0:00:02.1 Professor Walden: Alright, so we are live. So we’re gonna give it a few minutes and we’re gonna allow folks to kind of drop-in, pop in. This is exciting, I know several of you were waiting for this, and that you were excited to hear from the pharmacist themselves about these blood pressure medications. So hopefully, this gives you a little bit of clarity. But again, just kinda giving it full minute to load and drop in, so we’ll do that and while we’re kind of sitting here waiting and do that, hopefully everyone is doing well on this summer hot day, so let me get set as well. So, you guys will be just fine. Alright, cool. So it looks like everyone is kind of popping in, and we are going to get started, so fantastic. So, again, I’m excited. Hey guys, it’s Professor Walden, we’re here, and we are going to get started ’cause as always super respectful of your time and we’re gonna kinda try to keep it through this hour for you. So we have our pharmacist in the hot seat today, so she is with us today, and she is excited. I’m excited for the information and the material that she’s going to present, so hopefully, she will give you some clarity on things.
0:01:19.8 Professor Walden: And of course, if you guys have questions, please let us know and we will either get back to you and answer them or we will have Kendolyn back and hopefully, she can answer those questions for you. So let’s start off with a bio as always, as I like to do. So Dr. Kendolyn Smith is a consultant pharmacist, advocating for medication safety, medication compliance, Public Health literacy and overall medication management services, as well as she is faculty. She is an Associate Professor of Clayton State University, the healthcare management programme, and has served as adjunct faculty for Mercer University School of Medicine’s Master of Public Health programme. So, Dr. Kendolyn Smith completed her Doctor of Pharmacy degree at Creighton University. Hopefully, I’m saying that right… [chuckle] The correct Medical Centre School of Pharmacy and Allied Health Professions. A Master of Public Health and Health Policy and Management at Emory University’s Rollins School of Public Health, and she’s also an undergraduate alumnus of the University of Georgia.
0:02:23.7 Professor Walden: Her career has included leadership within a top tier pharmaceutical company, AstraZeneca, many of you know that one, focused on cardiovascular, gastrointestinal, and hypertensive medication. In addition to industry expertise, she has worked as a pharmacist in the local community, geriatric and academic settings. So, she’s got multiple publications, which we’re not gonna go into now, so she is well published and she has a depth of knowledge that we are excited that she’s gonna bring to the table. During COVID-19, this pandemic, she has been essential in immunising pharmacists and many… Immunising the local communities within the State of Georgia. So we are excited to have her with us, so I’m gonna bring her on screen. Here we go. Alright, there we are. Hi, Dr. Smith.
0:03:15.0 Dr. Kendolyn Smith: Hi, everybody. How are you guys? Thank you so much. Thank you so much. I am excited to be here with you guys as well. Now, I can’t see anybody yet, so I wanna make sure that everybody can see and hear me fine.
0:03:31.7 Professor Walden: Yes. So we all hear you, I hear you. So as long as I hear you, they can hear you, so you’re good to go there.
0:03:38.3 Dr. Kendolyn Smith: Okay. Yes, oh, that’s perfect.
0:03:40.4 Professor Walden: So we have your PowerPoint up, so what I’m going to do right now, guys, I… Oop, I stopped my camera by accident. [laughter] What we’re gonna do is, we are going to share our PowerPoint. Here we go. So there’s that. So, without further ado, we are not gonna waste any time. Dr. Smith, I’m gonna hand it over to you and you can get started.
0:04:03.3 Dr. Kendolyn Smith: Alright, and so you’re gonna be my one person with my PowerPoint here, so we can go ahead to the next slide, and the first thing I want to do is say that there’s so much information about hypertension out there. And so, some of this stuff may be repetitive at the beginning, and there’s a lot more information that’s out here on blood pressure medications, and of course, an hour doesn’t do us all justice, so I’d be happy to come back at any time to dig a little bit deeper if we need to. But first, let’s just talk about hypertension in general. These are some of the basics. We know for sure that hypertension is called either high blood pressure, HTN or HT, HBP, but the most important thing that we as people who work in healthcare like to consider for the patients is that hypertension is really the silent killer. And by silent killer, we just mean that lots of times people really walk around with hypertension and they have no knowledge that they have it, or because they don’t feel sick or because they’re not feeling ill, they really don’t pay attention to it.
0:05:12.1 Dr. Kendolyn Smith: They don’t try to make any lifestyle modifications or anything until they start showing signs, signs or symptoms of something that has impacted them, where they need to either go to the doctor or the doctor’s office has recognised that there’s something going on. So, you all probably already know this without a doubt, that hypertension is really the force of blood that goes up against the walls of the artery. If it does that for too long and consistently, it gets too high, that pressure ends up causing problems. And it doesn’t just cause problems for one thing, it can cause problems for many things. And so, we’re gonna go to the next slide and look at some of the symptoms of hypertension. And so, we know that it is measured in systolic over diastolic pressure, so that’s not anything new, but some of the common things that patients will actually experience, the main thing we always hear about is I have a headache, I’m lightheaded and dizzy.
0:06:09.6 Dr. Kendolyn Smith: There are people who actually have nose bleeds from hypertension, they’re tired, they’re drowsy, they get confused. The blurry vision is another thing that we actually hear a lot about. Now, some of the more severe symptoms that people can attribute to other things outside of hypertension are like, chest pain and difficulty breathing, the irregular heartbeat, and then also, there can be blood in the urine, and that really is a signal of something being wrong, no matter when that happens. But the lightheadedness and the dizziness and the headaches are really those things that we look at or we hear from patients most often. So, we all know that… And we can move to the next one when we talk about hypertension, that there are so many medications. We’re gonna focus on the medications, but I don’t want to disregard in any way, even as a pharmacist, that there are many, many excellent non-pharmacological recommendations that are out there, but for today’s conversation, we’ll just focus on therapy, and that’s pharmacologic therapy.
0:07:16.3 Dr. Kendolyn Smith: Now, when we talk about hypertension, even if you talk to people in community, they really just say, well, it’s treated so much or they’ve given me all this medicine, or sometimes patients will have more than one medicine to treat hypertension, and they’re thinking, why do I have all of this to treat just one situation or one condition? Even patients who have other concomitant disorders like diabetes or cardiovascular disease, will say, “Well, why do I need to be on three medications for my blood pressure?” And of course, there are lots of ways that we can look at that. And let’s look at this schematic that I have on the next slide. When we look at this, there are so many hypertensive medications, because hypertension affects so many different places in our bodies, and it can have an outcome that actually produces any of these things.
0:08:11.4 Dr. Kendolyn Smith: So obviously on here, I have stroke, heart failure, renal dysfunction, kidney disease or kidney failure, heart attack and vision loss. So, hypertension really does impact all parts of the body. It is truly one of the disorders that is progressive if it’s not treated, and it’s definitely multifaceted. So, what do we do? Well, we in the community, and we as nurse practitioners, physicians, a pharmacist, those people who are working in healthcare, we look at different ways that we can try to resolve the patient’s issue as best we can. We learn as we grow, and so some medications are super old and they’re still being used and then others are super new and there’s some concern about using them.
0:09:00.1 Dr. Kendolyn Smith: So what we wanna do is look at some of the common medications, some of the common things, and we wanna look at where in the body these things happen. Now you will see this schematic again, what I’ve done here, and I love this schematic, because it touches on every place that an antihypertensive medication, the most common ones that we see, where they impact the patient. Just like we just mentioned on the previous slide, you see the kidney here, you see here are the beta blockers working here. You can see over here, the blood vessels, the ACE inhibitors, the angiotensin receptor blockers, so we’re gonna hit on those, because every single one of those are important to lowering a patient’s blood pressure, and also, hopefully salvaging those organs and that in organ damage that can be contributed to hypertension. Alright, so let’s look at some of the first line treatments for stage one hypertension.
0:09:57.3 Dr. Kendolyn Smith: Now, I listed them out right over here. And they’re small here, but we’re gonna talk about each one of these in just a moment. So, you’ve got your thiazide or thiazide like diuretics, which we can call water pills or diuretics. We got the calcium channel blockers, the angiotensin converting enzymes, those are our ACEs, and then our angiotensin receptor blockers. So, let’s start with our diuretics. So, everybody probably has heard of a diuretic, when the patients come, they’re gonna be saying my water pill, they’re gonna say the blue water pill to the pharmacist or the pink water pill. They’re gonna say, they put me on something, I don’t know what’s in it, but it makes me pee or it makes me go to the bathroom, that is most likely a diuretic. Now, thiazide diuretics are, for all practical purposes, utilised the most and they’re most common because first we wanna relieve some of the pressure, get some of that water off. And one of the things that we want to do is, I’m not sure if you can see this as clearly, but this shows you where right in here, the thiazides work here, on the distal convoluted tubule.
0:11:17.0 Dr. Kendolyn Smith: And right in there, you can see where it crosses the sodium layer. Thank you very much. This is where your thiazides are gonna work. Now, thiazide diuretics are not the only types of diuretics. So, when we look at our thiazides and we’re looking at how they work across the distal tubule, because they’re really inhibiting the sodium chloride’s importer in that tubule, and they’re gonna reduce the water reabsorption there, so that it eventually comes out of the body, and that’s why it’s causing the patient to go to bathroom. Now, they don’t… They are not the only ones that cause patient go to bathroom, all of them usually do. Now, there’s been a uptake in looking at thiazide and thiazide like diuretics. So, things like chlorthalidone, which you’ll hear about a little bit later in another patient type, but for diabetics and stroke patients, these particular diuretics do look like they do provide longer activity for the patient and they do reduce some of the cardiovascular events, that’s what some of the studies have recently shown.
0:12:28.9 Dr. Kendolyn Smith: And so, they typically will use chlorthalidone with those patients. However, you’ve got several different types of diuretics, you’ve got these thiazides, you’ve got the furosemides, which are your loop diuretics, and then you’ve got your spironolactone, which are your potassium sparing diuretics. So let’s go. We’re gonna take a look at some of the common ones. And these are the examples. Okay, so, here are some examples. I tried to highlight some of the main ones that you will see used. The bolded ones are the ones that we definitely know you will see without a doubt. Bumetanide, chlorthalidone, chlorothiazide, you got your furosemide, which is Lasix, which is oldest forever, but still so widely used. You’ve got your hydrochlorothiazide, that’s gonna be the main diuretic that’s gonna be used, your indapamide, metolazone, and torsemide. Now, the others you will see used depending on what setting you’re in, but these that are bolded are definitely some of the most widely used diuretics.
0:13:40.2 Dr. Kendolyn Smith: And because they are widely used, you wanna make sure that you understand that they are used as individual medications, but they’re also used, particularly hydrochlorothiazide as a combination agent. Hydrochlorothiazide is used in combination with lots of other medications, ACE inhibitors, ARBs, they’re utilised with lots of other drugs. So, when your patients are on one medication, meaning one diuretic, they’re gonna be on something like hydrochlorothiazide, something like furosemide or Lasix, they can go from Lasix 10 all the way up to Lasix 80. Lasix is a definite diuretic that is going to work in the loop of henle, okay? And it’s going to cause that patient to really, really use the bathroom. It’s almost like…
(Laughter)
0:14:47.6 Dr. Kendolyn Smith: And if a patient is on a Lasix, they’re definitely not gonna wanna be able to sit anywhere for a long period of time, ’cause they’re gonna have to go. But these are ones that you definitely will see and you definitely will see used.
0:15:00.4 Dr. Kendolyn Smith: And like I mentioned, diuretics, that’s their function, to get that urine, that volume off of the patient, reducing the sodium uptake, lower the blood pressure by lowering the volume, okay? Alright. So, I think that I’m gonna go to the next slide where we talk about some of the other side effects of a diuretic. Now, with a diuretic, remember I said that we have different types of them. So, even though this diuretic is working so well to go across the sodium chloride channel, it is also potentially capable of causing patients to have hypokalemia, which is low potassium. And that is important, because again, remember our original little schematic, where we talked about all of the different ways that the diuretics will impact a patient, well, this way that it’s impacting a patient is because if you have low potassium levels that can indeed impact the heart and the function of the muscular function of the heart, so that’s a problem.
0:16:21.1 Dr. Kendolyn Smith: We don’t want there to be such a significant potassium loss. Then you also can have gout, you can have dehydration, because most times when patients are peeing so much or using the restroom so much, they’re not really truly drinking or taking in enough fluids, because it’s just coming off, coming off. You can also have things like changes in blood sugar, blood sugar levels, and most times, many hypertensive patients do have diabetes as well, or they’re pre-diabetic. So you have multiple things going at one time. Alright? Then you have your potassium-sparing diuretics, like spironolactone. Spironolactone is a potassium-sparing diuretic, but it also is used off-label for dermatology needs, for acne. So, be mindful that patients can actually be on a spironolactone, not be a hypertensive patient, but experiencing some of these symptoms associated with a diuretic side effects, but they’re really a patient that’s a dermatology patient, and they’re basically being treated for acne, alright? So, let’s look at our next slide. So, one of the things that I just mentioned about the potassium, potassium is a really, really big deal, because a lot of times people think that… We don’t think about potassium as much.
0:17:54.9 Dr. Kendolyn Smith: We think about sodium intake a lot, a lot of people think about water intake, but potassium is really needed to make sure that some of our bodily functions operate properly. And if you don’t have that mineral inside of your body or if you’re deficient of it, you can get things like, we talked about the heart, but also when patients come in and they’re saying that their legs are aching and they’ve been on a diuretic, or they’re so tired and weak and they can’t get up, we usually think about a beta-blocker, but sometimes it’s a diuretic that can be contributing to this type of side effect or this type of comment that you’re hearing from the patients. It is a very wise and very typical thing to do to ask people who are experiencing potassium deficiency to make sure that they’re intaking things like bananas or like orange juice or any other foods that actually might be a good potassium booster. A lot of times we give supplemental potassium 10 millieqs or something like that, sometimes 20, but if they’re really low in potassium, you wanna make sure they get something onboard to balance out that potassium loss. Now, here are some of the ones that are widely used. I mentioned spironolactone, that is a potassium-sparing diuretic.
0:19:21.0 Dr. Kendolyn Smith: Then I also have on here, amiloride, that’s also one and triamterene, now triamterene and spironolactone are gonna be your most common ones, triamterene and spironolactone are the most common potassium sparing ones that are used. However, you have to look at the combinations that I mentioned as well. So remember I talked about having multiple agents on board for the patient, so this potassium sparing diuretics actually can be combined with your hydrochlorothiazides as well. And these are very common combination diuretics. So the one here, Aldactazide, that’s spironolactone and hydrochlorothiazide, then you got the Maxzide or the Dyazide, which is probably very commonly thought of, and that’s the triamterene with the hydrochlorothiazide, and then you also have the Moduretic, which is the amiloride and the hydrochlorothiazide. So any of these can be utilised with hydrochlorothiazide. Remember our schematic that looked at the diagram of where these diuretics work. Your furosemide right here, thank you. So remember, you’ve got a thiazide and you’ve got a spironolactone over here, and you’ve got a furosemide, so your thiazide up here at the top in the distal convoluted tubule, and then you’ve got your spironolactone down here in the lower distal.
0:20:55.9 Dr. Kendolyn Smith: Well, if you can get that volume off with both of those medications, there’s a real need and a real interest in having both of those medications on board, because you can actually get that volume off and that fluid off of the patient, knowing that you’ve got a potassium sparing diuretic on board, as well as a thiazide, and you know that they’re tried and true agents, so you can get that water off coming off of them like that. Okay, alright. So let’s look at our calcium channel blockers. So I am going to say that I kind of wish that the calcium channel blockers had a name, but they don’t really have a name, we just call them CCBs, and they’re reasonably easy to understand, their names kind of give them away because they’re calcium channel blockers. I think they’re probably pretty easy to understand because what they do is they block the calcium channel, that seems pretty easy to understand, but the one thing you have to remember about them, they are going to reduce the blood pressure because they relax the blood vessels and reduce the heart rate. So if you have where the calcium is going through, let me see if I can…
0:22:25.7 Dr. Kendolyn Smith: Right in here in the middle of your schematic here, you can see this, I think you can see, and I can blow these up a little bit more to make them easier, but this is where it’s gonna work, so you’re gonna actually see where the calcium increases the strength of the force of the contractions in the heart and blood vessels, and then it blocks the entry into the smooth muscle tissues, and that’s what reduces the effect for the calcium channel blockers. The calcium channel blockers block the calcium channel. Alright, so when we talk about calcium channel blockers, there’s one thing that stands out about them that you should know in terms of… And you can go to the next slide, I’m gonna show them a couple of the popular ones, which they probably already have heard of ad nauseam, the amlodipine, which is the Norvasc, diltiazem, nicardipine, nifedipine, nisoldipine, and verapamil, these ones are used all of the time, but the problem with some of the calcium channel blockers is that they cause some issues for patients with swelling, okay, so their main issue is that they cause swelling. Now, amlodipine is…
0:23:42.5 Dr. Kendolyn Smith: It comes also with multiple strengths, 5 milligrams, 10, 20, you can go up in strength; however, with the calcium channel blockers, as you go up in strength, many times what you end up having is more of that swelling side effect. So a lot of times people will not want to have that particular side effects, so that’s why they typically wanna come off of the calcium channel blocker. Let’s go over to the next slide, look at some of the other side effects that are associated. So when a patient is on a calcium channel blocker, it’s very, very likely that they’re going to have that ankle swelling, but they also can end up having a lot of flushing and a lot of dizziness, some patients do complain of heartburn and nausea, the reason why that becomes an issue for patients is because if they are feeling the heartburn piece, then you don’t know when… If they go and they say, well, my chest is hurting, because that’s how they present with heartburn. Most times they’ll say it, my chest is hurting, and then they go and they’re seen. And they get there and you’re thinking, I think having a heart attack.
0:24:56.2 Dr. Kendolyn Smith: Is it angina, what’s going on with the patient. It’s really heartburn and note the patients do not want to nor do providers, you all, as providers, want to have patients showing up thinking they’re having a heart attack and it’s a heartburn from their blood pressure medication. So those are things to think about with your calcium channel blockers. Alright, so let’s go into our next group, and that would be our ACE inhibitors, now our ACE inhibitors or our angiotensin-converting enzymes, they actually do have a name, and so what they do though, if you look at your schematic here you see angiotensins… Angiotensinogen is converted into angiotensin I. ACE comes in and it converts it into angiotensin II, and so when it’s converting, if you look up from the very top of the screen, your renin, your renin that’s coming from the kidney, and you see where the angiotensinogen is there, it’s being catalysed into angiotensin I, then it uses ACE, which is the angiotensin-converting enzyme to catalyse into angiotensin II, and then it goes on into the next stages using ARBs, but this is where your ACE will work.
0:26:15.2 Dr. Kendolyn Smith: Your angiotensin is this hormone and it does cause blood vessels to narrow in there, and what you want to do is you wanna decrease the amount of that, and then you want to decrease this angiotensinogen, and you don’t want to have angiotensin I to convert into angiotensin II, because you really want the blood pressure to go down instead of up. And so by stopping this conversion, I don’t know if you can see my arrow that I’m pointing to here, but by stopping this conversion, it allows you to be able to stop that process from happening, you’re stopping that hormone from actually being able to narrow, and you know that if the blood vessels narrow, then that’s gonna cause the pressure to go up. So that’s the premise of why the actual blood pressure will increase.
0:27:12.7 Dr. Kendolyn Smith: So if you go on a little bit further and look at this particular schematic, you can see if ACE was not there, if it wasn’t in there, then what would happen is this angiotensin I would convert to angiotensin II, and it will go ahead and in its conversion there, what it would end up doing is it would increase the blood pressure because you’ve got your aldosterone, you’ve got your angiotensin II breaking off into two areas here and both end up causing an increased workload for the blood pressure. If you look… We’re gonna talk about it. I think if you look where the ACEs fit, you’ll see this little arrow, it’s pretty obvious here, between angiotensin I, ang-1 and ang-2. I’m not sure if that’s a terminology that you all have used, ang-1 and ang-2, but that’s where it inhibits, between that conversion of ang-1, ang-2 to stop that blood vessel narrowing in that area, okay? So here are some of the common ACE inhibitors. You got the benazepril, the captopril, enalapril, and obviously, lisinopril is so widely used, everybody knows lisinopril, quinapril, ramipril, and trandolapril.
0:28:30.6 Dr. Kendolyn Smith: Now, ACEs actually have a name, like I said, and they’re called the prils, obviously because all of them end with pril, and they’re easy to remember that way. So if you’re looking for the ones that are most common, it would be lisinopril at this time. You’ll hear it called Zestril and Prinivil, but those are the old branded names before they became generic. The reason that we try to use generic names more often is because, in pharmacy land, the law requires us to utilise a generic before we use a brand anyway, and many times the branded medications are not even available any longer, and so, therefore, the generic names make more sense because there can be multiple companies that make generic medications, but the generic name remains the same. So lisinopril, enalapril, benazepril are usually the most common ones and captopril, it comes behind that one. Alright. So let’s look at some of the side effects, and the main side effect that we can think about is the cough. The ACE inhibitors are notorious for this dry cough. And if you’ve ever seen or if you’ve ever known someone who’s on an ACE inhibitor, you will have recognised if they have this particular side effect, they usually get very annoyed. And before Covid, it was really a big deal because it would be a cough kinda like a…
(Laughter)
0:30:05.3 Dr. Kendolyn Smith: I know that’s a little animated, but you get my point. So it’s a dry cough like that and it’s kind of annoying, and if nothing’s really wrong, like you don’t have a cold or you’re not sniffing or anything, it does bother the patient, and so that’s really one of the reasons why they looked into what other types of medications can be used similarly to the ACE inhibitors, and hence we have the ARBs. So the ACE inhibitors have an ability to reduce the blood pressure, they can reduce it a lot and they do also have some impact on the patient’s side effect profile from headaches to dizziness and things like that, but hypotension is really the main thing. Hypotension, meaning they have… That it lowers it too much, and obviously, we don’t want that to happen at all. And so the dry cough and hypotension are really the things that actually impact the patients when they’re thinking about having to be on an ACE inhibitor, but the cough does go away, but it can take weeks to do so, alright?
0:31:15.8 Dr. Kendolyn Smith: So let’s look at the ARBs. These are our ARBs. Our ARBs, our angiotensin receptor blockers. Now, I put up this little schematic, but I talked a little bit about how it works in the other slide as well. So when we have our ARBs, we look at how that same angiotensinogen converting to angiotensin I or ang-1 converting to ang-2 and after it converts that ang-2, it can then start to do other things in the adrenal gland, and then it also can break off and look at the urine output and things like that. So it can affect urine output, the adrenal glands, and both those things can cause retention of sodium as well as water reabsorption and water retention, and obviously, we just talked about why water retention is a problem, and that’s a problem because it’s gonna cause pressure to increase. So angiotensin receptor blockers also narrow the blood vessels, but they have to find somewhere to bind, and so they bind to this receptor. So when they bind, if you can see… Let me see if I can make this any bigger. So when they bind to the receptor.
0:32:34.8 Dr. Kendolyn Smith: Then that’s where they cause a decrease in production in activity over here in that cascade from your angiotensin I to 2, and then when it breaks off into the adrenal gland, that’s where they can make their best impact. Now, they prevent the angiotensin from binding to the receptors on the blood vessels, and that’s how they help to lower the blood pressure. So they are receptor blockers. So they actually don’t allow the receptor and the binding to take place, okay? So they stop that process of the production of the aldosterone, and they stop the process of the binding so that there’s the adrenal gland, and so that the aldosterone are not produced. So I’m gonna say it again, the angiotensinogen converts the angiotensin I, angiotensin II. The ACE is gonna work right in the conversion from Ang I to Ang II. The ARB is gonna work after that. The ARB is gonna work by… Thank you, I appreciate that. So the ARB is gonna work after the conversion of Angiotensin II. So, that’s the difference between where the ACE and the ARB works.
0:34:04.3 Dr. Kendolyn Smith: They’re on the same cascade of events of that renin-angiotensin system, but one works at the conversion of Ang I to Ang II, the other works after angiotensin II is reduced. Okay? Alright, thank you. Okay, can we go back… Yup, right there, thank you. And the ARBs are called our sartans. So our sartans are obviously, our candesartan, most commonly used now, valsartan, losartan, olmesartan and telmisartan. Your irbesartan used to be very commonly used, but now, candesartan, losartan, olmesartan, telmisartan, and valsartan, well, valsartan used to be, but olmesartan, telmisartan, losartan, and candesartan are the ones that really definitely are commonly used now, and these are our sartans. Alright? And we can go to the next slide. So again, the common side effects is not a cough. So, patients who want to get that same effect or the providers who want that same effect for the patient, I should say, but they don’t want the cough, really will transition over to the ARBs.
0:35:27.8 Dr. Kendolyn Smith: So, really the common side effect, of course, is they’ll have more potassium levels, okay? That’s hyperkalemia, meaning, higher potassium levels, so they don’t cause a decrease, they may cause a little bit of an increase. And it’s not odd for a patient to say that they’re dizzy, maybe a little tired, but that’s not something that would keep a patient… It’s not so much that would keep a patient from actually taking the medication. They do have sometimes experienced GI issues like diarrhea, stomach upset, and things like that. Alright? So now, we’re gonna move to our beta blockers, which I think if you wanna take notes on a beta blocker, beta blockers have mnemonics, it’s always good to have some type of mnemonic to remember them. Now, your beta blockers, they’re gonna lower blood pressure in a couple of ways, so they really either act on the heart or the lung.
0:36:25.1 Dr. Kendolyn Smith: So, the beta blockers reduce heart rate, and they allow the pumping of the heart not to be as fervent. So, they’re gonna reduce that heart rate, and that’s how they’re gonna reduce the volume that’s being pushed through the heart. So, the way that we remember the beta blocker actions is the beta blocker, beta 1 receptor blockers had… They work on the heart. Beta 2 receptor blockers work on the lungs. You have one heart and two lungs. The other mnemonic that we can use here for remembering beta 1 versus beta 2 is over here on this other little schematic. Beta blockers, the site of action for a beta blocker right there is on the heart, beta 1 heart, beta 2 lungs. Then you also can decide if this makes sense to you as a mnemonic. Beta blockers… The beta 1 selective blockers versus the beta 1, 2 non-selective blockers, you remember those by using A through N as your mnemonic.
0:37:26.7 Dr. Kendolyn Smith: If it’s an A through N name, then they are beta 1 selective. The acebutolol, the atenolol, esmolol, metoprolol. Our beta blockers are lols, LOLs, and then if they are beta 1, beta 2 non-selective, they’re gonna be your O through your Z names. So that’s your pindolol, your propranolol and your timolol. If that works for you, that’s a really good mnemonic to use, but you would have to really learn your beta blockers in order to be able to remember that. So, you wanna make sure you make notes for the beta blocker class, because it is important for you to really associate the beta 1 blockers and the beta 2 blockers. But these are some good mnemonics that I think will work for you that might be helpful. Alright? Now, there are tons of beta blockers as well, but here are some of the highlighted ones, everybody probably is familiar with atenolol, bisoprolol, obviously, carvedilol, labetalol, metoprolol, nadolol, nebivolol, and propranolol.
0:38:41.0 Dr. Kendolyn Smith: Those are really our common ones. I wanna go back to metoprolol tartrate and metoprolol succinate. So, this is one of the most confusing parts of the beta-blocker class. Metoprolol tartrate and metoprolol succinate are two different drugs. Lopressor and Toprol XL. Now, they both have metoprolol, but their delivery system is different. The extended release, the extended release is going to be your succinate. Now, I will tell you one of the mnemonics that I’ve used forever, it’s metoprolol succinate, because it’s extended release, I always said, you can have success with Toprol XL. Why do I say that? Well, because as you know, I worked for a drug company at one point in my life, and Toprol XL was actually one of the drugs that I actually… We actually carry. And so, Toprol XL stuck out to me and metoprolol succinate, succinate means success with an extended release. So that’s the way I remember. May not work for you. I’m just throwing it out there, but it may be a way that you can kinda remember that there is an XL, and they both have a same name, but one is success with succinate, and one is a tartrate, okay?
0:40:03.6 Dr. Kendolyn Smith: I don’t quite have a mnemonic for tartrate, so, I’m sorry. But atenolol is also hugely used, carvedilol as well, and carvedilol is actually utilised in a lot of different settings. Propranolol is used also off-label as well, it’s used for other things besides being just a beta blocker for blood pressure. Alright, so let’s go… I feel like I’m running out of time. I’m sorry, guys, am I talking too slow?
0:40:34.5 Professor Walden: You’re fine, you’re fine, you’re fine, you’re fine. Yeah.
0:40:37.6 Dr. Kendolyn Smith: Okay, sorry. So beta blockers, we just mentioned they slow down the heart, so one of the things that you’re gonna recognise with the beta blockers is that they’re going to cause a patient to be relaxed, feel a little less upbeat, because they’re slowing the heart rate. They don’t want the patient to have a heart that’s beating so fast, but that can be a problem if you’re talking about a 40-year-old person, or somebody that’s active and they wanna be active, they don’t wanna feel sluggish, they wanna be out and about and doing their thing. So, that can be a real issue for the patient. And you should not take a patient off of a beta blocker spontaneously, because it could result in a heart attack or it could result in a sudden death, because those patients can actually… Because we just said they work on the lungs as well, they could cause a patient to have difficulty breathing, chest pain, and those kinda things. So you have to be mindful that they need to taper off of those medications. Okay?
0:41:41.2 Dr. Kendolyn Smith: Alright. So, let’s see here. I’m gonna go into some of the additional agents. Now, these agents are ones we call… Every one of these agents are unique in their own right, I put up these because they should not be forgotten, they’re not used as frequently, but they’re also utilised for blood pressure, so you’ve got your alpha blockers, your alpha-2 receptor agonists, the central agonists, the peripheral adrenergic agonists, and then your vasodilators. I’ve listed a couple of them here, I wanna touch base on the alpha blockers. For the main part, they’re gonna dilate blood vessels also, which we just said, but cause the blood pressure to decrease, but they also are used for enlarged prostate in men. So you’ve got your doxazosin, your prazosin, and your terazosin. And then, you can jump over to the central agonists, your guanfacine, and your clonidine, these can cause patients to be drowsy, but they work on the central nervous system more than they work on a specific, like a heart or a lung per se.
0:42:52.3 Dr. Kendolyn Smith: Your alpha-2 blocker is important, this is the one, the methyldopa, it is old, and some people say old is dirt, but it’s used first line in pregnancy, because it’s got a lot of success with that. And I mentioned that in another slide, because it actually is utilised very well in pregnancy, because it doesn’t affect the fetus, in the development of that fetus. Then you’ve got your reserpine. So reserpine over in the peripheral adrenergic agonist, they’re only used… These two are only used when other stuff has failed, when you actually can’t get success with other things, but reserpine does have lots of side effects. So it’s not widely, widely used. You have your vasodilators, which relax the artery walls, and that hydralazine is very commonly used… The Apresoline, and the minoxidil. We know that minoxidil is also used for hair growth, but it’s also used for severe hypertension. So it is also used for other reasons outside of hypertension. Alright?
0:44:06.7 Dr. Kendolyn Smith: So let me look at some of the common side effects with you of these. So I think I mentioned a couple of them. The alpha blockers can cause that postural hypertension, which is basically when a patient notices a sudden drop in blood pressure when they stand up, so they usually are asked to stay seated in the longitudinal position before they just jump up, okay? It can cause a patient to faint or anything like that, and it can result in increased heart rate, headache, nausea, those kinda things. The methyldopa, that’s the one that I said was old, is well tolerated, but it does have a number of these side effects that patients don’t want, if they don’t have to have them. And they can be a little bit more than what is normal for a patient. Dry mouth in particular is one of the things that nobody really cares to want if they can use something else. Alright? So the next slide is gonna talk about some of the additional, the central agonists, which I mentioned that a lot of people take clonidine, lots and lots of people.
0:45:10.0 Dr. Kendolyn Smith: It comes in multiple different deliveries. It comes as a tablet, as well as a patch. So it can be delivered in different ways. The patch usually the only thing you’ll have with that in terms of a side effect is that it will actually irritate a patient’s skin, that’s usually what they complain about most, but other than that, they don’t really have a main complaint. I mentioned the minoxidil can cause hair growth, because it’s used for hair growth, and so, patients don’t really wanna take that for their blood pressure if it’s gonna cause hair growth. I can imagine that would be a problem, especially for a certain population of the patients who just feel like there’s no need for me to have hair growth with my blood pressure. No, thank you. And then, hydralazine, of course, it’s very much used, but it does have some headaches and can cause palpitations for the patient and some of the aches and pains in the joints. Okay?
0:46:08.4 Dr. Kendolyn Smith: Alright. So now, we get to our special population of patients, and we’ve got our pregnant women, our older adults, ’cause I don’t like the word, “elderly,” and we’ve got our African-American population. So with our pregnant women, I mentioned to you that for those people methyldopa is used first line if patients develop hypertension during pregnancy, because it’s least likely to affect that developing fetus, and that’s what we want, and of course, protecting the mom with the fetus during pregnancy. Then you have the ACEs and ARBs, they should not be used in a pregnant patient, unless there’s some specific reason outside of my scope of practice that the patient should be given a ACE or ARB, because there are other agents that can be used and because of how they impact the renal development. You know where they work based on that schematic, and so that’s just not what we want, if it can be helped. With our older patients, chlorthalidone is usually the option. I mentioned earlier that chlorthalidone has had some good impact for patients who have other health conditions, diabetes and cardiovascular events and those things.
0:47:23.1 Dr. Kendolyn Smith: So, that works really well for them. They can also be used with other agents as well. So the chlorthalidone is a really good agent to use. And when you are dosing a patient that’s an older patient, you really can use multiple medications at lower doses instead of using a higher dose of one medication, okay? I’m almost on target. Alright, so let’s look at our African-American patient population, I think that they would be our next one. And everybody knows that African-American population has a very large number of people who tend to have hypertension. Yes, it does happen earlier in life for more reasons, and… For some reason, and it tends to be more severe in African-Americans than in others.
0:48:17.1 Dr. Kendolyn Smith: There are lots of different ways that the hypertension is attacked depending on that patient, it’s very patient-specific. We do try to have people use thiazide diuretics or calcium channel blockers as first line agents for those patients as well, just to be protective of the kidney, just to try to get some of that volume off, and also, many of the African-American patients are diabetic, so we treat them accordingly to ensure that they can actually get the full benefit of being treated for hypertension and diabetes. And we already know that we treat a diabetic patient as a cardiovascular patient as well. Okay? So, I think that I have made it by the timeline. And I am going to stop there, because we can dig into every single one of these things even more. And so, that is what I have to start you out with your hypertensive medications. Professor Walden?
0:49:20.7 Professor Walden: I’m here, I’m here. So, fantastic. No, it was exciting. So, [chuckle] I don’t know if you saw or were able to see, but the comments were absolutely flowing.
0:49:33.0 Dr. Kendolyn Smith: No, I couldn’t see anything.
0:49:34.6 Professor Walden: No? [chuckle] It’s okay, it’s okay, it’s perfectly great. So, no, there were absolutely some takeaways. You had… Oh, oh, we lost you off camera. But we definitely…
0:49:46.7 Dr. Kendolyn Smith: I see you. My camera… My power is going out…
0:49:51.2 Professor Walden: Oh, okay.
0:49:53.6 Dr. Kendolyn Smith: And so, I wanna make sure I can still hear you.
0:49:56.9 Professor Walden: Oh no, you’re fine, you’re fine. So, we just were able to… I think people were having some light bulb moments, I know there were some notes being taken. So I just wanted to address a few things that you mentioned.
0:50:09.0 Dr. Kendolyn Smith: Yes.
0:50:10.3 Professor Walden: One was… Well, there was a question more so than anything, not anything you mention. There was a question, and I think you addressed it more towards the end, which was…
0:50:18.2 Dr. Kendolyn Smith: Okay.
0:50:18.7 Professor Walden: “Do we give calcium channel blockers or an ACE inhibitor to our patients who have hypertension?” And for me, the answer is as a clinician, it depends on your patient. [chuckle] Right?
0:50:34.8 Dr. Kendolyn Smith: Yes.
0:50:35.5 Professor Walden: It depends on your patient. We know that we’re kind of… We’re using AHA Guidelines, but we’re using some intricacies of JNC 8 that are still relevant to us, so you’re really gonna have to look at your patient, being mindful of, is your patient Black, is your patient Caucasian or Asian? Because in that case, I’m more inclined to give an ACE.
0:51:00.7 Dr. Kendolyn Smith: Right.
0:51:00.8 Professor Walden: If they are White or Asian versus if I have an African-American patient, I might be a little hesitant, so I might start out with the calcium channel blockers and the thiazides to see if those work. So, I don’t know how you feel about that or any input.
0:51:19.7 Dr. Kendolyn Smith: Well, actually, I think that that is… You know, in today’s world that we have, we have so many diverse situations with patients, and it’s not really a one-size-fit-all any more. We can use our protocols, and we can use the guidelines, but we have to really look at the patients, because they’re individualised. When they come in, you listen to what they’re saying that’s going on, and then you have to treat accordingly. We… I, as a pharmacist, am on another side of the spectrum, so many times we see them where they’ve been treated so many different ways, they’re kinda throwing different things at them just trying to help them get to a goal of some sort. Because some patients are so out of whack with their blood pressure, and then they have other concomitant disorders that it makes it very difficult to just stick to solely the guidelines. But you definitely… If you’re treating based on demographics, African-American patients, you’re gonna see those patients present with hypertension probably much sooner, much earlier and much more advanced. I’ve seen people walking around with blood pressure 200, and they’re unbothered, they’re fine, walking around, but then all of a sudden they have a stroke.
0:52:30.9 Professor Walden: Yeah. Right.
0:52:32.1 Dr. Kendolyn Smith: So, you know, it’s really… Yeah, it’s patient-dependent.
0:52:35.3 Professor Walden: Absolutely. So I’ve experienced the same thing, so you just kinda have to keep that in mind. I did answer as best to your ability. So, the medications that act on the CNS system, so that would be like your clonidines. I have experience where I have had patients, like you said, who have been prescribed clonidine, and they might have been on it for a long time. It is not a favourite situation of mine, I feel like when that happens, it is because we have a resistant blood pressure. And at this point, the previous clinician has thrown up their hands and said, I don’t know what else to do.
0:53:19.1 Dr. Kendolyn Smith: Okay.
0:53:20.7 Professor Walden: So, how long does those medications affect the CNS system? So, if I give someone clonidine in my office, how… We’re supposed to have them sit there and watch them, but how long does that take to actually go into effect?
0:53:41.8 Dr. Kendolyn Smith: You mean like, to make sure that they don’t get up spontaneously and go out?
0:53:46.8 Professor Walden: Mm-hmm.
0:53:47.3 Dr. Kendolyn Smith: Usually, we tell patients… Well, we tell people, probably, you’re supposed to let them sit for about 15 minutes?
0:53:53.0 Professor Walden: Right.
0:53:54.7 Dr. Kendolyn Smith: Yeah, but… I mean, if you can do that, if you have the luxury of being able to do that, and if they’ll sit there…
(Laughter)
0:54:01.1 Professor Walden: Right.
0:54:01.7 Dr. Kendolyn Smith: Just like with the COVID vaccine, they’re supposed to sit for 15 minutes and they’re like, I’m not doing it. So, usually about 15 minutes, you really kinda have to just… I would say, tell the patient what is going to happen, what you’re looking for, you don’t want them to pass out, you don’t wanna them fainting, you don’t wanna have this whole dizzy, whole situation.
0:54:22.8 Professor Walden: Right.
0:54:23.8 Dr. Kendolyn Smith: Clonidine is a really interesting drug, like you’re saying. It comes in so many different strengths, and it comes in so many methods, like a patch and all of that. For some reason, it is a drug that clinicians do like to keep people on.
0:54:44.9 Professor Walden: Yeah.
0:54:46.2 Dr. Kendolyn Smith: And sometimes we don’t really quite understand why that is, and it may be true what you’re saying and is that, they don’t know what else to do for the patient. But I would think that that may be a patient that may need some further assessment in terms of why that blood pressure may not be coming down or getting to where it needs to be, or they’re still having episodic issues.
0:55:09.6 Professor Walden: Yeah, that is exactly my point, and that is exactly what I was getting into, because I have had the same experience. And after having multiple collaborating doctors, they have… They too are not super fans, which I’ve been very lucky, they are not super fans of clonidine, and I had some learning in that aspect, but I just wanna talk to the students and to these new NPs, when you guys have someone you inherit or a new patient who comes to you and they are on clonidine and they tell you, well, this is the only thing that seems to work, you need to start doing a lot of questioning. Because it’s not typically a blood pressure medications that we do long-term, when you actually start looking at the research. They are good for trying to get it down quickly and trying to manage it quickly, but if you have a patient who tells you that, that also tells me that there is a resistant high blood pressure, I instantly think of the figures that Dr. Smith has shown us, and I think about their kidneys, what’s happening to their kidneys?
0:56:20.6 Professor Walden: We know that resistant blood pressure tends to [0:56:23.9] __ itself in the kidneys, and that’s just an area where you need to start sending your patient for some further testing and doing some further investigation. Because in most aspects, blood pressure will respond to medications and like she’s presented with, there are so many that clearly there is common… And you kinda wanna look at that for a second, okay? There was one other thing that I wanted to mention, [chuckle] and we might be losing Dr. Smith, but the other thing that I wanted to mention also is in about amlodipine. Amlodipine is a starter, right? And so, we will typically have patients come to us that have been on amlodipine for a while. But amlodipine is typically a weak drug. So it is the weaker of the medication, so I just kinda wanna put that out there, so if you can’t go up anymore and it is not responding, it’s fine, don’t panic, just change the medication. Find something else that works. Let’s see if we can bring her back. There you go. Are you there? Now she…
0:57:45.0 Dr. Kendolyn Smith: That was weird.
(Laughter)
0:57:46.9 Professor Walden: Yeah, that’s okay. [laughter] That’s okay, I was talking about amlodipine and so, how amlodipine is typically one of the weaker blood pressure medications in my experience. So, I… Don’t panic if it does not seem to be… Your patient doesn’t seem to be responding, they just might need something a little bit stronger.
0:58:08.7 Dr. Kendolyn Smith: Yes, I would agree. It’s very widely used, but you’re definitely right, a lot of times it does not give a good solid blood pressure control.
0:58:18.8 Professor Walden: Yeah, yeah, it doesn’t. And I know we try to combine it with the diuretics and we try to do the whole thing, and that is normal, you will see that, but just know, it is literally one of the weakest. So, if it is not… You know, if your patient is not responding, don’t panic, just go ahead and change the medication, find something else that works for your patient, and you’ll be good to go.
0:58:38.9 Dr. Kendolyn Smith: Right. Because they have multiple strengths of it, you can start low and go up and see if that works better. And a lot of times people decide whether to use the combination or whether to try to use those two drugs and full with the dosing that they’re gonna do. The only bad part about that is that sometimes it can be more costly to the patient to do that.
0:59:02.5 Professor Walden: Right. Right. Right. And so… Yes.
0:59:03.8 Dr. Kendolyn Smith: And so… Yeah.
0:59:04.7 Professor Walden: Yeah. So keep that in mind, a lot of these medications that Dr. Smith mentioned some of them… You know, I’m in Georgia, so I know what is on our list at Publix or Kroger and it’s free or a couple of dollars for our patient. Keep in mind that some of these medications, they may work amazingly well, but they may not be cheap for your patients. So, depending on your population that you’re serving, you also have to start keeping that in mind when you are prescribing like… What is that good… What is the…
0:59:36.7 Dr. Kendolyn Smith: With the advance programme?
0:59:37.6 Professor Walden: Yes.
0:59:37.6 Dr. Kendolyn Smith: [0:59:38.8] __ Yeah. Definitely…
0:59:38.9 Professor Walden: Yes. Correct. Try to think about how much it might cost before you provide it, if you know that your patient might be questioning dollars. Okay?
0:59:47.5 Dr. Kendolyn Smith: Yeah.
0:59:48.0 Professor Walden: So that’s kinda important, but I’m super excited. This was great. We’re gonna absolutely have homework, and so, Dr. Smith I so appreciate it.
0:59:56.3 Dr. Kendolyn Smith: Oh, absolutely, absolutely. Thank you guys so much, I appreciate your time, and if there are any other questions that I can answer, feel free to let me know. You know how to find me.
1:00:05.5 Professor Walden: I do, I do, absolutely. Thank you so much. Alright guys, so that was wonderful, I hope that it was just as exciting and as amazing for you. I know that was a lot of information, but also, very good review, especially if that is not your strong point, and just being able to kinda figure out. If you have a better understanding of how the medications work and where they work, and then in addition to what other comorbidities your patient might have, you are better able to treat your patients and better able to do a better job. So, Dr. Smith will be back, [chuckle] she has agreed to kind of come back and let us know, and teach us some more things and go even more in-depth if we want or not. So she will be back, you will see her, she will be a regular with us with the NP collective, so we’re already starting that. But I am super excited you all were here. I’m glad you guys enjoyed it. Don’t worry if you caught on late, you can watch the replay. I do wanna let you know that if you pull up the PowerPoint, which we will load for you, so, if you pull up the PowerPoint, you’ll be able to see her figures much easier.
1:01:18.5 Professor Walden: So it’d be much clear and things like that, so you can… Those figures that we were circling and kind of looking at, you’ll be able to see that much better. So we’ll make sure that we upload that for you as well. Alright, guys. So, we’ll talk to you soon. But I’m so glad that you enjoyed it. If you have any questions, throw them in the group or let us know. Alright, talk to you soon. Bye.