Correction to your Assertion
While some of your assertion are correct, not all are true.
1. Angiotensin Receptor Blockers, Angiotensin Converting Enzymes, Direct Renin Inhibitors also have diuretic like properties by decreasing angiotensin II utilization ( either blocking receptors or decreasing corvesion of active metabolite) along the renal tubule specially in the proximal part and in ADH control in collecting duct, so not all diuretics with exception of potassium sparing agents cause hypokalemia. ARB's and ACEI's definitely cause hyperkalemia and definitely should not be in combination with potassium sparring agents. They are mention in a separate class because diuretic effect is less potent than other diuretiucs and also have cardioprotective effect in improving survival.
Note #1: While digoxin is not a diuretic, it also raises potassium levels (hyperkalemia), and it should be noted because it is usually recommended for CHF patients with reduced fraction ejection that already are taking ACEIs or ARB's ( beware of digoxin toxicity), and diuretics
Note#2: Osmotic diuretics can cause either hypokalemia or hyperkalemia, it is dependant on dosage and kidney disease
2. Epithelium sensitive sodium channel blockers ( Triamterene and Amiloride), classified as part of the potassium sparring agents do not have antiandrogenic properties as you stated, and there have been rare cases of eplerenone causing breast tenderness or gynecomastia although less tha 1%.
3. All diuretics have sulfa allergy because sulfa group needed to be lipophylic for better bioavalaibility it is not only loop diuretics, the only exception is etachrynic acid.
4. Osmotic diuretic also presents with metabolic acidosis and in the proper medical scenario they could all potentially exacerbate acidosis.
5. While USMLE doesnt give its proper importance, loop diuretics do cause hyperglycemia also as thiazides because they open atp sensitive potassium channels in beta cells.
While some of your assertion are correct, not all are true.
1. Angiotensin Receptor Blockers, Angiotensin Converting Enzymes, Direct Renin Inhibitors also have diuretic like properties by decreasing angiotensin II utilization ( either blocking receptors or decreasing corvesion of active metabolite) along the renal tubule specially in the proximal part and in ADH control in collecting duct, so not all diuretics with exception of potassium sparing agents cause hypokalemia. ARB's and ACEI's definitely cause hyperkalemia and definitely should not be in combination with potassium sparring agents. They are mention in a separate class because diuretic effect is less potent than other diuretiucs and also have cardioprotective effect in improving survival.
Note #1: While digoxin is not a diuretic, it also raises potassium levels (hyperkalemia), and it should be noted because it is usually recommended for CHF patients with reduced fraction ejection that already are taking ACEIs or ARB's ( beware of digoxin toxicity), and diuretics
Note#2: Osmotic diuretics can cause either hypokalemia or hyperkalemia, it is dependant on dosage and kidney disease
2. Epithelium sensitive sodium channel blockers ( Triamterene and Amiloride), classified as part of the potassium sparring agents do not have antiandrogenic properties as you stated, and there have been rare cases of eplerenone causing breast tenderness or gynecomastia although less tha 1%.
3. All diuretics have sulfa allergy because sulfa group needed to be lipophylic for better bioavalaibility it is not only loop diuretics, the only exception is etachrynic acid.
4. Osmotic diuretic also presents with metabolic acidosis and in the proper medical scenario they could all potentially exacerbate acidosis.
5. While USMLE doesnt give its proper importance, loop diuretics do cause hyperglycemia also as thiazides because they open atp sensitive potassium channels in beta cells.
