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Flashcards in Diuretics Deck (25):

Fluid flow through the kidneys

Blood plasma entering the kidneys is filtered from the glomerular capillaries into Bowman's capsule then
Proximal convoluted tubule
Descending loop of Henle
Ascending loop of Henle
Distal convoluted tubule
Collecting tubule and duct


Proximal convoluted tubule

Located in the cortex of the kidney, nearly all glucose, bicarb, amino acids and other metabolites are reabsorbed.
2/3s of Na+ is also reabsorbed
Carbonic anhydrase in the luminal membrane and cytoplasm of proximal tubular modulates reabsorption of bicarb
Site of the organic acid and base secretory system, which secretes uric acid, some antibiotics and diuretics.


Descending loop of Henle

Remaining filtrate from proximal tubule is isotonic, enters the descending loop of Henle, then into the medulla of the kidney. The osmolarity increases along descending portion of loop, resulting in 3 fold increase in salt concentration.
Osmotic diuretics exert part of their actions in this region


Ascending loop of Henle

Cells here are impermeable to water
Active reabsorption of Na+ K+ and Cl- os mediated by a Na+/K+/2Cl- contransporter.
Approx 25-30% of tubular sodium chloride returns to interstitial fluid.
Drugs affecting this size (loop diuretics) have the greatest diuretic effect because it is a major site for salt reabosprtion


Distal convoluted tubule

Also impermeable to water
10% of filtered sodium chloride is reabsorbed via a Na+/Cl- transporter that is sensitive to thiazide diuretics
Calcium reabsorption is mediated by passage through a channel then transported by a Na+/Ca2+ exchanger into interstitial fluid.
Ca2+ is regulated by parathyroid hormone in this portion of the tubule


Collecting tubule and duct

Principal cells of collecting tubule and duct are responsible for Na+, K+, and water transport, and intercalated cells affect H+ secretion.
Sodium enters principal cells through channels which are inhibited by amiloride and triamterene. Once inside Na+ reabsorption relies on Na+/K+-ATPase pump, which when combined increase Na+ reabsorption
ADH receptors promote reabsorption of water from collecting tubules and ducts


Thiazides and related agents

Sulfonamide derivative
Effect distal convoluted tubule, and all have equal max (called low ceiling diuretics) diuretic effects (varying in potency)


Chlorthalidone (thalitone) is a



Hydrochlorothiazide (microzide) is obvi 5 a



Indapamide is a



Metolazone is a



Bumetanide is a

Loop diuretic


Ethacrynic acid (edecrin) is a

Loop diuretic


Furosemide (lasix) is a

Loop diuretic


Torsemide (demadex) is a

Loop diuretic


Amiloride (midamor) is a

Potassium sparing diuretic


Eplerenone (inspra) is a

Potassium sparing diuretic


Spironolactone (aldactone) is a

Potassium sparing diuretic


Tramterene (dyrenium) is a

Potassium sparing diuretic


Acetazolamide (diamox) is a

Carbonic anhydrase inhibitor


Mannitol (osmitrol) is a

Osmotic diuretic


Mannitol (osmitrol) is a

Osmotic diuretic


Sulfa allergies diuretics don't haves

Loop, carbonic anhydrase inhibitors and thiazides


Thiazide fun facts!

Chlorthalidone, indapamide, and metolazone are referred to as thiazide-like because they contain the sulfonamide residue in their chemical structures and their MOA is similar. However, not truly thiazides
Treatment for severe edema (hepatic cirrhosis and heart failure)


Thiazide MOA

Act mainly in cortical region of the ascending loop of Henle and distal convulted tubule to decrease reabsorption of Na+ by inhibition of Na+/Cl- cotransporter on luminal membrane of tubule
Increases concentration of Na+ and Cl- in tubular fluid
Because site of action is on luminal membrane, drugs must be excreted into tubular lumen to be effective, and so with decreased renal function, they lose efficacy
NSAIDS inhibit production of renal prostaglandins, thereby reducing renal blood flow