhibit this?
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hypotension &/or syncope with the 1st dose; dose should be low and admin at night
prazocin |
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What is the significance of beta blocking diabetic patient?
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beta blockade blocks the feedback mechanism of tachycardia, a warning sign of impending hypoglycemia
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nebivolol
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beta blocker
in kidneys - blocks renin release; induces NO formation via beta 2 agonism in renal artery and glomerulus -->renal vasodilation |
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True or False
Chronic beta blockade produces receptor up regulation |
TRUE
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beta blocker(s) with ISA
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pindolol
carvedilol |
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True or False
Skeletal muscle is affected by calcium channel blockers |
FALSE
calcium is stored in sarcoplasmic reticulum in skeletal muscle and is not dependent on extracellular calcium levels |
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common side effect of CCB
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gingival hyperplasia
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What drugs produce the side effect of gingival hyperplasia?
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CCB
phenytoin cyclosporin |
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Which vasodilator has the side effect of cyanide toxicity?
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nitroprusside
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Which anti-HTN have a side effect of a dry cough?
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ACEI
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alliskerin
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direct renin inhibitor - inhibits angiotensinogen conversion
no need to adjust dose for renal or hepatic impairment, or for the elderly |
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side effect of alliskerin
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angioedema
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antiarrhythmics work in one of 4 ways. List them.
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block sodium channels
block calcium channels influence potassium channels block sympathetic effects |
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What is considered slow conduction tissue(s) in the heart?
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SA & AV nodes
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What is considered fast conduction tissue(s) in the heart?
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purkinje fibers
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class I antiarrhythmics
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block sodium channels
Ia-"use dependent"; slows phase 0 (depolarization) and delays phase 3 (repolarization) Ib- blocks sodium and enhances potassium channels Ic- "non-use dependent"; slows phase 0 with little effect on phase 3 |
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class II antiarryhthmics
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beta blockers - slows HR & decreases AV node conduction velocity
propanolol, acebutolol, esmolol |
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Give examples of class I antiarrhythics.
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Ia - quinidine, procainamide, disopyramide
Ib - lidocaine, tocainide Ic - encainide, flecainide I(other) - mexiletine |
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class III antiarrhythmics
Give examples. |
block potassium channels - increases refractoriness, QT interval & ERP
bretyllium, amiodarone, sotalol |
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class IV antiarrhythmics
Give examples. |
block calcium channels - slows HR & decreases AV conduction velocity
verapamil, diltiazem |
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class V antiarrhythmics
Give examples. |
adenosine agonists --> decreases AV node conduction velocity
adenosine |
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What drug is the protype class Ia antiarrhythmic? How does it work?
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quinidine
it blocks sodium channels; slows phase 0 (decreases conduction velocity) and delays phase 3 (increased refractoriness) it is dose dependent, i.e. use-dependent |
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Why are antiarrhythmics more effective on atrial tissue than ventricular?
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because of the direct effect on sodium channels and indirect anticholinergic effects --> both decrease conduction velocity and increase ERP
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How does quinidine work in a-flutter?
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it decreases conductive velocity and increases" the circuit
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quinidine works best in atrial or ventricular tissue? Why?
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atrial
ventricular function is driven by calcium. Quinidine blocks sodium channels |
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major side-effects of quinidine.
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Torsade de Pointes
hypokalemia prolonged QT cinchonism embolism (quinidine is highly protein bound and can displace anticoagulants) |
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In what class is procainamide? what are its side effects?
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antiarrhythmics Ia
systemic lupus like rxn |
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antiarrhythmic class Ib is used for?
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ventricular arrhythmias
they have a short half life |
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primary use of class II antiarrhythmic drugs?
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SVT caused by AV node re-entry
PVC's suppress ectopic pacemaker |
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amiodarone toxicity results in:
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corneal deposits
photosensitivity torsade de pointes |
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phase 0 - sodium influx
phase 1 - chloride movement phase 2 - calcium & sodium channels are fighting with each other phase 3 - potassium eflux phase 4 - resting potential |
ID the various phases of this action potential
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