Diuretics & RAAS Antagonists Flashcards Preview

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Flashcards in Diuretics & RAAS Antagonists Deck (28):

What are the three specific goals of pharmacologic management?

1. Reduce congestion - diuretics
2. Modulate neurohormonal activity - RAAS antag., BB
3. Improve flow - vasodilators


So vasodilators aren't very effective. But which vasodilators (nitrates/ hydralazine) are used for decreasing:
1. Preload
2. Afterload

1. Nitrates: venous dilation
2. hydralazine: arterial dilation


Diuretics reduce congestion and also preload. But which diuretics are preferred because they are the most efficient?

Loop diuretics (furosemide)
*Can be used acutely and chronically


Which subsequent medication should you start during or after optimization of diuretics?

ACE inhibitors


Beneficial actions of ACE inhibitors on the failing heart include..?
A. Decreased adrenal release of aldosterone
B. Increased vascular resistance
C. Decreased cardiac output
D. Reduced preload
E. Reduced heart rate
F. Decreased cardiac remodeling action of angiotensin II

A. Decreased adrenal release of aldosterone
D. Reduced preload
F. Decreased cardiac remodeling action of angiotensin II


How do aldosterone antagonists work and what do they do?

= Blocks aldosterone effect on kidney
-Diuretic = produces Na+/ fluid loss at kidney
-Anti-remodeling action
(cause increase in K+ and H+ ions usually excreted with aldosterone)


What is your biggest concern with aldosterone antagonists?

Hyperkalemia - K+ sparing

-monitor Serum K


Describe the beneficial effect of spironolactone (aldosterone antagonist):
A. Promotes K excretion
B. Promote Sodium retention
C. Activates aldosterone receptors
D. Blocks cardiac hypertrophy and fibrosis
E. Decrease renin release

D. Blocks cardiac hypertrophy and fibrosis


Where in the kidney do the following act?
1. aldosterone/ aldosterone inhibitors
2. loop diuretics
3. thiazide

1. collecting duct
2. thick ascending limb
3. distal convoluted tubule

*Most diuretics exert effects at luminal (urine) surface of renal tubule cells


Which diuretics are K+ wasting? What medications are K+ sparing

Loop diuretics

Aldosterone inhibitors


Why are we concerned with hypokalemia?

= decreases conductance!
-predisposes to digoxin toxicity
-^ sensitivity to class III anti-arrythmic drugs
-Prolonged QT interval > Torsade de pointe


You look at someones ECG and see a prominent U wave. What's wrong?



What effect does hyperkalemia have on conductance?

= increase conductance
-reduced action potential duration
-increased bradycardia & conduction disturbance > heart block

*ECG shows peaked T waves


A 52-year-old woman is admitted to the ED with a history of drug treatment for several conditions. Her serum electrolytes are found to be as follows:

Na+: 140 mEq/L (135-145) K+: 2.5 (3.5-5)
Cl−: 100 mEq/L (98-107) pH: 7.3 (7.31-7.41)

In view of the electrolyte panel shown the patient would be most at increased risk to the toxic actions of which drug?

A. Lisinopril
B. Digoxin (positive inotrope)
C. Dobutamine (-1 selective agonist)
D. Spironolactone
E. Epinephrine

B. Digoxin

*Low potassium


What causes hypokalemic alkalosis?

Loop diuretics/ thiazide
-A decrease in Na+ reabsorption (proximal to aldosterone site) means more Na+ at collecting tubule, ultimately resulting in more K+ and H+ loss


Why are loop diuretics so much more effective (high ceiling)?

Most Na reabsorption occurs at thick ascending limb!
-it blocks Na/K/Cl transporter there

*When you get to where thiazides act, all but 5-10% has been reabsorbed


Why do patients taking diuretics have increased uricemia?

Loop diuretics/ thiazides get secreted into urine from blood
-Go through same transporter as uric acid
-compete against uric acid secretion


So loop diuretics are used in HF patients with volume overload. What considerations should be taken if unresponsive to furosemide?

-Efficacy is enhanced with salt restriction

If lack response:
-increase dose
-switch to bumetanide or torsemide
-IV administration may be required initially
-ethacrynic acid can be used if sulfa allergies


Patients with HF have reduced diuretic response. What other meds can you add in addition to loop diuretics?

-Thiazide: block other Na reabsorption site

Aldosterone inhib.:
-enhance diuresis
-counter hypokalemia
-also reduce remodeling


An elderly female with a history of heart disease is brought to the emergency department with difficulty breathing. Examination reveals that she has pulmonary edema. Which is treatment is indicated?

A. Metoprolol
B. Dobutamine
C. Furosemide
D. Hydrochlorothiazide
E Spironolactone
F. Lisinopril

C. furosemide


What effect does Loop diuretic + thiazide have? How does it compare in efficacy?

Greater efficacy than just loop diuretics
Greater K+ loss as well :(

Good for use with refractory anemia


Which receptor does thiazide act on? What ionic effects does it have?

Na/Cl transporter in distal tubule (vs. loop diuretics Na/K/Cl transporter in ascending loop)

Decreased plasma Na levels
Increased Ca reabsorption (not sure why, but this is opposite of loop diuretics)


A 52-year-old woman is admitted to the ED with a history of drug treatment for several conditions. Her serum electrolytes are found to be as follows:

Na+: 140 mEq/L (135-145) K+: 6.5 (3.5-5)
Cl−: 100 mEq/L (98-107) pH: 7.2 (7.31-7.41)

This patient has probably been taking:

A. Spironolactone
B. Atenolol
C. Digoxin
D. Lisinopril
E. Furosemide

A. Spironolactone
D. Lisinopril


What is the major reason for taking aldosterone antagonists?


Used primarily for their anti-remodeling actions via block of cardiac aldosterone receptors (RAAS antagonist function)

*Remember that all but 2-5% of sodium has been reabsorbed by the time it gets to the collecting duct, so AA's have minimal effect


How does spironolactone inhibit aldosterone?

Competitive antagonist at aldosterone receptor

FYI mentions other Ald. Antag. like triamterene/ amiloride which block Na channels >> no utility in HF


What are the adverse effects of AAs? What increases the risks?

-risk increased by: age, renal dysfxn, high doses, combined use of ACEI/ARBs, use of NSAIDS

Endocrine abnormalities (gynecomastia)


8. A male patient is placed on a new medication for heart failure and notes that his breasts have become tender to the touch. Which medication is he most likely taking?

A. Carvedilol
B. Eplerenone
C. Furosemide
D. Hydrochlorothiazide
E. Spironolactone
F. Lisinopril

E. Spironolactone

(Yes eplerenone is also an AA, but doesn't block androgen receptors)


9. Beta-blockers improve cardiac function in heart failure by:

A. Increasing heart rate
B. Decreasing cardiac output
C. Increasing renin release
D. Cardiac anti-remodeling effects
E. Reducing epinephrine release from the adrenal gland

D. Cardiac anti-remodeling effects