2007 Exam Flashcards
The antiarrhythmic mechanism of adenosine (Adenocard) involves blockade of
A. Na channels
B. Ca channels
C. K channels
D. None of the above
D. None of the above
Which of the following drugs is contraindicated in patients with myocardial infarction?
A. Lidocaine (Xylocaine)
B. Propafenone (Rythmol)
C. Amiodarone (Cordarone)
D. Quinidine (Quinidex)
B. Propafenone (Rythmol)
Class I antiarrhythmic drugs
A. Decrease action potential threshold.
B. Cause positive entropy.
C. Are only used for supraventricular arrhythmias.
D. Are more effective in rapidly beating myocardium.
C. Are only used for supraventricular arrhythmias.
Class IV antiarrhythmic drugs
A. Increase the QT interval on the electrocardiogram.
B. Increase refractoriness.
C. Act on G protein coupled receptors.
D. Are used to treat life-threatening arrhythmias.
E. Do none of the above.
E. Do none of the above.
Which physiological mechanism does NOT contribute significantly to the efficacy of antianginal drugs?
A. Increasing diastolic interval
B. Decreasing myocardial contractile force
C. Increase in total coronary blood flow
D. Reduction in venous return to the heart
C. Increase in total coronary blood flow
Beta-adrenergic receptor antagonists are useful antianginal drugs because they
A. Attenuate exercise-induced tachycardia.
B. Reduce cardiac contractility.
C. Relax venous smooth muscle thereby reducing preload.
D. Do A and B only.
E. Do A, B,and C.
D. Do A and B only.
When used for the treatment of angina which of the following statements about nitroglycerin (Nitrostat) is FALSE?
A. It reduces myocardial work by decreasing preload and afterload.
B. It has a high bioavailability when dissolved in the mouth.
C. It directly reduces cardiac rate and contractility.
D. It is effective in relieving unstable angina due to inhibition of platelet aggregation.
C. It directly reduces cardiac rate and contractility.
Mechanisms that contribute to reduce mortality in the pharmacological treatment of heart failure include
A. Interference with the actions of angiotension II.
B. Partial blockade of cardiac beta 1 adrenergic receptors.
C. Increase myocardial contractility.
D. A and B only.
E. A, B, and C.
D. A and B only.
When used for the treatment of heart failure which of the following statements about angiotensin converting enzyme inhibitors is false?
A. They reduce peripheral resistance. B. They promoted sodium excretion. C. They increase glomerular filtration. D. They reduce aldosterone secretion. E. They can produce a persistent cough.
C. They increase glomerular filtration.
Which of the following statements about digitalis glycosides is false?
A. The margin of safety between therapeutic doses and toxic doses is narrow.
B. They inhibit Na/K ATPase in all excitable cells.
C. They increase the intracellular free Ca concentration in cardiac myocytes.
D. They reduce peripheral vascular resistance.
D. They reduce peripheral vascular resistance.
Which of the following statements is true regarding low-density lipoprotein (LDL)?
A. Regulation of liver LDL receptor levels is the dominant mechanism for controlling LDL levels in humans.
B. LDL is anti-atherogenic.
C. Lowering plasma LDL levels has no effect on coronary heart disease mortality.
D. LDL transports dietary lipids from the intestine to peripheral and hepatic tissues.
E. Cholestyramine (Questran) is the most effective drug in controlling plasma LDL levels.
A. Regulation of liver LDL receptor levels is the dominant mechanism for controlling LDL levels in humans.
Exetimibe (Zetia)
A. Is the first choice drug for any patient with elevated LDL levels.
B. Binds to the nuclear receptor PPAR alpha.
C. Increases the activity of lipoprotein lipase.
D. Acts locally in the small intestine.
D. Acts locally in the small intestine.
Cardiovascular reflexes resulting from pharmacological vasodilation can include
A. Reduced cardiac output.
B. Increased parasympathetic nervous system activity.
C. Reduced aldosterone released from the adrenal gland.
D. Increased heart rate.
E. All of the above.
D. Increased heart rate.
The antihypertensive mechanism of action of clonidine (Catapres) involves
A. Antagonism of beta-1 adrenergic receptors
B. Activation of central nervous system alpha-2 adrenergic receptors leading to a reduction in sympathetic outflow from the brain.
C. Depletion of neurotransmitters stored in postganglionic sympathetic neurons.
D. Blockade at angiotensin converting enzyme.
E. An ability to accumulate in synaptic vesicles and be released as a ‘false’ neurotransmitter.
B. Activation of central nervous system alpha-2 adrenergic receptors leading to a reduction in sympathetic outflow from the brain.
What blocks the synthesis of thromboxane A2 (TXA2) in platelets?
A. Enoxaparin (Lovenox) B. Streptokinase (Streptase) C. Warfarin sodium (Coumadin) D. Aspirin E. Abciximab (ReoPro)
D. Aspirin
