What's a diuretic?
It's a drug that makes you pee more.
Classification
Loop diuretic (aka high ceiling), which may cause substantial diuresis of up to 20%, of filtered load of NaCl and water (cf normal renal sodium reabsorption which leaves only about 0.4% of filtered sodium in the urine), by inhibiting reabsorption of sodium at the ascending loop of Henle [of the nephron], leading to an excretion of water in the urine, as water follows sodium. They are more effective in Pt's with impaired kidney function. Examples include:
Furosemide (Lasix, previously, frusemide)
Bumetanide
Ethacrynic acid
Torsemide
Carbonic anhydrase inhibitors, which inhibit the enzyme carbonic anhydrase, which is found in the PCT. This causes reduced reabsorption of NaCl and bicarbonate at the PCT. It includes:
Acetazolamide
Methazolamide
Thiazides (aka low ceiling), which act on the DCT (see page)
Potassium-sparing diuretics, which don't promote secretion of potassium into urine as with other diuretics. These include:
Aldosterone antagonists, mainly, which competitively antagonize aldosterone. Aldosterone normally adds sodium channels in the principal cells of the collecting duct and late DCT of the nephron. It thus helps prevent sodium reabsorption. Examples include:
Spironolactone
Eplerenone
Potassium canreonate
Epithelial sodium channel blockers, e.g.:
Amiloride
Triamterene
Calcium-sparing diuretics, which are beneficial in hypocalcemia, or unwanted in hypercalcemia. It includes:
Thiazides, which cause a net decrease in calcium lost in urine
Potassium-sparing diuretics, which cause a net increase in calcium lost in rurine, but the increase is much smaller than the increase associated w/ other diuretic classes
In comparison, loop diuretics have significant increase in calcium excretion, which can increase risk of reduced bone density
Osmotic diuretics, which increase osmolality, but have limited tubular epithelial cell permeability. it works by expanding extracellular fluid and plasma volume, thus increasing blood flow to the kidney, particularly the peritubular capillaries. This reduces medullary osmolality, and thus impairs the concentration of urine in the loop of Henle
Patient information
Wow, that seems like a lot. What are the different types of diuretics?
There's loop diuretics, pretty popular, they prevent sodium from being taken back up at the LOOP of Henle... hence the name. This makes more sodium to pee out. Thiazides are similar, but rather than preventing sodium from being taken back up at the loop of Henle, it does this at the DCT. Carbonic anhydrase is again similar, but prevents sodium from being taken back up at the PCT, rather than the DCT.
Wait, can we start with high vs low ceiling, what's the difference?
So loop diuretics act on inhibiting sodium reabsorption at the ascending loop of Henle, whereas thiazides does this at the distal convoluted tubule. You might recall in the kidney, that the concentration of sodium in mOsmol/L, dramatically increases as water is pulled out as you go down the loop of Henle, and dramatically decreases as sodium is pulled out as you go up the loop of Henle. This increase in concentratino is then repeated again at the collecting duct, but this is because a lot of it is discarded as urea. Therefore, if you compare the effect of inhibiting at the loop of Henle vs the DCT, the effect of preventing sodium from escaping at the loop of Henle, is going to be far more effective than at the DCT.
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