Thiazide Diuretics | Mechanism of Action, Indications, Adverse Reactions, Contraindications

I ninja nerds in this video we are gonna talk about thiazide and thighs I'd like the Redax so let's going to get started alright so now what we got to do before we start talking about all the indications and mechanism of action side effects of thighs that heretics we got to go over the basic physiology within the nephron but we're focusing on here we're really zooming in on the cellular level at a particular part of the nephron and that's where these drugs primarily work what is that part well the main part that I want you to remember here is that these drugs act on the distal convoluted tubule well where is that so let's imagine here I have my Bowman's capsule proximal convoluted tubule thin descending limb of the loop of Henle then I got my hairpin turn I move up and I have my ascending limb and the ascending limb II know it has two portions right you have a thin portion and then you got that thick portion then after that it makes that turn around the cortex at the distal convoluted tubule and then it turns around again and works its way back down into the collecting duct we're focusing primarily on this portion we're zooming in on that area now one thing I want you to remember is is when we're talking about the eyes eyes eyes eyes I like redick's we're talking about their pertinents when it comes to high blood pressure right because they're commonly used in high blood pressure they have other indications we'll talk about but the way that they help with blood pressure is by controlling sodium chloride so what you need to remember here is that in the distal convoluted tubule around five to maybe ten percent of the sodium chloride is actually resorbed in that segment so if we can inhibit sodium chloride reabsorption what follow sodium chloride water so let's talk about how if we decrease sodium chloride absorption we decrease water reabsorption and therefore drop blood volume and blood pressure so let's look and zoom in on one of these distal convoluted tubules cells we have two of them here this is going to be where we talk about normal physiology and here we'll talk about how the drug works and its mechanism of action first thing you need to know on this apical surface right so we're zooming in if we were to kind of imagine where we are in this point we're zooming in and we're looking at the cells at this point okay so right here we're looking at their luminal surface on this end here this is their basal lateral surface that's this portion and that's where the two pair tubular capillaries are gonna be present okay now first thing is imagine that the two Buhl is carrying with it filtrate and one of the main components of the filtrate in this area is sodium chloride there's a special transporter here and we're gonna call this in si si sodium chloride cotransporter okay what this does is is it move sodium and it moves chloride from the tubular lumen into the tubular cell so we're basically taking imagine here these little dots that sodium chloride or moving it from in the tubular lumen and into the cell okay now once they get into the cell here we're gonna have sodium here we're gonna have chloride again the main one I want us to focus on here is sodium now we have to get sodium into the blood because that's the whole goal here of this normal physiological process so how do we do that well what happens is sodium has two ways that it can get out of the cell one of the ways is there's a very special transporter here called a sodium potassium ATPase and it's a very prominent pump that's not on every cell in our body and it pumps out three sodium ions and pumps into the cell two potassium ions so that's how we get the sodium out into the blood that's one way the other way is that sodium also can get back into the cell all right you know how you know one of the big things here we get sodium out via the sodium potassium ATPase but then what happens is sodium will move from this exercise fluid some of it will move back into the cell when it moves back into the cell it actually allows for something to move out of the cell and what is that thing that thing that moves out of the cell as sodium moves into the cell is calcium now when calcium moves out here into the blood now the concentration of calcium when it moves from the cell and into the blood what happens to the concentration of calcium in this cell well the calcium concentration is going to decrease as a result there's a small amount of calcium that's remaining in the distal convoluted tubule and usually in order for it to get reabsorbed it's dependent upon a particular hormone called para thyroid hormone okay we're not gonna focus on all that right now I just want you to understand this basic concept now calcium concentrations might be a little bit higher out here now if the calcium concentration in the cell is low because we're pushing calcium out by bringing sodium in what does that do well that creates a concentration gradient where calcium is gonna want to move from the tubular lumen and into the cell and then from in the cell where does it go again utilized by that sodium calcium exchanger we pump sodium into the cell and pump calcium out of the cell and into the path through the capillary blood what's the result of all this well one is I can put calcium in the bloodstream more calcium in the bloodstream the other thing is I can increase my sodium concentration and the blood stream one thing you want to remember whenever you have a lot of salt concentration high salt concentration in the blood that creates an osmotic gradient and that osmotic gradient is gonna want to pull water which is also going to be in this tube the lumen it's gonna want to drag water via through the aquaporins it's gonna want to drag that water into the blood okay and as a result will bring decent amounts of water into the bloodstream so normal physiology is we're going to try to retain sodium and chloride thereby pulling water with us and we can also help to regulate the calcium levels in the blood well via that sodium calcium exchanger now what if I as I dare addicts do what I want you to remember is they do not like that sodium chloride co-transporter they're not a big fan of that sodium chloride cotransporter so what they're gonna do is they're going to inhibit him okay what does that do then well let's follow along remember what was responsible what this protein was responsible for doing what was responsible for moving sodium into the actual tubular cell and moving chloride into the tubular self from the tubular lumen but if you inhibit this that means that there's going to be less sodium being brought into the cell less chloride being brought into the cell now remember how to sodium get out of the cell remember sodium it gets out of the cell via this sodium potassium ATPase and remember what it does is it pumps three sodium ions out right but because there's less sodium coming into the cell via this sodium chloride cotransporter less sodium is coming in that means that less sodium is going to be pumped into the peritubular capillary blood via this sodium potassium ATPase it's simple logic there right less sodium in the cell less for us to pump out there's less sodium then that's one big goal remember we said that was one of the goals of thiazide and thighs that like heretics and again if you really want to remember chloride has its own special channel that it can actually also get out here as well and so we decrease chloride concentration remember what did I tell you happens though and if you if you really want we can also remember here that whenever you pump three sodium out you also pump two potassium in but again you're pumping less potassium into the cell because there's less activity of the sodium potassium ATPase so again decrease sodium potassium ATPase activity decrease sodium entry across via the sodium chloride cotransporter less sodium chloride in the blood now because there's less sodium okay now remember what happens here less sodium is in the cell right there's decreased concentration of sodium in the cell because you're not bringing sodium from the tubular loo into the tubular cell what does that do them now because this creates a concentration gradient now I know that I said there's low amounts of sodium in the blood but if you're comparing the sodium and the blood to the sodium in the tubular cell it's much higher in concentration so I'm just for a second I'm gonna flip this arrow and then the only reason I want you guys to remember this is because sodium concentration in the blood is much higher than the sodium concentration in the cell now because of that where's the sodium going to want to go from in from outside the cell inside the cell and it's gonna want to go a lot more than usual it's gonna flood in now every time these sodium molecules rush into the cell what has to rush out of the cell calcium so now because of that calcium is also going to have to rush out of a cell and into the blood so what does that mean that means I'm gonna have an increased calcium concentration in the blood now if I pull tons and tons and tons of calcium from inside of the cell into the blood what happens to the calcium concentration inside the cell then well it's going to drop a little bit because I'm pushing a lot of it out into the blood so what's that gonna do now now the calcium that's out here in the tubular lumen it's gonna get driven in to the cell and get utilized to get pumped where out of the cells of a pitcher for the capillaries if we go back to what we said here before there's less sodium less chloride that means there's less salt less of an osmotic gradient to drive water movement that means that if we think about the movement of water from the tubular lumen and into the blood what's gonna happen there's gonna be less movement of water now what does that overall tell you the overall purpose here we're going to decrease sodium and chloride movement into the blood right as a result that's going to decrease water movement if I decrease the sodium chloride and water movement what's that going to do to the overall blood volume it's got to decrease my blood volume okay and that can play a role within blood pressure and in fluid overload States the other thing I want you to remember is what else do we say that the highs a diuretic do they pull calcium into the bloodstream and so they can also increase the calcium reabsorption and if we increase calcium reabsorption there's a benefit of that especially in patients who may be arras t.o.p mnek osteoporotic or patients who have already have a high amount of calcium in their kidneys and their kidney tubules what kind of people have lots of calcium in their kidney tubules and it can crystallize and precipitate make nasty little stones people who are more prone to calcium oxalate calcium phosphate kidney stones so that's where we can see the significance of these drugs okay now that we understand the overall mechanism of action let's talk about the two different types of drugs again what do we say that there were there were thiazide diuretics so again one are gonna be the thiazide diuretics and the others are going to be the thiazide like diuretics I want you to remember particularly to thighs I diabetics in 2000 lee utilized one of the thiazide diuretics that are commonly utilized you hear a lot is called hydro chloro thiazide sometimes abbreviated h ctz the other type is going to be chloro thiazide now the other drugs that I want you guys to remember here or going to be the thighs I'd like to retic so remember these all have pretty much the same mechanism of action they inhibit the sodium chloride cotransporter the thiazide diuretic like directs are a little bit also interesting because some of them have been shown to be a little bit more effective one of them is called klore valadon so chlorothalonil ii utilized is called Mottola zone and if you guys remember from the congestive heart failure video we talked about how this can be utilized in patients with congestive heart failure whenever you're utilizing like a loop redick and he's just a little bit of extra sodium and water pull you can utilize this drug so again what I want you to remember is there's thiazide diuretics thiazide like the Redax both have the same mechanism of action hydrochlorothiazide clora is either part you're thiazide diuretics and the thiazide like diuretics or clora thousand and Mottola zone one other thing that I'm going to mention here is that the thighs I'd like diuretics have sulfa component to them okay so technically what you need to remember is that these technically have a sulfa component in their structure so why is that significant in patients who maybe have sulfa allergies you might not want to be giving these patients that kind of drug and we'll talk about why because it might lead to a particular type of reaction called an acute interstitial nephritis last thing I want to mention here with these thighs thighs iodized I like their etics is there's also been one other mechanism of action that's been proposed with these but again they don't know the complete underlying physiology of it but what they know is that thighs on thighs I'd like Doretta --xe have the ability to promote vasodilation and if you cause vasodilation what does that do well that decreases the total peripheral resistance and if you decrease total peripheral resistance you decrease the blood pressure so this is another mechanism that they've seen associated with thighs I and thighs I'd like their attics they don't really know what's the thing responsible how do those eyes cause vasodilation they think it may be regularly responsible from prostaglandins through some way shape or form there's these prostaglandins and that thye azides by some way help to stimulate the prostaglandin production and that prostaglandins help to promote this vasodilation mechanism so now if we understand then that thighs and thighs I'd like their attics basically inhibit sodium and chloride reabsorption via the sodium chloride cotransporter less sodium chloride in the blood less water is going to be driven into the blood therefore there's a decreased blood volume that decreased blood volume can decrease blood pressure so we can see how this would be very helpful in patients with hypertension very very beneficial drug and hypertension here's another thing that I want you to remember so again go back to the whole concept here with these drugs you decrease sodium and you decrease chloride reabsorption that decreases the water reabsorption that decreases their blood volume and by decreasing blood volume you decrease blood pressure so that's how that would be helpful in this sense what about in other situations where they have a high blood volume right so someone has a large blood volume and you want to prevent that excessive continual fluid overload well what about in situations where someone has fluid overload maybe within their peripheral extremities maybe in their legs so someone has peripheral edema okay so they have peripheral edema what could that be due to there's multiple causes of peripheral edema it could be due to CHF could be due to cirrhosis it could be due to an acute kidney injury right or nephrotic syndrome something of that nature where they're basically accumulating fluid within the peripheral tissue spaces in the legs or another thing that can happen is besides having peripheral edema they can have pulmonary edema and this pulmonary edema again what could be the cause of it could be CHF it could be cirrhosis it could be acute kidney injury or some type of nephrotic syndrome and again what's happening is a lot of fluid is accumulating where well the fluid is accumulating particularly within the interstitial spaces and as that fluid starts to accumulate it makes it very difficult to breathe same thing as we start to accumulate lots of fluid in the legs that can lead to increased pressure pain swelling right what's another thing where there is someone it can be fluid overloaded another situation where someone could be fluid overloaded is maybe ascites and what could be the cause of ascites well again it could obviously be cirrhosis which is causing you know a backup a fluid through the portal circulation it might even be related to CHF we don't but there could be tons of different causes of why someone could have ascites but the whole point is with all of these the patient is fluid-overloaded well what can we do well if we give them a thighs outer thighs I'd like to retic these aren't the best with these but they can be utilized you're gonna decrease sodium and you're gonna decrease chloride reabsorption you're gonna decrease water pull into the blood which is gonna decrease blood volume wouldn't that be helpful and as someone who's already fluid overloaded and you don't want to continue to increase their blood volume this would be a situation where we could give these drugs are they the absolute best no he'd be more likely to use something like a loop diuretic but they can be utilized either alone or remember what I told you in combination with a loop diuretic so we could take a thighs I diuretic like Mottola zone the thighs I'd like there etic combined it with a loop diuretic and pull off some of the excess fluid and someone who has peripheral edema pulmonary edema or ascites due to an underlying etiology like CHF cirrhosis or Aki see that's what we understand about this drug okay now we understand it can be utilizing hypertension we know that it could be utilized either either mono therapy but more commonly dual therapy with a loop diuretic so it's important to remember that whenever we're talking about this situation of Dimity States pulmonary edema peripheral edema or ascites we could utilize these drugs either as mono therapy not as common but more commonly as dual therapy with and utilization of a loop diuretic like furosemide okay now that we understand that let's talk about the other indications for the stroke this next one's actually really interesting and someone who has what's called nephrogenic diabetes insipidus okay so diabetes insipidus is basically when someone doesn't make right of antidiuretic hormone okay so you know you're basically you have your hypothalamus and it has these neurons called super optic nucleus and it has the paraventricular nucleus which extend down into the poster pituitary and they release a hormone called ADH on diabetes insipidus nephrogenic diabetes insipidus the ADH production here's the key thing is normal okay so ADH what does it do it circulates through the blood and it comes to the area of the collecting duct you know in the collecting duct you have specific receptors here and these are called v2 receptors vasopressin that's another name for ADH what it does is it binds on to these v2 receptors and then it signals basically the end result here is it signals the production of aquaporins and it puts these little pores into the cell membrane here and as I put these little pores into the cell membrane the whole goal of this is that we're going to pull water from the tubular lumen into the tubular cell and as a result pull that water into the blood okay so then from here we know that this is going to go into the bloodstream okay but here's the problem and nephrogenic diabetes insipidus the v2 receptor doesn't function properly and so the ADH production is normal but the v2 respess scepter which responds to the ADH isn't functioning properly so the overall result is going to be the same there's not going to be the activation of the aquaporins if there's not aquaporins being pulled in what's going to happen that means less water and that little decrease in water in the blood is a problem here right because now what's gonna happen is you're gonna actually lose a lot of water into the urine tons of water into the urine now here's something you guys are probably trying to think about why in the world what I give someone a thiazide diuretic if they're already losing water because the aquaporin units aren't being you know basically synthesized properly and expressed on the cell membrane here's why I assign thighs I'd like tower etics produced what's called a mild hypovolemia right so in other words they decrease here's what I want you to remember what do we say happens there's a decrease in sodium and there's a decrease in the chloride reabsorption if there's a decrease in the sodium reabsorption decrease in the chloride reabsorption that's going to decrease the water reabsorption if you decrease the water reabsorption that's going to decrease the blood volume now here's what's really interesting if you decrease the blood volume you decrease the blood flow through the glomerulus a decreased blood flow through the glomerulus leads to a decreased glomerular filtration rate what that means is is now the proximal convoluted tubule has more time to reabsorb sodium chloride and thereby water okay so if you remember what we just talked about you decrease blood volume that means that there's less blood flowing through the glomerular capillaries that means that less blood is being filtered off into this Bowman's capsule and less of this actual filtrate is moving into the proximal convoluted tubule what that means is that's more time in the proximal convoluted tubule that we can reabsorb sodium reabsorb chloride and thereby water because in patients with diabetes insipidus what are they doing they're losing tons of water it may be even a little bit of salt if we give them a thigh outer thigh as I'd like to heretics you induce a mild hypovolemia which then triggers the proximal convoluted tubule ourselves to increase their reabsorption of sodium chloride water so now there's less sodium less chloride and less water getting down to the level of the collecting duct and so on I'll lose less water in the urine so that's trying to help me in the overall end so that's what's we're really cool about this drug in this situation here the next thing I want you to remember here and it's indications remember what I told you that in this area of the distal convoluted tubules what else did it do remember it help to transport calcium into the blood right there was an increase in the calcium movement into the blood if there's an increase in calcium movement into the blood why is that important well think about this what about in a situation where someone has high amounts of calcium in their urine what does that predispose them to especially if they have phosphates and oxalates that they can also combine with it increases the risk of renal stones so this would be helpful in somebody who actually forms kidney stones due to hyper Calci area there can be many different reasons for this we're not gonna go into detail on that but in someone who is predisposed because they've hypercalcemia you give them a thigh as I thighs I'd like their attic you're gonna pull some of that excess calcium out of the kidney tube was and prevent the formation of kidney stones what if I'm the person who's also osteo penis hole to increase the calcium reabsorption and if you increase calcium reabsorption you therefore help to do what stimulate calcitonin production and that calcitonin production is an increased osteoblastic activity and lead to bone deposition which is important at a person who already has very weak bones okay so indications that I want you to remember with this drug hypertension big one it can be utilized mono therapy less common and fluid-overloaded States more common dual therapy if necessary in utilization with a loop diuretic in situations like peripheral edema pulmonary edema or sides-- secondary to CHF cirrhosis or Aki or nephrotic syndrome it can also be used in nephrogenic diabetes insipidus which is in a situation where they have normal but abnormal v2 receptors so they don't reabsorb water and lose a lot of water into the urine if you give them thighs IDEs it helps to basically through a mechanism of causing mild hypovolemia increased reabsorption and chloride and water in the proximal convoluted tubule which helps to lead to less water loss and the last thing is it also increases calcium in the blood stream so it helps in patients who have increased risk of hyper calcia which can cause kidney stones as well as maybe those who are osteopenic who have very brittle weak bones okay it may be even osteo parodic individuals alright so now that we understand the mechanism of action the different drugs okay as well as the indications of thiazide and thigh as I'd like diuretics let's talk about some of the potential side effects and a DRS because these commonly come up and your boards okay so one of the big things that you want to remember is you know in the proximal convoluted tubules you have these specific types of transporters and they're called organic acid or an ion transporters so organic acid or an ion transporters and what they do is you have this molecule waste product called uric acid and uric acid is designed to be excreted via these transporters so in order for me to push uric acid from the blood into the tubular cell I need this organic I enter anti transporter then from here there's another transporter that's pushes this from the tubular cell and into the tubular lumen and then now there's uric acid that I push out here should then go and become excreted in the urine whenever you give drugs like thighs outer thighs I'd like to Redax what they do is through some mechanism they inhibit the organic and ion transporters so if you inhibit the transporter that pushes uric acid into the cell and thereby uric acid into the tubular lumen this can't get into the cell what happens to the uric acid level in the blood Rison so now the uric acid level and the blood is going to rise what do you call that whenever the uric acid level in the blood rises this is called hyper Yura C Mia what is the issue with hyperuricemia what kind of patients will we be very concerned about these sodium like these urate crystals getting deposited into particular joints like the metatarsal phalangeal joint in the big toe this could lead to it depositing into the joints and leading to gout because again these uric acid leads to monosodium urate crystals and they deposit into particular joints and one of the most common joints is the MTP the first MTP and it can lead to very exquisite pain and tenderness so that's one thing that we have to worry about that's a potential side effect the other side effect here is again remember we have again the sodium chloride okay code transporters and there again what did they do we'll remember that these thiazide and thiazide liked diuretics inhibit these and thereby this leads to less sodium being reabsorbed and less chloride being reabsorbed okay so now because of that because less sodium and less chloride are being reabsorbed that leads to more chloride and more sodium being retained in the kidney tubules as more sodium is retained in the kidney tubules you pee this out right so now what's gonna end up in the urine one of the things is gonna end up at the urine is more sodium than usual what does it call whenever you have low sodium now now there's less sodium that's being transported into the blood what's that call when there's less sodium in the blood less sodium in the blood is called hypo net remya okay so that's another potential complication of this another potential side effect the other thing is again you're gonna lose chloride in the urine so now you're gonna have lots of chloride that shows up in the urine and what's it called whenever you have low chloride in the blood so now less chloride is gonna get transported into the blood and this will lead to hypo chlorine eeeh now we're gonna talk about why that's significant in just a second the other thing I want you to remember is what else happened here remember that we had the sodium and we had the chloride and they move in via the sodium chloride cotransporter sodium moves out via the sodium potassium ATPase and then in order for the sodium to get back into the cell it allows for an exchange from sodium moving into the cell and calcium going out of the cell and ëthe of the blood this creates an osmotic gradient alright I'm sorry a concentration gradient that pulls calcium from the tubular lumen into the tubular cell and then that calcium again is going to get pulled via the sodium calcium exchanger into the blood what's that result in if there's increased calcium in the blood hyper Cassie Mia okay so we have hypercalcemia hypo chlorine a hyponatremia and hyperuricemia as potential side effects and again the overall concept here is that you're gonna get less calcium that's gonna get shown up in the urine now here's what it gets really interesting now if there's more sodium right because less sodium is hitting reabsorbed more sodium moving from the distal convoluted tubules into the collecting duct so now we're at the collecting duct more sodium is moving down through the collecting duct in previous alright what happens is this creates a concentration gradient where sodium is going to be in lower concentration inside of this tubular cell on the collecting duct and in higher concentration than usual in the tubular lumen and what happens is sodium is going to want to move a little bit of the sodium is going to want to move into this actual tubular cell and then from here again you have the sodium potassium ATPase as that pumps the sodium out and then we'll go into the blood here's the point that's really interesting if positive ions are moving into the cell because sodium is moving into the cell and positive ions are leaving the tubular lumen what happens to the charge inside of the tube of the lumen as you lose sodium it becomes negative as it becomes negative it attracts specific types of cations that are present inside the cell like potassium and protons and this potassium will leak out of the cell these protons will leak out of the cell more than usual and what's gonna happen now I'm gonna lose potassium more potassium than usual in the urine and I'm gonna lose more protons in the urine so as a result if someone has less potassium in the blood what is that called that's called hypo Kaleem iya and the other thing is if there's less protons because I'm excreting protons if there's less protons in the blood that can lead to alkalosis and this isn't related to the respiratory system this is related to your metabolic system so this is a metabolic alkalosis so do you see how there's some potential side effects from these drugs right so there's a potential of metabolic alkalosis there's the potential of hypokalemia hypokalemia hyponatremia hyperuricemia all right so this is actually really cool it took me a little bit to kind of figure out how sites can cause hyperglycemia because you want to understand why these things happen well here's one of the big things if there's less potassium in the blood we can kind of say that what's gonna happen is more potassium is gonna leave these cells to try to compensate for that so overall then what's gonna happen is the potassium concentration inside of the cell is gonna be lower than usual okay now here we have a specific cell and we're gonna focus on what's called the pancreatic beta cell now the pancreatic beta cell has specific types of blood train Porter's and what they do is they bring glucose from outside the cell and they bring it into the cell and then you guys know that what happens is glucose eventually through multiple mechanisms will lead to the synthesis of ATP ATP is very interesting because what happens is it has a very specific type of binding site on this ATP sensitive potassium channel and when ATP binds on to this channel it closes the potassium channel and so now potassium can't leak out okay but what happens is there's already less potassium inside of the cell so because there's less potassium than usual inside of the cell what happens as there's you know usually what happens is you have lots of positive ions that build up in the cell as this channel closes the potassium ions can't exit they accumulate inside of the cell and they cause a slight positive charge but there's less potassium in the cell so that's less of a positive charge that means less activation of these voltage-gated calcium channels so that what that means is less calcium is going to enter into the cell if there's less calcium why is that important because you know calcium is responsible for stimulating these vesicles which contain insulin and insulin wins when calcium rushes into the cell it causes this vesicle to fuse with the cell membrane and release insulin into the bloodstream but again we have low potassium inside of the cell normally the ATP binds to the ATP sensitive potassium channel and normally potassium can't leave the cell so it builds up inside the cell causes a positive charge enough to activate the calcium channels they open calcium rushes in and stimulates insulin release but because we have lower than normal potassium storage because of the thiazide thighs I like to etics there's less of a positive charge inside the cell and there's less activation of the voltage-gated calcium channels less calcium rushes into the cell and less insulin is released why is that important because if you remember here we'll have a cell and here we're gonna have an insulin receptor and what does insulin do insulin binds on to an insulin receptor and basically triggers the activation of transporters that will move glucose from outside the cell inside the cell okay and effectively the whole whole purpose of moving glucose into the cell is to decrease blood glucose levels well if you have less insulin being produced that means less glucose movement into the cell and that means that less blue blood glucose is getting cleared and put into the cell that means the blood glucose levels are going to rise and this can lead to hyper glycemia so this is how that actually happens it's actually pretty darn cool the last thing that I want to talk about here is again remember I brought up a point with that some of these drugs particularly the thighs I'd like diuretics they have a sulfur group and remember that sulfur group what it can do is it can if someone has a salt allergy or in general sulfa drugs can lead to a particular type of reaction and this reaction is called acute interstitial nephritis and with the cute interstitial nephritis what happens is a classic triad of symptoms that people can develop because of a reaction to this sulfa drug because again this is particularly from the thiazide like drugs that have that sulfur group this can create an acute interstitial nephritis via sulfa drug reaction and what can happen is this can lead to a triad of symptoms one is it can lead to arthralgias the other is it can lead to a rash the other classic symptom is acute kidney injury particularly in TRO renal if we really want to be specific intro a renal a ki another thing is if you actually check the blood stream one of the things that happens as a result of this actual drug and the sulfa drug reaction is if you check a CBC they also commonly have elevated eosinophils okay so this is another potential type of side effect or adverse drug reaction that can happen particularly to the thighs I'd like drugs because that's all family that they contain I engineers so in this video we talk about thighs I'd and thighs I'd like that Redax we discussed their mechanism of action the different types of drugs we talked about the indications that that can be commonly utilized for and we also talked about side effects and adverse drug reactions with these particular drugs I hope it all made sense I really hope that you guys did enjoy it if you guys did please hit that like button comment down the comments section and please subscribe as always an engineer until next time [Music]

Channel: Ninja Nerd Lectures

Views: 34,793

Rating: 4.9507523 out of 5

Keywords: hypertension treatment, HTN treatment, HTN, high blood pressure, hypertension, antihypertensives, diuretics, thiazide diuretics, thiazide, thiazide like diuretics, hydrochlorothiazide, HCTZ, chlorothiazide, Ninja Nerds, blood pressure, pharmacology, heart failure, hypertension pharmacology, Medical channel, metolazone, chlorthalidone, treatment of hypertension, treatment of high blood pressure, Ninja Nerd Science, Medicine, Ninja Nerd Medicine, lecture Ninja Nerd Science, medical channel

Id: chJK_EOnaDY

Length: 41min 15sec (2475 seconds)

Published: Fri Apr 17 2020