Clinical Problems Associated With Diuretics

Thiazides deplete potassium, sodium and magnesium (although thiazides aim for sodium loss, potassium and magnesium are also lost). Metabolic changes also occur, such as an elevation of uric acid leading to gouty symptoms. So to manage the gout, an anti-gout agent can also be prescribed if this is seen—not a good way to manage a patient. The metabolic changes also include elevation of blood sugar, lipid increase, and insulin receptor hyper-sensitivity.


Loop diuretics lead to hypkalemia. Also, high doses appear to damage CN VIII. Make sure that the patient has some sort of potassium source if they are on a loop diuretic (bananas, apricots, potassium tablets). Dose is very important if taking potassium tablets, we need at least 20 milli-equivalents.


Carbonic anhydrase inhibitors can cause metabolic acidosis, a term which is important in studying for the National Boards Exam and not much else since we don’t use these drugs anymore.


Potassium sparing diuretics can lead to hyperkalemia if dosages are too high, which leads to AV block and systole—hypokalemia usually increases the excitability, you get irregular heartbeats which can be life threatening, hyperkalemia can lead to conduction block. Gynecomastia (man-boobs and masculine nipple tenderness) is also a clinical problem with potassium sparing drugs (because Spironolactone is a estrogen derivative).



Thiazides can be used with beta-blockers, but they tend to increase the blood glucose when used together. When a thiazide is used with digitalis, the hypokalemia can cause digitalis toxicity. When a potassium sparing diuretic like Spironolactone is used with an ACE inhibitor, you get hyperkalemia. If you combine a loop diuretic with and aminoglycoside you get hearing loss. So all of these things are predictable based on the pharmacology of each class.

Category: Pharmacology Notes