Diuretics - Mechanism of Action of Different Classes of Diuretics, Animation
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- Опубліковано 30 вер 2024
- (USMLE topics) Pharmacology of diuretics: Mechanism of action of carbonic anhydrase inhibitors, osmotic diuretics, loop diuretics, thiazides , and potassium-sparing diuretics.
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Diuretics are commonly used to treat primary hypertension and edema. Changes in body fluid and electrolytes induced by diuretics can also be therapeutic for some other conditions.
Sodium and water are filtered in the glomerular capsule of nephrons, then reabsorbed back to the blood at various sites along the renal tubule. Different classes of diuretics prevent sodium reabsorption, and thus increase sodium loss, at different sites, by different mechanisms.
Carbonic anhydrase inhibitors inhibit the enzyme carbonic anhydrase, which is required for reabsorption of bicarbonate in the proximal tubule. Most of sodium lost at this early stage is reclaimed further down the renal tubule. Increased delivery of sodium to the collecting duct increases its reabsorption at this site through epithelial sodium channels, in exchange for a greater potassium loss, and may cause hypokalemia. Loss of bicarbonate also affects acid-base balance, producing metabolic acidosis. Carbonic anhydrase inhibitors are rarely prescribed for cardiovascular diseases; they are mainly used in the treatment of glaucoma.
Osmotic diuretics, such as mannitol, promote water loss directly through osmosis. Mannitol is effective in lowering intracranial pressure in patients with head injury, and lowering intraocular pressure in acute glaucoma.
Loop diuretics inhibit the sodium/potassium/chloride cotransporter in the thick ascending limb of the loop of Henle. These are very powerful diuretics because this transporter not only reabsorbs a large share of sodium, but is also responsible for the osmolarity gradient in the medulla that enables the collecting duct to concentrate urine. Side effects include electrolyte imbalances, metabolic alkalosis, hypovolemia due to excessive loss of water, loss of hearing due to inhibition of a similar transporter in the inner ear, and gout due to interference with transporters involved in urate secretion.
Thiazide diuretics inhibit the sodium/chloride cotransporter in the distal tubule, which reabsorbs about 5% of the sodium load, and are not as powerful as loop diuretics. However, thiazides also have a vasodilation effect by a still poorly understood mechanism. Thiazides are first-line drugs for uncomplicated hypertension and most effective for heart failure prevention.
Unlike loop diuretics, thiazides reduce calcium loss in urine and can be used to prevent formation of new calcium kidney stones. This is because lower intracellular sodium induced by thiazides leads to higher calcium reabsorption mediated by sodium/calcium exchanger located on the basolateral membrane. Other side effects are similar to those of loop diuretics and include hypokalemia, metabolic alkalosis and hyperuricemia.
Potassium-sparing diuretics act mainly in the collecting duct. Here, sodium reabsorbs through epithelial sodium channels, ENaC, then sodium/potassium pump, in exchange for potassium loss. Sodium influx into cells creates a negative lumen potential, which drives reabsorption of chloride and excretion of potassium and hydrogen. Both ENaC and sodium/potassium pump are induced by aldosterone.
Potassium-sparing diuretics include aldosterone receptor antagonists and direct ENaC inhibitors. They are called potassium-sparing because they do not increase potassium loss, unlike all other diuretics acting upstream. Instead, they reduce potassium loss because reduced sodium reabsorption decreases the electrogenic exchange for potassium. Aldosterone antagonists also directly inhibit the sodium/potassium pump, reducing potassium loss.
Because the collecting duct reabsorbs only a small amount of sodium, this class of drugs has only a mild diuretic effect. They are commonly used in conjunction with thiazide or loop diuretics to prevent hypokalemia. Side effects include hyperkalemia, metabolic acidosis, and effects associated with inhibition of aldosterone.
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My problem is that I wake up every night to pee at least once. It’s disturbing because it interrupts my sleep and I cannot fall back asleep when I return to bed. I’ve tried stopping all fluid intake after 6pm, not having any drinks or even soup and hydrating fruits. And still I’m waking up in the middle of the night to pee. I’m always exhausted when I’m awake. What should I do?
I believe that might be more connected with a physiological state of mind. I had an issue I had a similar issue however I tried to control my mind to avoid that feeling happy to say it works. Some of the environmental conditions also can trigger the same sensation I think it best to find the triggers. Additionally, the BPH condition might not allow the bladder to empty completely which need medicine
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▪︎CA inhibitors inhibit the enzyme (carbonic anhydrase) which is required for reabsorption of bicarbonate in PCT.
▪︎ This leads to greater sodium loss, in the form of sodium bicarbonate, and subequently greater water loss in the urine.
▪︎These inhibitors have the weakest druritic effect because most of sodium lost at this early stage is reclaimed further down the rend tubule
▪︎increased delivery of sodium do the collecting duct increases its reabsorption at this site, through epitelial sodium channels, in exchange for greater potassium loss, and Cause hypokalemia.
▪︎loss of bicarbonate also affects the acid-base balance, producing metabolic acidosis"."
▪︎CA inhibitors are ranely prescribed for Cardiovascular diseases; they are mainly used in the treatment of glaucoma.
▪︎Osmoticdiuretics, such as mannitol, promote water loss directly through
osmosis.
▪︎Being filtered without subsequent reabsorption, mannital stays in the renal tubule, creating a higher osmolality which attract water by osmosis.
▪︎It produces a greater loss of water compared a to sodium and potassium.
▪︎Mannitol is not usually used to treat edema because its initial presence in the circulation may acually further increase fluid volume to a dangerous level.
▪︎it is however effective in lowering intracranial pressure in patients with head injury, as well lowering intraocular pressure in (acute glocuma).
▪︎osmotic diuretics act only the entire renal tubule, with predominant effect on the PCT and the descending LH.
▪︎ Loop diuritics inhibite the sodium /potassium /cloride cotransporter in the thick ascending limb of the LH.
▪︎There are very powerful diuritics because these transporter not only reabsorbs a large share of sodium, but is also responsible for the asmolarity gradient in the medulla that enables the collecting tobules to concentrate urine.
▪︎As the loop diuritics cause the salinity gradient to diminish, the collecting duct loses less water , more water is excreted in urine.
• Because the Na + /K + / cl cotransporter acts in Conjunction with back diffusion of potassium to create a positive lumen potential that drives reabsorption of other positive ion, its inhibition by loop diuretics also induces greater loss of these ions.
▪︎Side effects include electrolyte imbalances, metabolic alkalosis, hypovolemia due to excessive loss of water, loss of hearing due to inhibition of a similar transporter in the inner ear,and gout due to interference with transporters involved in urate secretion.
▪︎Thiazide diuretics inhibit the sodium/chloride cotransporter in the distal tubule, which reabsorbs about 5% of the sodium load, and are not as powerful as loop diuretics.
▪︎However, thiazides also have a vasodilation effect by a still poorly understood mechanism.
▪︎Thiazides are first-line drugs for uncomplicated hypertension and most effective for heartfailure prevention.
▪︎Unlike loop diuretics, thiazides reduce calcium loss in urine and can be used to prevent formation of new calcium kidney stones.
▪︎This is because lower intracellular sodium induced by thiazides leads to higher calcium reabsorption mediated by sodium/calcium exchanger located on the basolateral membrane.
▪︎Other side effects are similar to those of loop diuretics and include hypokalemia, metabolicalkalosis and hyperuricemia.
▪︎Potassium-sparing diuretics act mainly in the collecting duct.
▪︎Here, sodium reabsorbs through epithelial sodium channels, ENaC, then sodium/potassium pump, in exchange for potassium loss.
▪︎Sodium influx into cells creates a negative lumen potential, which drives reabsorption of chloride and excretion of potassium and hydrogen.
▪︎Both ENaC and sodium/potassium pump are induced by aldosterone.
▪︎Potassium-sparing diuretics include aldosterone receptor antagonists and direct ENaC inhibitors.
▪︎They are called potassium-sparing because they do not increase potassium loss, unlike all other diuretics acting upstream.
▪︎Instead, they reduce potassium loss because reduced sodium reabsorption decreases theelectrogenic exchange for potassium.
▪︎Aldosterone antagonists also directly inhibit the sodium/potassium pump, reducing potassium loss
▪︎Because the collecting duct reabsorbs only a small amount of sodium, this class of drugshas only a mild diuretic effect.
▪︎They are commonly used in conjunction with thiazide or loop diuretics to prevent hypokalemia.
▪︎Side effects include hyperkalemia, metabolic acidosis, and effects associated with inhibitionof aldosterone.
thank you so much. Such a nice video and clear my concept in few minutes.
Must to watch ….thank dear..
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Best explained ❤
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What are the foods that disrupt the work of diuretics?
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