Diuretics

Pharmacology of diuretics: Mechanism of action of carbonic anhydrase inhibitors, osmotic diuretics, loop diuretics, thiazides , and potassium-sparing diuretics. This video is available for instant download licensing here https://www.alilamedicalmedia.com/-/galleries/all-animations/urinary-system-videos/-/medias/b1eb96d4-a43e-4fdb-af86-dd0149a1e37d-diuretics-narrated-animation
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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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Thiazide diuretics pharmacology nursing NCLEX review about the mechanism of action, side effects, nursing implications, and patient education.

Thiazide diuretics work to inhibit the sodium-chloride cotransporter (NCC) in the early part of the distal convoluted tubule. This will decrease sodium reabsorption…meaning less sodium will enter back into the blood. Instead, the sodium will stay in the filtrate. Therefore, this will cause more water to stay in the filtrate and less to be reabsorbed back into the blood…hence, leading to diuresis (increased urination).

Thiazides are used to treat hypertension, heart failure, and renal calculi that are composed of calcium.

Side effects of thiazides include hypokalemia, hyponatremia, hypercalcemia, hyperuricemia, hyperglycemia, metabolic acidosis, and orthostatic hypotension.

Nursing implication for thiazide diuretics are monitoring for signs and symptoms of dehydration (low blood pressure, fast heart rate), strict intake and output measure, daily weights, monitor labs for electrolyte imbalances, avoid digoxin and lithium toxicity etc.

#diuretics #thiazides #pharmacologynursing

Quiz: https://www.registerednursern.com/thiazide-diuretics-pharmacology-nclex-questions/
Notes: https://www.registerednursern.com/thiazide-diuretics-pharmacology-nclex-review/
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Potassium-sparing diuretics pharmacology review for nursing students in preparation for the NCLEX exam.

This review will discuss the mechanism of action of potassium-sparing diuretics, what conditions they treat, nursing responsibilities, side effects, and patient education.

Potassium-sparing diuretics inhibit the sodium channels in the last parts of the nephron, specifically the last part of the distal tubule and the collecting duct. When sodium channels are inhibited this will decrease the sodium and potassium exchange via the sodium-potassium pump within the nephron. This will cause sodium to stay in the filtrate instead of being reabsorbed, which causes water to stay with the sodium and this achieves the diuretic effect. Furthermore, this will limit potassium from leaving the bloodstream to enter the filtrate (hence SPARING potassium…this can lead to hyperkalemia in some patients).

There are two types of diuretics I discuss in this video: epithelial sodium channel inhibitors (Triamterene and Amiloride) and aldosterone antagonist (Spironolactone and Eplerenone).

Side effects of potassium-sparing diuretics include: hyperkalemia, dehydration, antiandrogen effects like gynecomastia, menstrual problems, decrease sex drive, upset stomach

Nursing interventions include: monitoring for dehydration, electrolyte imbalances, educating about limiting foods high in potassium/salt-substitutes, medication interactions with ACEI, ARBs, NSAIDs and Lithium etc.

#potassiumsparingdiuretics #diuretics #pharmacologynursing

Quiz: https://www.registerednursern.com/potassium-sparing-diuretics-nclex-questions-pharmacology/
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Where oh where do diuretics act in the nephron? A very common medical school and post graduate question, this VERY short video goes through all the major classes of diuretics and explains clearly WHERE and HOW they work to induce a diuretic effect.

A key concept is understanding that when SODIUM stays INSIDE the nephron tubules (and is NOT reabsorbed back into the body) it carries water with it, which is excreted. Nearly all the diuretics work by this principle.

Used widely in the community, hospitals and ICU, diuretics are an incredibly common medication – so you WILL be asked about them in nearly every specialty medical exam.

Find out more on www.propofology.com/resources and find Diuretics in the resource links with my full infogram on the topic!

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Cathy Parkes RN, covers Nursing pharmacology – Diuretics. The Nursing pharmacology video tutorial series is intended to help RN and PN nursing students study for nursing school exams, including the ATI, HESI and NCLEX.

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Loop diuretics pharmacology nursing review that includes the mechanism of action, side effects, nursing interventions, and patient education.

Loop diuretics mechanism of action is on the thick ascending limb of the loop of Henle. These medications will inhibit the sodium-potassium-chloride (NKCC2) cotransporter. When this cotransporter is inhibited, it will decrease the ions (sodium, potassium, and chloride) reabsorbed into the blood.

In turn, this will decrease sodium reabsorption in the loop of Henle (which normally reabsorbs about 25% of sodium) and decrease the tonicity of the medulla, which is normally hypertonic. The end result will be that the collecting ducts and loop of Henle will reabsorb less water back into the blood and more water will leave the nephron as filtrate.

Side effects of loop diuretics include: hypokalemia, hypocalcemia, hypomagnesemia, ototoxicity, metabolic aklaosis, and dehydration.

Loop diuretics are used to treat heart failure, pulmonary edema, hypercalcemia, and liver impairment (due to ascites).

Nursing interventions for loop diuretics: included in the video.

#loopdiuretics #diuretics #pharmacologynursing

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There are three different types of Diuretics that nursing students must review and know for their NCLEX and nursing exams. Diuretics are typically classified as either: potassium wasting diuretics (K+ wasting) or potassium sparing diuretics (K+ sparing). Potassium wasting diuretics include Loop diuretics like Furosemide, and bumetanide, as well as thiazide diuretics like HCT hydrochlorothiazide. Potassium sparing diuretics include spironolactone, which is easy to memorize their mechanism of action of blocking aldosterone hormone, since it sounds spironolactone sounds like aldosterone. In this video we cover a diuretic pharmacology nursing review of everything a student nurse must know for their nursing exams, ATI and HESI exit exams, as well as their NCLEX.

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