Diuretics

 

A- kaliuretic diuretics:

1- Loop diuretics:

* Molecules: furosemide; bumetanide

* Action Site: large segment of the ascending limb of the loop of Henle.

* Action: It inhibits the reabsorption of NaCl (25 to 30% of the filtered sodium)

NB -> this action persists in renal failure

2- Thiazides Related:

* Molecules: hydrochlorothiazide; indapamide (Fludex®)

* Target: the initial portion of the distal tube (dilution segment)

* Action: inhibits the reabsorption of sodium and chlorine; saldiurétique the action is gradual and moderate (5 to 10% of Na + filtered).

* Other: weak inhibitory activity of carbonic anhydrase => increased excretion of bicarbonate. decrease urinary calcium.

Carbonic anhydrase inhibitors -> acetazolamide (Diamox®): used to have no effect on acid-base balance and its extrarenal share (glaucoma)

B- sparing diuretics:

Molecules:

* Aldosterone antagonists -> spironolactone; potassium canrenoate (Soludactone®)

* Direct Diuretics -> amiloride (Modamide®); triamterene (in combination)

* The combination of any of these with a thiazide diuretic used to limit the urinary loss of K + (Modurétic®)

– These drugs work in the distal convoluted tubule to inhibit reabsorption of sodium in exchange for potassium excretion

– The non-aldosterone antagonist diuretics directly inhibit ion transport at the distal tubular cells

– Effects: mild increase the excretion of Na + with decreased excretion of K + and H + -> the urine becomes alkaline, the ammoniénémie and titratable acidity decreased while shedding bicarbonate.

– The spironolactone added back calcium excretion.

– The spironolactone has extrarenal effects: heart (LVH reduction and prevention of fibrosis); antiandrogenic effect.

* Comments

– Diuretics decrease initially and blood volume in a second time peripheral resistance

– Edema and ascites of cirrhosis -> spironolactone often associated with furosemide

– Indication of thiazide if stones -> decreased urinary calcium excretion

– The loop diuretics majorem the ear, and nephrotoxicity of aminoglycosides

– The combination of several kaliuretic diuretics majorem the depleting effect.

– The combination of a diuretic NSAIDs may induce acute renal failure with acute tubular necrosis and dehydration.

Diuretics - mode of action

Diuretics – mode of action

C- Side effects:

– The thiazédiques diuretics and loop diuretics can reduce glucose tolerance and promote the onset of diabetes; the thiazédiques may aggravate pre-existing diabetes; the hyperglycaemic effect could be due to a glycogenolytic Action

– Hyperuricemia is seen in most of the subjects treated with hypokalemic diuretics.

– Thiazide decrease renal calcium excretion => hypercalcemia. Conversely, furosemide increases urinary calcium and promotes calcium nephrolithiasis and nephrocalcinosis.

– The long-term use of diuretics thiazédiques increases in triglycerides and cholesterol.

– Acute Pancreatitis -> hydrochlorothiazide

– Dysmenorrhea and gynecomastia -> spironolactone

– Metabolic alkalosis hypokalemic

– Metabolic acidosis hyperkalaemic

D- notes:

– HTA

– Heart failure (loop diuretics, spironolactone)

– PAO (furosemide IV)

– Edema and ascites in cirrhotic spironolactone (often associated with furosemide)

– Calcium Nephrolithiasis -> thiazides (they decrease urinary calcium)

– Acute hypercalcemia -> furosemide is useful

– Acute glaucoma -> inhibitor of carbonic anhydrase (Diamox)

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