This quiz, titled 'Block 11 - Week 12 - Heart Failure Drugs', assesses knowledge on pharmacological treatments for heart failure, examining drug effects, mechanisms, and clinical applications through various patient scenarios.
Loop diuretics increase renin secretion
Loop diuretics are also weak inhibitors of carbonic anhydrase
The diuretic effect of thiazides undergoes partial tolerance
More sodium is physiologically reabsorbed at TALH than at DCT
The antihypertensive action of thiazides reduces GFR
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Isoproterenol
Atropine
Lidocaine
Potassium chloride
Atenolol
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Digoxin induced stimulation of vagal nucleus
Digoxin induced compensation of cardiac insufficiency
Direct depressant effect of digoxin on vasomotor center
Direct depressant effect of digoxin upon SA and AV node
Digoxin induced appearance of a ventricular pacemaker
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Activation of Na+ /K+ ATPase
Decreased intracellular Na+
Activation of cardiac M2 receptors
Inhibition of Ca++/Na+ exchanger
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Hydrochlorothiazide
Furosemide
Amiloride
Mannitol
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Inhibition of phosphodiesterase
Inhibition of Ca++/Na+ exchanger
Inhibition of Na+/K+ ATPase
Activation of beta-1 receptors
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Hyperkalemia increases the risk of digoxin toxicity
Hypokalemia increases the risk of digoxin toxicity
Metoprolol inhibits the metabolism of digoxin
Furosemide causes hemoconcentration
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Digoxin, hydrochlorothiazide, metoprolol, triamterene
Digoxin, furosemide, metoprolol, lisinopril
Digoxin, dorzolamide, furosemide, amiloride
Digoxin, acetazolamide, spironolactone, atenolol
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