0:00 In this video we are going to look at diuretics. 0:19 Diuretics works on the kidneys, the nephrons of the kidneys. 0:23 What are diuretics? 0:24 Diuretics are substances that help the body get rid of sodium and water. 0:32 Diuretics decreases blood pressure, because a decrease in plasma volume, a 0:37 decrease in 0:37 water, equals a decrease in blood pressure. 0:45 Hopefully the function of diuretics will make sense towards the end of this 0:49 video. 0:49 In this video we are going to look at four main types of diuretics, and another 0:53 one. 0:54 We will look at osmotic diuretics, lip diuretics, thiazide diuretics, and 0:59 potassium sparing 1:00 diuretics, and also the carbonic and hydrates inhibitors. 1:06 All these diuretics aim to reduce blood pressure by increasing the excretion of 1:14 water and sodium 1:16 in urine. 1:18 Those diuretics elicit its function on the nephron of the kidneys, let us again 1:23 recap 1:24 the structure of the nephron, and later see where these diuretics specifically 1:30 have its 1:31 function along the nephron tubule. 1:35 So here we have the glomerulus with the afferent arterial coming in, and the 1:39 efferent arterial 1:40 coming out. 1:41 Here we have the proximal convoluted tubules, the thick descending limb, the 1:46 loop of headly, 1:48 the thick ascending limb, the distal convoluted tubules, and the collecting 1:53 duct. 1:54 Now let us look where along this tubule of the nephron, sodium, and other 1:59 substances 2:00 can be reabsorbed from. 2:04 So for example, the main site of sodium reabsorption is in the proximal 2:08 convoluted tubules, where 2:10 it absorbs a proximal 65 to 70%. 2:14 Sodium bicarbonate can also be absorbed in the proximal convoluted tubules. 2:19 Water is reabsorbed within the descending limb, and in the thick ascending limb 2:26 we have a 2:27 transporter, a symptomer, which reabsorbs sodium, potassium, and chloride, 2:33 about 25% of sodium 2:35 is reabsorbed here. 2:37 And then we have in the distal convoluted tubules, another symptomer, 2:40 transporter, which reabsorbs 2:43 sodium and chloride ions, about 5% of sodium is reabsorbed, and finally in the 2:48 collecting 2:49 ducts we have a final transporter, which reabsorbs sodium, but secretes a 2:57 potassium, 2:59 and this only reabsorbs about 1% of sodium, so not that much. 3:07 Water can also be reabsorbed within the collecting duct. 3:11 Now what is very important to realize is that wherever along this tubule, 3:16 sodium is reabsorbed, 3:18 this will cause water to be reabsorbed as well, because the golden rule of the 3:23 kidneys 3:24 is that water tends to follow sodium, and therefore when we reabsorb water and 3:30 sodium, 3:31 this will indefinitely increase blood pressure. 3:38 This prevents the reabsorption of the sodium and water somewhere along this tub 3:44 ule, and 3:44 therefore aims to decrease blood pressure. 3:50 So now let's look at a scenario where we have an increase in blood pressure, 3:55 and see 3:56 how diuretics work to decrease blood pressure. 4:03 The first type of diuretics we'll talk about is osmotic diuretics, and they 4:07 work in the 4:08 proximal conflict with tubules, and also the loop of handling. 4:13 These are things such as manatol, urea, glycerin, and isosorbide. 4:20 Now they don't really sound like one of those drugs, because really what their 4:26 main function 4:27 is, is that they increase the solute concentration within the tubules, and 4:34 therefore causes water 4:37 to be retained within the tubules. 4:43 This is because it follows the osmosis rule, where if we have a higher 4:47 concentration of 4:48 solutes within a particular area, more water will tend to go there. 4:56 So for example here, we have the cells light in the tubule, here we have the 5:01 tubule lumen, 5:02 which is inside the nephron, and then we have the blood which is outside. 5:05 In the blood we have two solutes and two waters for example, but in the tubule 5:11 lumen we have 5:12 many solutes, these red things which can be manatol or urea, and therefore 5:17 there will 5:18 be a lot of water, and therefore water will not be reabsorbed because it has to 5:23 follow 5:23 the osmosis rule. 5:25 Hence the name osmotic diuretics. 5:29 Osmotic diuretics prevent the reabsorption of water from the tubule into the 5:34 blood, and 5:35 therefore it will decrease the blood volume, or the plasma volume, and 5:38 therefore decrease 5:40 blood pressure. 5:43 So osmotic diuretics, when taken orally or intravenously, they will enter the 5:47 bloodstream 5:48 and they will be freely filtered at the glomerulus and enter the tubule. 5:55 Their function is to limit the reabsorption of water in the tubule by 5:59 increasing the 6:00 osmolality in the redo tubule. 6:05 Their overall function is that they increase the excretion of sodium, potassium 6:10 , calcium, 6:11 magnesium, chloride, bicarbonate, and hydrogen, phosphate, and water. 6:20 So the absorption and elimination of these osmotic diuretics, well for the 6:25 absorption 6:25 manatol and urea are given intravenously, glycerin and isosorbide are 6:31 administered orally. 6:36 And so you'd expect if they are given IV, that's a quick response. 6:41 Elimination, they have a short duration of activity, and are quickly metabol 6:45 ized, and 6:46 they are eliminated or excreted through the uroic. 6:54 The next type of diuretics we will look at are the loop diuretics, and as a 6:58 name might 6:59 suggest, it works at the loop of handling, particularly it works at the thick 7:04 ascending 7:05 limb of the loop of Henle. 7:08 These are the drugs such as ferusimide and bumetenide. 7:11 Easy way is mide and nide. 7:14 Loop diuretics works on the symptoma, on the thick ascending limb of the loop 7:19 of Henle, 7:20 and thus prevent the sodium reabsorption. 7:22 Let's have a closer look. 7:24 Here we have the blood and the tubule lumen. 7:28 The tubule lumen is inside the nephron. 7:31 Here we have the transporter, which is within the tubule, within the tubular of 7:38 the lumen. 7:39 So this transporter typically transports sodium to chloride ions and potassium 7:47 through. 7:48 Loop diuretics prevents this chloride, or inhibits this chloride from being re 7:54 absorbed, 7:55 and thus will screw up the transporter and not cause the other ions to be re 8:02 absorbed. 8:04 In the long term, loop diuretics will also prevent the reabsorption of calcium 8:10 and magnesium 8:11 ions. 8:15 So loop diuretics prevents essentially the reabsorption of sodium, which 8:20 therefore prevents 8:22 the reabsorption of water, which therefore will decrease blood pressure. 8:27 Some information. 8:29 So loop diuretics will essentially increase the urine flow because it will 8:34 prevent the 8:35 reabsorption of all these things. 8:37 It increases sodium, chloride, potassium, water, calcium, magnesium excretion 8:45 in the nephron. 8:48 And because it increases the excretion of the substances, it will therefore 8:52 decrease the 8:53 plasma volume, right? 8:55 And thus, loop diuretics can actually induce renin release due to the plasma 9:02 volume depletion. 9:04 And renin, as you know, will want to increase blood pressure. 9:09 For the absorption and elimination of loop diuretics, about 60 to 90% is 9:14 absorbed when 9:15 given orally, and the elimination is that it's secreted via the proximal tubule 9:26 . 9:26 So let's look at now the third diuretic, which is the thiazide diuretics. 9:32 And these work on the distal, convoluted tubules, particularly the transporter 9:37 here, the symptom 9:38 of sodium and chloride. 9:42 Thyroid diuretics include names such as hydrochlorothiazide and chlorothiazide. 9:48 It's very easy to remember this because they're all in thiazide. 9:53 So let's look at how it works. 9:56 So here we have the cell, here we have the blood on the outside and the tubule 10:01 lumen 10:01 within the inside. 10:03 Thiazide essentially prevents sodium reabsorption by inhibiting this 10:07 transporter of sodium and 10:09 chloride. 10:12 In the long term, it will actually inhibit the secretion of calcium from the 10:17 blood to the 10:18 lumen, but it will promote the secretion of magnesium. 10:25 So thiazide diuretics, of course, increases the sodium excretion up to 5% of 10:30 the filtered 10:31 load, 5% because this transporter only roughly reabsorbs 5%. 10:37 Thiazide diuretics increases excretion essentially of sodium, chloride, 10:45 potassium and water. 10:48 In the long term, it will decrease the secretion of calcium but increase the 10:53 secretion of magnesium. 10:57 Very interestingly enough, thiazide diuretics increases the reabsorption, not 11:02 the excretion, 11:04 but the reabsorption of urea in the proximal cond related tubules. 11:09 If we increase the reabsorption of urea, this will increase plasma uric acid 11:15 levels. 11:16 And then if we have increased plasma uric acid levels, this might lead to gout, 11:21 gouty 11:21 arthritis, where it will accumulate within the joints and cause pain, etc. 11:28 The fourth major type of diuretics are the potassium sparing diuretics. 11:33 And there are two classes of these, you can say, and these work in the distal- 11:38 convolated 11:39 tubules, the very end of it, and as well as the collecting ducts. 11:45 Their major goal is to decrease the reabsorption of sodium but also prevent the 11:53 excretion of 11:54 potassium, hence the name potassium sparing diuretics. 11:59 Because if you haven't realized the other diuretics we looked at, the other 12:03 three, they 12:04 cause an increase in excretion of potassium. 12:11 And that is why potassium sparing diuretics is used in conjunction with other 12:16 diuretics, 12:17 to prevent the excretion of potassium. 12:20 Because sometimes potassium is very important in the body, actually potassium 12:24 is important 12:25 in the body. 12:28 So remember, there are two types of potassium sparing diuretics, let's look at 12:32 the first 12:33 one. 12:34 These are the one, these are things such as amyloride and triamitrine. 12:40 And they work on the principal cells of the collecting ducts and the late dist 12:44 al-convolated 12:44 tubules. 12:46 Normally, let's look at what happens normally, normally sodium is reabsorbed 12:51 from the lumen 12:52 of the nephron and then sodium will then be reabsorbed into the blood through a 12:59 transporter. 13:00 This transporter, when it reabsorbs sodium, it excretes potassium. 13:06 Potassium is then excreted into the tubular lumen. 13:11 The potassium sparing diuretics amyloride and triamitrine essentially inhibits 13:16 this sodium 13:17 reabsorption and thus inhibits sodium reabsorption and as well as inhibit 13:24 potassium excretion. 13:26 The other type of potassium sparing diuretics essentially are aldosterone 13:32 inhibitors such 13:33 as spironolactone. 13:36 And these work on the transporter within the collecting ducts. 13:40 They work on the intercolated cells where this transporter is located. 13:46 So what happens is, normally again, here we have the tubular lumen intercolated 13:52 cells 13:52 and the blood. 13:55 Within the blood, we have the hormone aldosterone which is secreted by the 14:00 adrenal glands, the 14:01 cortex of the adrenal glands. 14:05 Within the intercolated cells, we have the aldosterone receptor. 14:08 Aldosterone is a steroid so thus it will bind to the receptor within inside the 14:14 cell. 14:14 The receptor will bring the aldosterone into the nucleus where it will cause 14:20 the DNA to 14:21 make mRNA for potassium and sodium pumps. 14:27 So here we have a sodium and potassium pump. 14:30 This will go onto the surface of the cell next to the blood and will cause the 14:36 reabsorption 14:37 of sodium as well as the excretion of potassium. 14:44 What aldosterone inhibitors do such as spironolactone is that they inhibit this 14:52 binding of aldosterone 14:54 with the aldosterone receptor or inhibits just the formation and thus inhibit 14:59 the production 15:00 of the sodium-potassium pump thus prevent the excretion of potassium as well as 15:07 the 15:07 reabsorption of sodium. 15:10 So overall, these potassium-sparing diuretics, they increase the excretion of 15:15 sodium chloride 15:16 and water and therefore decrease blood pressure. 15:21 The absorption of potassium-sparing diuretics, well the absorption for spironol 15:27 actone is 15:27 that they are metabolized by the liver and they are actually highly protein 15:31 bound, meaning 15:32 that they travel within the blood by binding onto a protein, some kind of 15:37 protein. 15:38 The absorption is that they are secreted via the proximal condylated tubules. 15:44 Finally, there's another type of diuretic which is essentially the weakest di 15:50 uretic 15:50 and these are the carbonic anhydrase inhibitors and they work at the proximal 15:55 condylated tubules 15:56 and they prevent the reabsorption of sodium bicarbonate. 16:01 As I mentioned, they are the weakest diuretics and they are used to treat gly 16:05 cola for example. 16:07 How they work is that they essentially prevent the reabsorption of sodium bic 16:11 arbonate, which 16:12 means that it will cause less sodium to be reabsorbed and therefore decrease 16:17 blood pressure. 16:20 So I hope you enjoyed this video on diuretics. 16:23 We learned that diuretics essentially work to decrease blood pressure and 16:26 therefore they 16:26 can be used in cardiovascular, to treat cardiovascular diseases where we see 16:32 most often an increase 16:34 in blood pressure. 16:36 Thank you for watching. 16:37 Bye.
