Diuretics

Question 1

state the mechanism by which all diuretics increase urine production

Answer 1

BLOCK sodium

REABSROB chloride

Question 2

classify the follow as potassium Sparing or potassium wasting: thiazides, loop diuretics, spironolactone, triamterene

Answer 2

Potassium Sparing: Spironolactone and triamterene

potassium wasting: thiazides, loop diuretics

Question 3

why is knowing the effects of diuretics on renal potassium excretion clinically important?

Answer 3

to note the cause of lower potassium levels

Question 4

factors to consider when choosing a diuretic

Answer 4

state of renal function, the existence of certain co-morbid conditions, potential untoward drug actions, and possible interactions of diuretics with nutrients and with other drugs

Question 5

review a nephron structure and identify where the drugs listed above do their work.

(furosemIde, hydroCHLORathiazide, spironolActone, triamtErEnE)

Answer 5

a nephron has five parts: a glomerulus, a proximal tubule, a loop of Henle, a distal tubule, and a collecting duct.

FUROSEMIDE acts in the thIck segment of the ascending loop of Henle’s loop to block reabsorption of sodIum and chlorIde

HYDROCHLOROTHIAZIDE blocks the reabsorption of sodium and CHLORide in the early segment of the distal COnvoluted tubule.

SPIRONOLACTONE blocks the the actions of Aldosterone in the distAl nephron

TRIAMTERENE disrupts sodium/potassium Exchange in the distal nephron.

Question 6

state the normal range for K+ and how changes of serum K+ levels affect digoxin and the likely impact of hypokalemia or hyperkalemia

Answer 6

the normal range for potassium is 3.5-5.0 (you usually buy only 3-5 bananas at the store and bananas have potassium!)

Digoxin toxicity is
worsened by hypokalemia. Because digoxin binds to the K+ site of the Na+/K+-ATPase pump, low serum potassium levels increase the risk of digoxin toxicity. In contrast, digoxin efficacy is reduced by hyperkalemia.