My approach to diuretic questions
DDx of diuretics
- Loops
- Thiazides
- K+ sparing
- Acetazolamide
- Spironolactone (competitive aldosterone antagonist, also interferes with testosterone synthesis causing incr estradiol in treating hirsutism in PCOS. Spironolactone has been shown to improve mortality in patients with CHF by blocking the toxicity of aldosterone as it hits the heart. (Weird MOA)
- Amiloride (inhibits directly, the Na/K pump in the DCT)
- Triamterene (same MOA amiloride)
To separate all of the diuretics that cause hypokalemia, look at the [Ca++] to separate loops and thiazides.
- Loops lose everything including Ca++, so if the patient is hypokalemic and hypocalcemic, they are probably on a loop (furosemide, torsemide, ethacrynic Acid, bumetanide) be careful of ethacrynic acid, it's name doesn’t look like a loop at all!
- Thiazides cause increased Ca++ reabsorption from renal tubules so they cause hypercalcemia, but they are used to treat calcium renal stones because they decrease Ca++ in the tubules, where it is causing the problem.
- Acetazolamide is one of the few things that causes a metabolic acidosis with hypokalemia. Acetazolamide is a carbonic anhydrase inhibitor producing an alkaline diuresis. (you pee bicarb, and with the bicarb, Na follows). Usually, acidosis goes with hyperkalemia. Acetazolamide is also used to decr aqueous humor production and to treat acute mountain sickness.
ACE-I and Digoxin causes hyperkalemia so watch these drugs with spironolactone.
If you get a question w/ Bartter’s Syndrome (mutation of the Na+/K+/2Cl- cotransporter in TAL, just look for the lab values that match a loop diuretic (remember loops LOSE everything). You must rule out diuretic abuse in a patient you suspect has Bartter’s Sydrome.
1 comment:
this stuff is amazing! how did you come up with this info?
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