Podcasts about arbs

Heart failure management has evolved dramatically, and nurses are central to optimizing outcomes and preventing hospital readmissions. In this episode, we break down the core medication classes used in heart failure, including ACE inhibitors, ARBs, beta blockers, mineralocorticoid receptor antagonists, diuretics, and newer agents like ARNIs and SGLT2 inhibitors. You'll learn how these medications improve symptoms and survival, key monitoring parameters such as blood pressure, potassium, and renal function, and common adverse effects to watch for. We'll also review practical bedside considerations and patient education pearls that improve adherence and safety. Your support helps me provide more free resources like this! Consider supporting and getting more amazing pharmacology content! Head on over to meded101.com/nurse

Hypertension medications are a cornerstone of nursing practice, and understanding how they work can dramatically improve patient safety and outcomes. In this episode, we break down the major antihypertensive drug classes, including ACE inhibitors, ARBs, beta blockers, calcium channel blockers, and diuretics, in a practical and easy-to-understand way. You'll learn how each class lowers blood pressure, key monitoring parameters, common side effects, and important nursing considerations. We'll also cover when to hold medications, what lab values matter most, and how to educate patients to improve adherence. Your support helps me provide more free resources like this! Consider supporting and getting more amazing pharmacology content! Head on over to meded101.com/nurse

Episode 212: Managing HFpEFHyo Mun and Jordan Redden (medical students) explain how to manage HFpEF with medications and touch some basics about nonpharmacologic treatments. Dr. Arreaza asks insightful questions to guide the discussion. Written by Hyo Mun, MSIV, American University of the Caribbean; and Jordan Redden, MSIV, Ross University School of Medicine. Comments by Hector Arreaza, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.Treatment of HFpEFArreaza: Mike, if you had to name the one therapy everyone with HFpEF should be on, what is it?Mike: That's easy! SGLT-2 inhibitors. This is the one slam-dunk we have in HFpEF. Empagliflozin (Jardiance) or dapagliflozin (Farxiga) should be started in essentially every patient with HFpEF, and it doesn't matter if they have diabetes or not.Jordan: And that's worth repeating, because people still think of these as “diabetes drugs.” They're not anymore. In HFpEF, SGLT-2 inhibitors reduce heart-failure hospitalizations, improve symptoms, improve quality of life, and even reduce cardiovascular death.Dr. Arreaza: They're also simple. Empagliflozin 10 mg daily or dapagliflozin 10 mg daily. No titration, no drama. The effectiveness of these meds was established around 2019 with DAPA-HF and later with DELIVER. These were trials thatdemonstrated that dapagliflozin reduces worsening heart failure and cardiovascular events across the full spectrum of heart failure, from reduced to preserved ejection fraction, independent of diabetes status.Mike: And the number needed to treat is about 28 to prevent one heart-failure hospitalization. That's excellent for a disease where we historically had almost nothing that worked.Jordan: They're also safe in chronic kidney disease down to an eGFR of about 25, which makes them even more useful in this population.Dr. Arreaza: Alright. We got SGLT-2 inhibitor, what's next?Mike: Volume management. Loop diuretics are still the backbone of symptom control in HFpEF. If the patient is volume overloaded, you diurese, and you diurese aggressively.Jordan: The goal is euvolemia. Dry weight, no edema, no orthopnea, no waking up gasping for air. A lot of these patients end up needing chronic oral loop diuretics to stay there.Dr. Arreaza: Something to remember: HFpEF patients don't tolerate congestion well, and being “a little wet” is not benign. Let's move into RAAS inhibition. Where do ARBs and ACE inhibitors fit in?Mike: Between ARBs and ACE inhibitors, ARBs are the winners in HFpEF. They actually reduce heart failure hospitalizations—drugs like candesartan, losartan, valsartan. ACE inhibitors? Not so much. They showed minimal benefit in older HFpEF patients, which is why we go with ARBs instead.Jordan: But a lot of clinicians get nervous about ACE inhibitors and ARBs because of kidney function, so it's worth talking through how these drugs actually work in the kidney.Dr. Arreaza: Yes, misunderstanding may lead to unnecessary drug discontinuation.Jordan: Under normal conditions, the afferent arteriole brings blood into the glomerulus, and the efferent arteriole is constricted by angiotensin II. That constriction keeps pressure high in the glomerulus and maintains filtration.Mike: Here's what happens with an ACE inhibitor: you block angiotensin II, the efferent arteriole relaxes, glomerular pressure drops, and GFR dips slightly. Creatinine bumps up a little, and that scares people, but that's actually the whole point—that's how you get kidney protection long-term.Jordan: High intraglomerular pressure causes hyperfiltration injury and scarring over time. Lowering that pressure protects the kidney long-term. The short-term GFR drop is the price you pay for long-term benefits.Dr. Arreaza: So let's talk about CKD, because this is where people panic.Mike: Right. ACE inhibitors and ARBs are not contraindicated in chronic kidney disease. In fact, they're recommended even in advanced stages. They reduce progression to kidney failure by about a third.Jordan: The key is how you use them. Start low. Check creatinine and potassium one to two weeks after starting, then periodically. A creatinine rise up to 30% from baseline is acceptable. That's not kidney injury, that's physiology.Dr. Arreaza: And what about potassium creeping up?Mike: You adjust the dose or add a potassium binder. You don't just automatically stop the drug.Dr. Arreaza: Now there is one absolute contraindication everyone needs to know about! (board exam test)Jordan: Bilateral renal artery stenosis. This is the big one. In these patients, the kidneys are completely dependent on angiotensin II–mediated efferent constriction to maintain GFR. Take that away, and GFR collapses.Mike: Creatinine can jump dramatically within days. If you see a creatinine rise of 20% or more shortly after starting an ACE inhibitor, you should be thinking about bilateral renal artery stenosis and stopping the drug immediately.Dr. Arreaza: After revascularization, though, many patients can tolerate ACE inhibitors again, so this isn't always permanent. What about cardiorenal syndrome? That's where things get uncomfortable.Mike: It is uncomfortable, but cardiorenal syndrome isn't a contraindication. These patients have severe heart failure and kidney disease, and their mortality is actually higher than patients with heart failure alone.Jordan: ACE inhibitors still reduce mortality and slow kidney disease progression in this group. Studies show that stopping ACE inhibitors during acute heart-failure admissions increases in-hospital mortality three- to four-fold.Dr. Arreaza: So we are cautious, but we don't avoid it.Mike: Exactly. Start low, titrate slowly, monitor labs closely, accept up to a 30% creatinine rise. You only stop if kidney function keeps worsening, or potassium gets dangerously high.Dr. Arreaza: Alright. Let's move on. What about mineralocorticoid receptor antagonists… MRA?Jordan: Spironolactone or eplerenone might reduce hospitalizations in HFpEF, but the data is mixed. This is more of a “select patients” situation.Mike: And you have to watch potassium and kidney function carefully, especially if they're already on an ACE inhibitor or ARB.Dr. Arreaza: What about sacubitril-valsartan, also known as Entresto®?Mike: Entresto may help patients with mildly reduced EF roughly in the 45 to 57% range. It's not first-line for HFpEF, but in select patients, it's reasonable.Dr. Arreaza: Now let's clarify one of the biggest sources of confusion: beta blockers.Jordan: Beta blockers are not a treatment for HFpEF itself. They're only indicated if the patient has another reason to be on them, like coronary disease or atrial fibrillation.Mike: And timing really matters here. You absolutely do not start beta blockers during acute decompensated heart failure. Their negative inotropic effects can make things worse when patients are volume overloaded.Jordan: But, and this is critical, you also don't stop them if the patient is already taking one. Abrupt withdrawal causes a sympathetic surge and dramatically increases mortality.Dr. Arreaza: If a patient is admitted on a beta blocker, what do we do?Mike: Continue it at the same dose or reduce it slightly if they're really unstable. Once they're euvolemic and stable, you can carefully titrate up.Jordan: And watch for chronotropic incompetence. HFpEF patients often rely on heart-rate response to exercise, and beta blockers can worsen exercise intolerance.Dr. Arreaza: Beyond medications, HFpEF is really about treating comorbidities. Aerobic activity can be an initial strategy to improve exercise intolerance and has evidence of improving aerobic function and quality of life. Sodium restriction: improves symptoms, does not decrease risk of death or hospitalizations.Mike: Hypertension control is huge. For diabetes, the SGLT-2 inhibitors will perform double duty. For obesity, weight loss improves symptoms, and GLP-1 agonists like semaglutide are absolute gamechangers.Jordan: Don't forget sleep apnea, atrial fibrillation, and lifestyle. Exercise improves the quality of life, even if it doesn't change hard outcomes. Lifestyle is the main treatment. Dr. Arreaza: And when should you refer to cardiology?Mike: You should refer when the diagnosis isn't clear; symptoms are not responding to treatment, difficult volume management, end-organ dysfunction, or if you are concerned about advanced heart failure.Dr. Arreaza: So, it has been a great discussion. What is the takeaway?Mike: HFpEF treatment isn't about one magic drug -- it's about volume control, SGLT2 inhibitors, smart use of RAAS blockade, and aggressive management of comorbidities.Jordan: And it's understanding the physiology, so you don't withhold life-saving therapies out of fear.Dr. Arreaza: Well said. If you found this helpful, share it with a friend or colleague and rate us wherever you listen. This is Dr. Arreaza, signing off.Jordan/Mike: Thanks! Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References:Barzin A, Barnhouse KK, Kane SF. Heart Failure With Preserved Ejection Fraction. Am Fam Physician. 2025;112(4):435-440.Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure. Circulation. 2022;145(18):e895-e1032.Kittleson MM, Panjrath GS, Amancherla K, et al. 2023 ACC expert consensus decision pathway on management of heart failure with preserved ejection fraction. J Am Coll Cardiol. 2023;81(18):1835-1878.Anker SD, Butler J, Filippatos G, et al. Empagliflozin in heart failure with a preserved ejection fraction. N Engl J Med. 2021;385(16):1451-1461.Solomon SD, McMurray JJV, Claggett B, et al. Dapagliflozin in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2022;387(12):1089-1098.Pitt B, Pfeffer MA, Assmann SF, et al. Spironolactone for heart failure with preserved ejection fraction. N Engl J Med. 2014;370(15):1383-1392.Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction. Lancet. 2003;362(9386):777-781.Solomon SD, McMurray JJV, Anand IS, et al. Angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med. 2019;381(17):1609-1620.Kosiborod MN, Abildstrøm SZ, Borlaug BA, et al. Semaglutide in patients with heart failure with preserved ejection fraction and obesity. N Engl J Med. 2023;389(12):1069-1084.Xie Y, Xu E, Bowe B, Al-Aly Z. Long-term cardiovascular outcomes of COVID-19. Nat Med. 2022;28(3):583-590.Puntmann VO, Carerj ML, Wieters I, et al. Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from COVID-19. JAMA Cardiol. 2020;5(11):1265-1273.Basso C, Leone O, Rizzo S, et al. Pathological features of COVID-19-associated myocardial injury. Eur Heart J. 2020;41(39):3827-3835.Nalbandian A, Sehgal K, Gupta A, et al. Post-acute COVID-19 syndrome. Nat Med. 2021;27(4):601-615.Badve SV, Roberts MA, Hawley CM, et al. Effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in adults with estimated GFR less than 60 mL/min per 1.73 m². Ann Intern Med. 2024;177(8):953-963.Navis G, Faber HJ, de Zeeuw D, de Jong PE. ACE inhibitors and the kidney: a risk-benefit assessment. Drug Saf. 1996;15(3):200-211.Textor SC, Novick AC, Tarazi RC, et al. Critical perfusion pressure for renal function in patients with bilateral atherosclerotic renal vascular disease. Ann Intern Med. 1985;102(3):308-314.Hackam DG, Spence JD, Garg AX, Textor SC. Role of renin-angiotensin system blockade in atherosclerotic renal artery stenosis and renovascular hypertension. Hypertension. 2007;50(6):998-1003.Ronco C, Haapio M, House AA, et al. Cardiorenal syndrome. J Am Coll Cardiol. 2008;52(19):1527-1539.Prins KW, Neill JM, Tyler JO, et al. Effects of beta-blocker withdrawal in acute decompensated heart failure. JACC Heart Fail. 2015;3(8):647-653.Jondeau G, Neuder Y, Eicher JC, et al. B-CONVINCED: Beta-blocker CONtinuation Vs. INterruption in patients with Congestive heart failure hospitalizED for a decompensation episode. Eur Heart J. 2009;30(18):2186-2192.Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

  Genes. Glands. Vessels.

In this podcast episode, an in-depth discussion is provided on the drug Telmisartan, commonly used for lowering blood pressure. The host elaborates on how it belongs to a class of medications known as angiotensin receptor blockers (ARBs) and stands out due to its 24-hour half-life and partial PPAR-gamma agonist activity.  The episode explores Telmisartan's potential benefits for longevity, including its properties that reduce cardiovascular mortality, renal decline, and metabolic issues. It also compares Telmisartan with other ARBs and addresses its unique ability to improve myocardial efficiency, reduce arterial stiffness, and support neuroprotection. Detailed explanations are given on technical concepts such as pulse pressure and its relevance to arterial compliance, and the necessity to consult a doctor before taking the medication is emphasized.   Telmisartan / ARBs (main topic) Telmisartan — MedlinePlus drug info: https://medlineplus.gov/druginfo/meds/a601249.html Blood pressure meds overview (includes ARBs): https://medlineplus.gov/bloodpressuremedicines.html Key mechanisms mentioned PPARγ (PPARG) — NCBI Gene: https://www.ncbi.nlm.nih.gov/gene/5468 Endothelium + nitric oxide (NO) — NCBI Bookshelf: https://www.ncbi.nlm.nih.gov/books/NBK534266/ Angiotensin / aldosterone / "fight-or-flight" Aldosterone test — MedlinePlus lab test: https://medlineplus.gov/lab-tests/aldosterone-test/ Sympathetic nervous system ("fight-or-flight") — Cleveland Clinic explainer: https://my.clevelandclinic.org/health/body/23262-sympathetic-nervous-system-sns-fight-or-flight Lab tests mentioned in the episode Fasting insulin ("Insulin in Blood") — MedlinePlus lab test: https://medlineplus.gov/lab-tests/insulin-in-blood/ Hemoglobin A1C (HbA1c) — MedlinePlus lab test: https://medlineplus.gov/lab-tests/hemoglobin-a1c-hba1c-test/ C-reactive protein (CRP) — MedlinePlus lab test: https://medlineplus.gov/lab-tests/c-reactive-protein-crp-test/ Arterial stiffness / pulse pressure (longevity framing) Pulse pressure & arterial stiffness as risk predictors — PubMed: https://pubmed.ncbi.nlm.nih.gov/11224702/ Visceral fat resource mentioned Dr. Sean O'Mara website: https://drseanomara.com/   Show Notes   00:00 Welcome to the Hart2Heart Podcast. 01:22 Understanding Angiotensin and Its Effects 02:14 How ARBs Work and Their Benefits 03:00 Unique Properties of Telmisartan 03:36 Comparing Telmisartan with Other ARBs 04:44 Telmisartan's Impact on Endurance and Fat Loss 05:59 Telmisartan and Cardiovascular Health 09:57 Blood Pressure Basics and Pulse Pressure 18:54 Telmisartan's Role in Longevity and Dosing 27:28 Conclusion and Final Thoughts   The Hart2Heart podcast is hosted by family physician Dr. Michael Hart, who is dedicated to cutting through the noise and uncovering the most effective strategies for optimizing health, longevity, and peak performance. This podcast dives deep into evidence-based approaches to hormone balance, peptides, sleep optimization, nutrition, psychedelics, supplements, exercise protocols, leveraging sunlight, and de-prescribing pharmaceuticals — using medications only when absolutely necessary. Beyond health science, we explore the intersection of public health and politics, exposing how policy decisions shape our health landscape and what actionable steps people can take to reclaim control over their well-being. Guests range from out-of-the-box thinking physicians such as Dr. Casey Means (author of "Good Energy") and Dr. Roger Sehult (Medcram lectures) to public health experts such as Dr. Jay Bhattacharya (Director of the National Institutes of Health (NIH) and Dr. Marty Mckary  (Commissioner of the Food and Drug Administration (FDA) and high-profile names such as  Zuby and Mark Sisson (Primal Blueprint and Primal Kitchen). If you're ready to take control of your health and performance, this podcast is for you.We cut through the jargon and deliver practical, no-BS advice that you can implement in your daily life, empowering you to make positive changes for your well-being.   Connect with Dr. Mike Hart Instagram: @drmikehart Twitter: @drmikehart Facebook: @drmikehart

Kiera is joined by the tooth-healer himself, Jason Dent! Jason has an extensive background in pharmacy, and shares with Kiera where his pharmaceutical experience has bled over into dentistry. This includes the difference between anti-quag and anti-platelet and which medications are probably safe, what to do to shorten the drag time in the pharmacy, how to write prescriptions most efficiently, and more. Episode resources: Subscribe to The Dental A-Team podcast Schedule a Practice Assessment Leave us a review Transcript: The Dental A Team (00:00) Hello, Dental A Team listeners. This is Kiera and today is a really awesome and unique day. It is, think the second time I've had somebody in the podcast studio with me live for a podcast and it's the one and only Jason Dent. Jason, how are you? I'm doing well. Good morning. Thanks for having me. It is crazy. I I watch Instagram real like this all the time where people are like in the podcast and they're hanging out on two chairs and couches and now look at us. We're doing it. Cheers. Cheers.   That was a mic cheer for those of you who are only listening, but yeah, Jace, how does this feel to be on the podcast? It's weird. Like I was not nervous at all talking about it. I got really nervous as soon as you hit play. So if I stumble over my words, please forgive me ahead of time. Well, Jason, I appreciate you being on the podcast because marketing had asked me to do a topic about teledentistry and I was like, oh shoot, that's like not my forte at all. so   You and I were actually chatting in the hot tub. call it Think Tank session and you and I, we have a lot of good ideas that come from that Think Tank. A lot of business. no phones. That's why. We do leave our phones out. But I was talking to Jason and this is actually a podcast we had talked about quite a while ago. Jason has a lot of information on pharmacy. And if you don't know, Jason isn't really, we were going through all of it last night. It's kind of a mock in the tub. And I think it's going to be great because I feel like this is an area, I'm working at Midwestern and   knowing about how dentists, pharmacology was surely not your favorite one. Jason actually helps a lot of dentists with their clearances. And so we were talking about it and I like it will just be a really awesome podcast for you guys to brush up on pharmacology, different things from a pharmacist's side. So Jason, welcome. Thank you. Yeah, no, we were talking about it and here's like, what should I talk about on the podcast next? I have all these different topics and she's like, what do you know? And the only real interaction I have with dentists is doing clearances for procedures. We get them all the time, which makes sense.   Lots of people are on blood thinner, I've always told Kiera, like, hey, I could talk about that. Like, that's kind of a passion of mine. I'm not a dentist. Or my name is Jason Dent. So in Hebrew, Jason means tooth. No, no, no, sorry. Nerves are getting to me. Jason means healer and Dent means tooth. So my name means tooth healer. So, here's a little set. Hold on, on, hold Can we just talk about? I brought that up before you could talk about it more. So.   My name means tooth healer but I did not become a dentist. I know you wanted me to become a dentist. did. I don't know why. I enjoy medicine. I know what you're going to get to already. The things you're going to ask me. There's been years of this. But nevertheless, that's my name. We'll get that out of the way. But you did give me a great last name. So I mean, it's OK. You're All is fair and love here. SEO's up for that. But yeah, Jason, I'm going to get you right into the show. And I'm going to be the host. And we're going to welcome to the podcast show. Jace, how are you?   Good, good, good. Good, good, good. So by getting into clearances, right? This is what you're kinda talking about with you know, before we get to clearances, I actually wanted Jason, for the listeners who don't know you, who haven't talked to you, who don't know, let's kinda just give them like, how did you go from, Kiera wanted you to be a dentist, to now Jason, you are on the podcast talking as our expert on pharmacy. fantastic. I've always really loved medicine, a ton. As a kid getting headaches and taking Excedrin, like you just feel like a miserable pile of crap.   and then you take two pills and all of a sudden you feel better. Like that's amazing, like how does that happen? Also getting ear aches as a kid, just being in so much pain and then taking some medicine and you start feeling a lot better. I always had a lot of appreciation for that. I've always been mechanically inclined. I went to, started doing my undergrad and took biology and learned about ATP synthase, which is a spinning enzyme that's inside the mitochondria, like a turbine engine. I used to work on small engines on my dirt bike and thought that is so cool. So I really got wrapped up into chemistry.   All the mechanics of chemistry really pulled me in. I'm not getting goosebumps. checking. I usually get goosebumps when I think about chemistry. But it's so cool. You think an engine's awesome, like pistons and camshafts and pressures, the cell is the same thing. It's not as loud, so it's not as cool. But it's fascinating. that's why we're like. ⁓   chemistry and really got into coagulation. So I did my residency after pharmacy school. we went to Arizona for three years. ⁓ You did and your main focus, you were never wanting to be the guy behind the counter. No, I haven't done that. Yeah. No, I love them though. I've always really want to go clinical. ⁓ But I love my retail ⁓ pharmacists. They're amazing resources. And ⁓ I use the retail pharmacist every day still to this day, but I went more the clinical route, really love the chemistry aspect of it.   did my doctorate degree and then I did my residency in Reno. Reno's kind That's how we got here everybody. Welcome to Reno. Strategically placed because I was really interested in critical medicine and where we're located we cover a huge area. So we pull in to almost clear, we go clear to Utah, clear to California, all of Northern Nevada. We get cases from all over. So we actually are kind like the first hub of care for lot of areas. So we really get an eclectic mixture of patients that come in that need-   all kinds of different cases that are coming to them. So it's what I really wanted. So I did my residency in critical care there. And then for the next 10 years, I worked in vascular medicine with my final five years being the supervisor of the clinic. Ran all the ins and outs of that. So my providers, two doctors were on our view. So when we talk about dentistry, talk about production, those kinds of things, totally get it. My doctors were the exact same way, my vascular providers. ⁓   There's some pains there, right? You wanna be seeing patients as much as possible, being able to help as many people, keeping the billing up. And had other nurse practitioners, four practitioners, a fleet of MAs, eight pharmacists. We also had that one location we had, going off the top of my head, I think we had eight locations running as well. And we took care of all the different kinds of vascular cases that came to us. Most common was blood clots, ⁓ which is just a...   which is an easier way of saying VTE. There's so many different ways to say a blood clot. Like you might hear patients say, I've had a PE or a DVT or a venous thromboembolism or a clot in my leg, right? They're all clots, but in different locations. Same with an MI, and MI can be a clot as well. ⁓ there's a lot of, everybody's kind of saying the same thing, but sometimes the nomenclature can make it sound hard, but it really is actually pretty simple.   No. And Jason, I love that you went through, you've been in like, and even in your, ⁓ when you were getting your doctorate, you were in the ER. You also worked in retail pharmacy. remember you having a little sticker on your hand. And retail pharmacy, I have a lot of respect for those guys. They have a lot of pressure on them. and then you also, ⁓ what was that test that you had to take that? I don't know. You were like studying forever for it. ⁓ board certification for, ⁓ NABP. Yeah. So I did that board certification as well.   And now you've moved out of the hospital side onto another section in your career. Now in the insurance, right? So it's really, really interesting. So now I'm on the other side reading notes and evaluating clinical appropriateness and trying to help patients with getting coverage and making those kinds of determinations. So yeah, I've really jumped all over. Really love my clinical days. I know. don't I don't I do miss them. But yeah, kind of had a good exposure to a lot of.   pharmacy a lot a lot of dentists actually with all the places that come through which Jason I really appreciate that and honestly I know you are my spouse and so it's fun to have you on but when I go into conversations like this I don't know any of this information and so finding experts and Jason I think here's me talk more about dentistry and my business than I do hear about him on pharmacy so as we were chatting about this I really realized you are a wealth of knowledge because you've been on the clinical side so you've done a lot of patient care and you've seen how   medications interact and I know you've had a few scares in your career and ⁓ you've known some physicians that have had a few scares and ⁓ you've seen plenty of patients pass away working in the ER and gosh in Arizona drownings were such a big deal. I remember when you were in the ER on your rotations I'd be like who died today? Like tell me the stories and you've really seen and now going on to the insurance side I felt like you could just be such a good wealth of knowledge because I know dentists are sometimes so   I would say like maybe just a little more anxious when it comes to medications. I know that dental students from Midwestern were like here was like four months and we had to like pass it, learn it. And Jason, you've done four years plus clinical residency, plus you've been in it. And something I really love about Nevada Medicine is they've been so collaborative with you.   like your heart, your cardiologist, they diagnose and then they send to you to treat with medicine and... Yeah, I've been really lucky being here in Reno too. The cardiology team has been amazing to work with. We started a CHF program, sorry, congestive heart failure program for patients. So we would collaborate with cardiologists. They'd see the cardiologists and then they send them to the pharmacist to really manage all the medications. So there's pillars of therapy ⁓ called guideline directed medical therapy and the pharmacist would take care of all that. So that's gonna be your...   your beta blockers, your ACEs, your ARBs, your Entresto, which would be a little bit better, spironolactone. So just making sure that all these things are dosed appropriately, really monitoring the heart, and make sure that patients are getting better. we've had real positive outcomes when the, sorry, this is totally off topic. do, talk about that study. When we looked at when patients were coming to see our pharmacists in our clinic that we started up, the patients were half as likely to be readmitted. And this was in 2018, and our pharmacists,   We're thinking about all the medications. We're usually adjusting diabetes medications too at the same time. Just kind of naturally just taking care of all the medications because we kind of got a go ahead from the providers, a collaborative practice agreement that we could make adjustments to certain medications within certain parameters. So we weren't going rogue or maverick, but we were definitely trying to optimize our medications as much as possible. And then years later, some studies came out with, I'm sure you've seen Jardins and Farseegh. not trying to, I'm not.   I don't get any kickback from them. I have no conflicts to share. But because our pharmacists were really optimizing that medication, those medications were later shown to reduce hospitalizations and heart failure, even though they're diabetes medications. Fascinating. So it wasn't really the pharmacists. It was just the pharmacists doing as much as they can with all the tools that were in front of them. And then we found out that the patients were going back to the hospital.   half as much as regular patients. So, yeah, being here, it's been so amazing to work with providers here. the providers here want help, want to help patients, don't have an ego. I mean, I just, it's awesome. I love it. I do love how much I think Jason sees me geek out about dentistry and I watching Jay's geek about his pharmacy and how much he loves helping patients. And ⁓ really that was the whole idea of, all right.   Dentistry has pharmacy as a part of it. And I know a lot of dentists are sending in clearances and I know working in a chair side, it would be like, oh no, if they're on warfarin or on their own blood clot, you guys, honestly don't even know half of what I'm talking about because this is not my jam, which is why Jason's here. But I do know that there was always like, well, we got to talk with their provider. And so having Jason come in and just kind of explain being the pharmacist that is approving or denying or saying yes or no to take them off the blood thinners in different parts, because you have seen several dental   I don't know what they're called. What is it? Clarence's? that what comes to you? don't even know. All day my mind, it's like, here is the piece of paper that gets mailed to you to the pharmacist and then you mail it back. So whatever that is. But Chase, let's talk about it because I think you can give the dentist a lot of confidence coming from a pharmacist. What you guys see on that side. When do you actually need to approve or disapprove? Let's kind of dig into that. Yeah. Well, first of all, I think I'm not a replacement for any kind of clinical judgment whatsoever. Every patient's different. But the American Diabetes Association, you   I work with diabetes a lot. American Dental Association has some really great guidelines on blood thinners and I would always reference them. I actually looked at their website today. Make sure I'm up to speed before I get back on this again. They have resources all around making decisions for blood thinners. And I think the one real important thing in putting myself in the shoes of a dentist or any kind of staff that's around a patient that's in a chair, if they say I'm on a blood thinner, right, a flag goes up. At least in my mind, that's what goes up.   Like, okay, how do we get across this bridge? And I think the important thing to really distinct right then when they say they're on a blood thinner is that is kind of a slang word for a lot of different medications, right? Like it's the overarching word that everybody pulls up saying, I'm on a blood thinner. It's like, okay, but I don't know what say. It's like, I have a car. You're like, okay, do you have a Mazda? Do you have?   Toyota, Honda, what do you have? or even worse it'd be like saying I have a vehicle, right? So when somebody says they're on a blood thinner, it opens up a whole box of possibilities of what they're Blood thinners are also, doesn't, when they're taking these types of medications that are quote unquote a blood thinner, it doesn't actually thin the blood, like adding water to the blood, if that makes sense, or like thinning paint, or like thinning out a gravy, right? It doesn't do the same thing. Blood thinners, really what they're doing is they're working on the blood, which.   which is really cool, try not to tangent on that. ⁓ When they're working on the blood, it's not thinning it per se, but it's making it so that the proteins or platelets that are in it can't stick together and make a cloth quite as easy. So whenever somebody's on a blood thinner, I usually ask, what's the name of the blood thinner that you're on? It's not bad that they use that slang, that's okay, on the same page, but it's really broken into two different classes. There's anticoagulant and antiplatelet.   And a way to kind of remember which is which, when residents would come through our clinics, the way that I teach them is a clot is like a brick wall. You know, it's not always a brick wall. Usually the blood is a liquid going through. But once they receive some kind of chemical message, it starts making a brick wall with the mortar, which is the concrete between the and the bricks, the two parts. When it's an anti-quagent, it's working on that mortar part. When it's an anti-platelet, it's working on the bricks part, right? You need both to make a strong clot or strong brick wall.   But if you can make one of them not work, obviously like if your mortar is just water, it's not working, right? You're not gonna make a strong brick wall. So that's kind of the two deviants right there. So that's what I do in my mind real quickly to find out because antiplatelets are usually, so that's gonna be like your Plavix, Ticagrelor, Brilinta. And hold on, antiplatelets are bricks? Good job, bricks. They're the bricks. And so the reason I was thinking you could remember this because I'm, antiplatelets, it's a plate and a plate is more like a brick.   And anti coagulant, I don't know why quag feels like mortar to me, like quag, like, know, it's like slushy in the blood, like it's coagulating. It's a little bit of that, like, honestly, I'm just thinking like coagulated blood is a little bit more mortar-ish. And so platelet is your plate, like a brick, and anti-quag is like.   the gilly between the bricks. Okay, okay, I got it. Yeah, so there's an exception to every rule, but when they're on that Don't worry, this is Kiera, just like very basic. You guys are way smarter listening to this, and that's why Jason's here. No, no, you helped me pass pharmacy school. When we were doing all the top 200, you helped me memorize all know what flexorill is, all right? That's a muscle relaxant. Cyclo? I don't know that part. It's a cyclo, because you guys are cycling and flexing. I don't actually know. just know it's a muscle relaxant, so that's about as far as I got. When we're looking at antitick platelets, so that's the brick part, so that's going to be your, you know,   Hecagrelor, Breitlingta, Clopidogrel is the most common one. It's the cheapest one, so probably see that one the most. Those, I mean, there's an exception to every rule, but that's generally being used after like a stent's placed in the heart. It can be used for VTE, there's some out there, but that's pretty rare. But also for some valves that are placed in the hearts, it can be used for that as well. So antiplatelet, really thinking more like a cardiac event, right? Like I said, there's always an exception to every rule, but that's kind of where my mind goes real quickly, because we're gathering information from the patient.   They're on anticoagulant. Those are like going to be the new ones that you see commercials for all the time. So Xeralto, Alequis, those are the two big ones right now. They're replacing the older one. And also we were supposed to do a disclaimer of this is current as of today because the ADA guidelines do change. this will be current as of today. And Jason, as a pharmacist, is always looking up on that. I had no clue that you are that up to speed on dental knowledge. so just throwing it out there that if you happen to catch his podcast,   a few years back that obviously check those guidelines for sure. But the new ones are the Xarelto and Eloquist. They're replacing the older ones of warfarin. Warfarin's been around for a really long time. We've seen that one. Those are anti-coagulants. So when you're looking, when a patient says that, generally they're on that medication because they've possibly had a clot in the past or they have a heart condition called atrial fibrillation. Those are kind of the two big ones. Like I said, there's always caveats to it, but that's kind of where my mind goes real quickly. And then,   as far as getting patients cleared, the American Dental Association has really good resources on their website. You can look at those and they're always refreshing that up. They even say in their own words that there's limited data around studying patients in the dental chair and with anticoagulants or anti-platelets. It's pretty limited. There's a few studies, some from 2015, some from 2018. There's one as recent as 2021, which is nice. But really, all of those studies come together and it's really more of an expert consensus.   And with that expert consensus, they have kind of simplified things for dentistry, which is really nice. ⁓ comparing that to, we have more data for like total hip replacement, total knee replacement. We have a lot of data and we know really what we should be doing around then. But going back to dentistry, we don't have as much information, so they always say use clinical judgment, but they do give some really great expert guidance on that. So if a patient's on an anticoagulant, ⁓   they generally recommend that it doesn't need to be stopped unless there's a high bleeding risk for a patient. as a provider or as a clinician in the practice, you can be looking at high bleeding risk. Some things that make an oral procedure a little bit lower risk is one, it's in the compressible site, right? Like we can actually put pressure on that site. That's the number one way to stop bleeding is adding pressure. It's not like it's in the abdominal cavity where we can't get in and can't apply pressure. So number one, that kind of reduces the bleeding risk.   is number one. Two, we can add topical hemostatic agents. Dentists would know that better than me. There's a lot of topical ways to do that. So not only pressure, but there's those things as well. And also, but there are some procedures that are a little bit more likely to bleed. And that's where you and dentists would come in hand in What's the word in APO? Oh, the APOectomy. I got it right. Good job. like, didn't you tell me last night that the ADA guideline was like what?   three or four or more teeth? great question. So you can extract one to three teeth is what their expert consensus One to three teeth without. Without really managing or stopping anticoagulation or doing anything like that. I think that's some good guidance from them. I'm gonna add a Jasonism on that though. So with warfarin, I do see why dentists would be a little bit more conservative or worried about stopping the warfarin because warfarin isn't as stable as these newer agents. Warfarin, the levels.   quote unquote levels can go really high, they can go really low. And if the warfarin levels are high, they're more likely to bleed. So I do think it makes sense to have a really recent INR. That's how we measure what the warfarin's doing. I think that makes a lot of sense, but the ADA guidelines really go into the simplification version of all these blood thinners. Generally, it's recommended to not stop them because the risk of stopping them outweighs the benefit of stopping them in almost every case. Almost every case.   ⁓ So when you're with that patient, right, they say I'm on a blood thinner, finding out which kind of blood thinner that they're on, you find out that they're on Xeralto, right? How long have you been on Xeralto for? I've been on it for years. You don't know exactly why, but if they haven't had any recent bleeding, you're only gonna remove one tooth. ⁓ You can do what's called a HasBlood score. That kind of looks at the bleeding risk that they'd have. That'd be kind of going a notch above, but in my mind, removing one tooth isn't a real serious bleeding risk. I'd love to hear from my dentist friends if they...   disagree, right, but ADA says one to three tooth removals, extractions, that's the fancy word. Extractions, yeah, for extracting teeth out. Is not really that invasive. Sure. It's not that high risk, so it's usually perfectly fine. So if a patient was on Xarelto, ⁓ no other, this is in a vacuum, right? I'm not looking at any other factors, which you should be looking at other factors. I would be perfectly fine to just remove one to two.   And when those clearances come in, because dentists do send them, talk about what happens. You guys were working in the hospital and you guys would get these clearances all the time. do. We get them so often. I mean, we get like four or five a day. We'd love to give it to our students, student pharmacists, and ask them what to do. And they would usually look up the American Dental Association guidelines and come up with something. We're like, yep, that's what we say too. In fact, we say it so many times a day that we have a smart phrase.   which just blows in the information real quickly and faxes it right back to the So it's like a copy paste real quick. So what I wanted to point out when Jason told me this is dentists like hearing this and learning this, this can actually save you guys a ton of time to be able to be more confident, to not need to send those clearances on. And we were actually talking last night about how I think this might be a CYA for dentists. like, as we were talking, I think Jason, you seeing so many other aspects of medicine, like you've literally seen patients die, you've seen other areas.   And so coming from that clinical vantage point, we were realizing that dentists, we are so blessed to live in an injury. I enjoy dentistry because possibly there's someone dying, not super high, luckily in dentistry. The only time that I have actually had a doctor have a patient pass away, and it was only when they were completely sedated and doing ⁓ some other things, but that was under the care of an anesthesiologist. And so that's really our high, high risk. And so hearing this, Jason,   That was one of the reasons I wanted him to come on is to give you doctors more confidence of do we have to always send to a pharmacist? I mean, hearing that on the pharmacy side, they're just sending these back and not to say to not see why a to not cover this because you might be questioning like, well, do I really need to? But you also were talking about some other ways of so number one, you guys are just going to copy back the 88 guidelines. So so 88 guidelines. Yeah. And I think that that gives a lot of confidence to a provider or a dentist is that you can go to the 88 guidelines and read them, right? Like you're listening to some   nasally monotone pharmacist on a podcast. Rumor has it, people love him at the hospital. were like, you're the voice, he's been told he has a good radio So for the clinic, I was the voice. Like, yeah, you've reached the vascular clinic, right? And they're like, oh my gosh, you're the voice. But sorry, you me distracted. That'll be your next career, Jace. You're going to be a radio host. OK. I would love that. I love music. But you're hearing from a nasally guy, but you can actually read the ADA guidelines. You just go right to the ADA, click on Resources, and under Resources, it has the   around anticoagulants, I think that's the best way to get a lot of confidence about it because they have dentists who are the experts making calls on these. I'm just reiterating what they say, but I think it makes a lot of sense to help providers. And the reason why my heart goes out to you as well is having the providers that used to work underneath me, they're always looking for our views, which is a fancy way of making sure that they're drilling and filling. Can I say that? Yeah, can say drilling and filling. They're being productive, right? They're being productive, right?   They're always looking to make sure if a patient's canceling, like get somebody in here. Like I need to be helping people all day long. That's how I, we keep the lights on. That's how I help as many people. And so if you have a patient coming in the chair and it has an issue, they say I'm on Xeralto. Well, you can ask real quickly, why are you on Xeralto? I had a clot 10 years ago. my gosh. Well, yeah, we're pretty good to go. Then I'm not worried. We're only removing one tooth or we're just doing a cavity or a cleaning. Something like that. Shouldn't be an issue whatsoever because there's experts in the dental. ⁓   in the dental society, the ADA guidelines that recommend three teeth or less, minimally invasive. They really recommend if it's gonna be really high bleeding risk. And clinically, that's where you would come in, ⁓ or yourself. know, apioectomy is one that's like on the fence line. I don't know where implants set. though, and like we were talking, implants aren't usually like a date of procedure. Most people aren't popping in, having tooth pain, and we're like, let's do an implant. Now sometimes that can be the case, but typically that one's gonna have   a few other pieces involved. And so that is where you can get a clearance if you want to. ⁓ But we were really looking at this of like so many dentists that I know that you've seen will just send in these clearances because they are. And I think maybe a way to help dentists have more confidence is because you know, I love routines. I love to not have to remember things. So why don't we throw it in, have the team member set it up where every quarter we just double check the ADA guidelines. Are there any updates? Are there any other things that we need to do on that? That way you can just see like   getting into the language of this, of what do I need to do? Because honestly, you guys, know pharmacy was not a big portion for it, so, recommending different parts, but I think this is such a space where you can have confidence, and there's a few other things I wanna get to, and I you- I some pearls too. Okay, go. I'm so when she get me into talking about drugs, I'm not gonna stop. So, some other things around that too is these newer blood thinners like Xarelto Eloquist, they now have reversal agents, so a lot of providers in the past were really worried about bleeding because we can't turn it off. We can turn those off. Warfarin has reversal as well, right?   So I'm looking at these patients. It's really low risk. It's in the mouth, generally speaking. Very rarely are they a high bleeding risk. Now if you're doing maxillofacial surgery, this does not apply, right? This does not apply whatsoever. you're like general dentist, you're pediatric dentist. Yeah, yeah, and it's kind of on the fly. So just trying to really help you to be able to take care of those patients on the moment, have that confidence, look at the ADA guidelines, have that in front of you. I don't think it's a bad thing to ever...   check with their provider if you need to. If you're thinking, I feel like I should just check with the provider, I would never take that away from you. But I just want to kind of steer towards those guidelines that I have to help. But what did you want to share? No, yeah, I love that. And I think there were just a few other nuggets that we were chatting about last night that can help dentists just kind of get things passed a little bit easier. So you were mentioning that if they were named to their cardiologist, what was it? was like, who is the last? Great question. Yeah, when a patient's on a blood thinner,   It could be prescribed by the cardiologist. It could be prescribed by the family provider or could have been punted to like a vascular clinic like where I was working. It can go to any of those. And when you send that fax, right, if it goes to the cardiologist and it's supposed to go to the family care provider, like it just kind of goes, goes nowhere, right, from there. So I think it's a really good idea to find out who prescribed it last. If the patient doesn't know who prescribed their blood thinner last, you can call their pharmacy. I call pharmacies all day long.   I have noticed in the last year, they are way easier to get a hold of, which has made my job a lot easier, working on the insurance portion. So reaching out to the pharmacy, finding out who that provider is and sending it to them, because they should be able to help with that. I thought that was a good shift in verbiage that you had of asking instead of like the cardiologist, because that's who you would assume was the one. But you said like so many times you guys would take care of them, and then they go back to family practitioner, and you guys would get the clearances, but you couldn't clear because you weren't overseeing. So just asking the patient.   who prescribed their medication for them last time. That way you can send the clearance to the correct provider. then- And they might not know. You know patients, right? They're like, I don't know, my mom's or else, I don't know who gave it to me. Somebody told me I need to be on this. But at least that could be another quick thing. And then also we were talking last night about-   ⁓ What are some other things that dentists can do when like writing scripts to help them get what I think like overarching theme of everything we discussed is one how to help dentists have less I think drag through pharmacy. ⁓ Because pharmacy can take a little while and so perfect we now know the difference between anti-quag and anti-platelet. We know which medications are probably safe. We know we can check the ADA guidelines so that we were not having to do as many clearances. We also know if they're on a medication to find out and we do need a clearance.   who we can go to for the fastest, easiest result. And now, in talking about prescriptions, you had some really interesting tips that you could share with them. Yeah, so with writing prescriptions, right, pharmacies are pharmacies. So I'm not gonna say good thing or bad thing. There are challenges working with pharmacies. I'm not gonna play that down at all. ⁓ If you're writing prescriptions and having issues and kickbacks from pharmacies, there's some interesting laws around ⁓ writing prescriptions. Say that you're trying to ⁓ prescribe   augmentin, you know, 875 BID, and you tell the patient, hey, I want you to take this twice a day for seven days, and then you put quantity of seven, because you're moving fast, right? You want it for seven days, quantity of seven. Quantity would actually be 14, right? It's not that big of a deal. Anybody with common sense would say if you're taking a pill for twice a day for seven days, you need 14 tablets. But LAHA doesn't allow pharmacists to make that kind of a change, unfortunately. They have to follow what you're saying there. So you're going to get a...   An annoying callback that says, you wrote for seven tablets. I know you need 14. Is that OK? Just delays things, right? So ⁓ I really like the two letters QS. That's Q isn't queen. S isn't Sam. Yeah. It stands for quantity sufficient. So you don't have to calculate the amount of any medication that you're doing. So for me, as a pharmacist, when I was taking care of patients, I hated calculating the amount of insulin they would need for an entire month. So I would say.   Mrs. Jones needs 15, I'd say 15 units ⁓ QD daily. ⁓ And then I say QS, quantity sufficient, ⁓ 90 day supply through refills. So the pharmacy can then go calculate how much insulin that they need. I don't have to even do that. So anytime you're prescribing anything, I like that QS personally. So that lets the pharmacy use ⁓ common sense, as I like to call it, instead of giving you a call. I think that's super helpful. I also thought of one thing too.   going back to blood thinners is when it's kind of like a real quick, like they're not gonna have you stop the blood thinner at all. like you're seeing if you can stop the blood thinner for a patient, there's some instances it's just not gonna happen. And that's whenever they've been, they've had a clot or a stroke or a heart attack within the last three months. Three months. Yeah, that's kind of like the.   Because so many people are like, they had a heart thing like six years ago. And so I think a lot of my dentists that I worked with were like, we got to stop the blood thinners. But it sounds like it's within three months. Yeah, well, I'm just the time. Like this is general broad strokes. What I'm just trying to say is when you want to expect a no real quick. Got it. Right. So because benefits of stopping a blood thinner within those first three months of an event is very, very risky versus the, you know, the benefit of reducing a little bit of blood coming out of the mouth. Right. Like that's not that bad.   when somebody's had a stroke or a heart attack or pulmonary embolism, a clot in the lung, like we can't replace the lung, heart or brain very easily. We can replace blood a lot better. We've got buckets of it at most hospitals have buckets of it, right? So I'm always kind of leaning towards I'd rather replace blood than tissue at all times. So that's kind of a quick no. If they've had one those events in the last three months, we are really, really gonna watch their brain instead of getting.   root canal, right? Like really worried about them. So you'll just say no. And they could the dentist still proceed with the procedure or would you recommend like a three month wait? Or is it provider specific way the pros and cons because sometimes you need to get that tooth out. Great question. think then it's going to come into clinical. That's that's when you send in the clearance, right? Like, and it's great to reach out to the provider who's managing it for you. But I think it's kind of good to know exactly when you get a quick no quick no is going to be less than three months.   ⁓ Or when it's going to be like a kind of a typical, yeah, no problem. If it's been no greater than six months, they're on the typical anticoagulants or alto eloquence. Nothing crazy is going on for them. You're only removing two teeth. This is very, very low risk. But again, I'd urge everybody to read the ADA guidelines. That way you feel more comfortable with it. I'm not as eloquent as they do. They do a real good job. So I don't want to take any of their credit. I think they do a real good job of simplifying that and making you feel confident with providing.   more timely care for patients. Which is amazing. And Jayce, one last thing. I don't remember what it was. You were talking about the DEA and like six month rule. yeah. Let's just quickly talk about that and then we'll wrap this because this is such a fascinating thing for me last night. Yeah. So when comes to prescribing controlled substances, most providers have to have a DEA license. OK. First of all, though, what's your take on dentist prescribing controlled substances? ⁓ I don't think, you know, I worked on the insurance side of things. Right. And I look at the requirements for the   as the authorizations, what a patient, the criteria a patient needs to hit in order to qualify for certain medications. A lot of times for those controlled substances, they have pretty significant issues going on, like fibromyalgia or cancer-related pain or end-of-life care versus we don't, in all my scanning thread, I don't have a ⁓ perfect picture memory. Sure. But I don't usually see oral.   pain in there. There is some post-operative pain that can be covered for those kind of medications but I really recommend to keep those lower and in fact in a lot of our criteria it recommends you know have they tried Tylenol first, they tried, have they filled NSAIDs or are they contraindicated with the patient. So really they should be last line for patients in my two cents but there's always going to be a caveat to the rule right? Of course. comes through that has oral cancer and you're taking   like that would make sense to me. Got it, so then back to the DEA. Yeah, okay. Okay, ready. So as a provider, you should be checking the, if you're doing controlled substances, you should be checking the prescription drug monitoring program, or sometimes called the PDMP, looking to see if patients are getting ⁓ controlled substances from another provider. So it's really just a check and balance to make sure that they're not going from provider to provider to getting too many narcotics and causing self harm or harm to others.   And so with checking that PDMP before prescribing, I think a lot of providers do that. A lot of softwares that I'm aware of, EMRs, electronic medical records, sometimes have links so that you can do that more quickly. However, I don't think it's as intuitive that they need to be checking that every six months in some states. And like here in Nevada, you're supposed to be checking it every six months, not for a patient, but for your actual DEA registration to see if anybody else is prescribing underneath you. Because if you don't check that every six months, you could get in some serious trouble with...   not only DEA, but even more the Board of Pharmacy and your state. Now, I don't know all 50 states, so I check with your state to see if you need to be checking that every six months, but set an alarm just to check that real quickly, keep your nose clean. ⁓ I've had providers, I've had to remind to do that. And if somebody was using your account, prescribing narcotics, you'd never know unless you went and checked that PDMP.   Yeah, I remember last night you were like, and if that was you, I would not want to be you. The Board of Pharmacy is going to be real excited to find you. So that was something where I was like, got it. So, and we all know I'm big on let's make it easy. And Jason, I love that you love this so much and you just brought so much value today. And like also for me, it's just fun to podcast. fun. Yeah. But I got a nerd out on my world a little bit. Bring it into yours. I work with dentists or at least you know, when I was working in Vascular Clinic all day long. Great questions that would come through. Yeah.   So I think for all of us, as a recap on this is number one, I think setting yourself ⁓ some cadences. So maybe every quarter we check our ADA guidelines and we check our, what is it, PDMP. PDMP. so each state, so they call it Prescription Drug Monitoring Program. We need that. Yeah, but there are different acronyms in different states, though. That's just what it's called in Nevada. I forget what it is in California, but you can check your state's prescription monitoring program, make sure that opioids aren't being prescribed under your name. Got it. So we just set that as a cadence.   We know one to three teeth most likely if they're on a blood thinner is According to the 88 as of today is good to go You know things that are going to get a quick know are going to be within the last three months of the stroke the heart attack or the Clot I'm thinking like the pulmonary embolus. Yeah, that's what we're trying to prevent   Those are gonna be quick knows and then if we're prescribing, let's do QS. We've got quantity is sufficient so that we're not getting phone calls back on those medications that we are. And then on narcotics, just being a bit more cautious. Of course, this is provider specific and in no way, or form did Jason come on here to tell you you are the clinical expert.   Jason's the clinical expert on medications. And if you guys ever have questions, I know Jason, you geek out and you want to talk to people so that anyone wants to chat shop. Be sure to reach out and we'll be able to connect you in. we've even talked about possibly, so let me know listeners. You can email in Hello@TheDentalATeam.com of ask a pharmacist anything. I talked to Jason. I was like,   We'll just have them like send in questions and maybe get you back on the podcast or we do a webinar. But any last thoughts, Jace, you've got of pharmacy and dentistry as we as we wrap up today? No, I think that's pretty much it. So check the ADA guidelines. I think it's really good to have cross communication between professions. Right. If you're working with the pharmacy, CVS, Walgreens or something like that or Walmart, I know that it can be challenging. Right. They're under different pressures. You're under different pressure. So I think ⁓ just coming in with an understanding, not being angry at each other.   you know what mean, is super beneficial and working together. When it comes to it, every dentist that I've talked to is actually worried about their patient. Every pharmacist that I've worked with is really worried about the patient as well. So we're trying to accomplish the same thing, but we have different rules and our hands are bound in different ways that annoy each other, right? Like I know Dr. Jones, want 14 tablets, but you said seven. And I know Common Sense says I should give them 14, but I've got to make that change.   knowing that their hands are tied by the law. They can't use as much common sense, which is aggravating. I mean, that's why I love what I gotta do here. I gotta just kind of help a lot more and use common sense and improve patient care. But those kinds of things I think are really beneficial as you work together and then not being so afraid of blood thinners, right? So I think those guidelines do a great job of giving you confidence and not worrying about the side effects. And there's a lot of things that you can do locally for bleeding.   You have a lot of control over that. I think that's pretty cool, the tools they have. Yeah. And at the end of the day, yes, you are the clinician. You are the one who is responsible for this. so obviously, chat, but I think collaborating, talking to other pharmacists, talking to them in your state, finding out what are the state laws, things like that I think can be really beneficial just to give you peace of mind and confidence. And again, dentistry, are maybe a bit more risk adverse because luckily we don't have patients dying That's great thing. Yeah, that's fantastic. I want my dentists to be risk adverse. I think so too. But Jason, I appreciate you being on the podcast today.   And for all of you listening, ⁓ more confidence, more clarity, more streamline to be able to serve and help our patients better. if we can help you in any way or you've got more questions, reach out Hello@TheDentalATeam.com. And as always, thanks for listening. I'll catch you next time on the Dental A Team podcast.  

Doctors Lisa and Sara talk to Consultant Nephrologist Dr Darren Green about patients with Type 2 Diabetes who also have Chronic Kidney Disease and Heart Failure.  We go through a hypothetical case to illustrate some of the finer points of management that can commonly get missed or might not be appreciated. A really detailed talk full of useful practice enhancing tips for this complex group of patients.  Disclaimer: All educational content in this podcast was developed as part of the Circulation Health collaborative working project between Boehringer Ingelheim Limited, Greater Manchester Primary Care Provider Board and Health Innovation Manchester. Content has been created by Circulation Health Clinical Leads for educational purposes, reflecting NHS Clinical Lead and guideline-based recommendations. Boehringer Ingelheim had no input into content development. They have provided financial resources to support Podcast recordings related to this project. Darren would like us to make you all aware that he has working relationships with pharmaceutical industry partners. Specifically, that he has received speak fees and consultancy fees from AstraZeneca, GSK, Novartis, Boehringer Ingelheim, Bayer, and Lilly, and has been part of collaborative working agreements with Novartis, Boehringer Ingelheim, and AstraZeneca. You can use these podcasts as part of your CPD - we don't do certificates but they still count :) Resources: Dr Kevin Fernando counselling diabetic patients starting an SGLT2 Inhibitors like Dapagliflozin or Empagliflozin: https://www.youtube.com/watch?v=pc99SdtlsyU Diabetes UK counselling sheets on SGLT2 inhibitors: https://www.diabetes.org.uk/about-diabetes/looking-after-diabetes/treatments/tablets-and-medication/sglt2-inhibitors Kidney Care UK Patient Booklets: https://kidneycareuk.org/get-support/free-resources/patient-information-booklets/ Pumping Marvellous Heart Failure Charity with patient resources: https://pumpingmarvellous.org/ International Society for Nephrology Toolkit for Initiating or Changing RAASi - Renin Angiotensin Aldosterone System Inhibitors (like ACEis such as Lisinopril or Ramipril, or ARBs like Candesartan on Losartan): https://www.theisn.org/initiatives/toolkits/raasi-toolkit/ Royal College of General Practitioners Acute Renal Failure Toolkit: https://elearning.rcgp.org.uk/course/info.php?id=899 CONFIDENCE trial: Finerenone with Empagliflozin in Chronic Kidney Disease and Type 2 Diabetes | New England Journal of Medicine: https://www.nejm.org/doi/full/10.1056/NEJMoa2410659 ATLAS trial: Efficacy and safety of high-dose lisinopril in chronic heart failure patients at high cardiovascular risk, including those with diabetes mellitus: https://pubmed.ncbi.nlm.nih.gov/11071803/ Metformin lactic acidosis Metformin in Patients With Type 2 Diabetes and Kidney Disease: A Systematic Review: https://jamanetwork.com/journals/jama/article-abstract/2084896 UK AKI Summit report UKKA AKI Summit Report + Recommendations: https://share.google/7uw1GPQ5sV2riJtiV RCGP AKI follow up  post discharge recommendations: https://bjgpopen.org/content/early/2020/06/15/bjgpopen20X101054/tab-figures-data?versioned=true ___ We really want to make these episodes relevant and helpful: if you have any questions or want any particular areas covered then contact us on Twitter @PCKBpodcast, or leave a comment on our quick anonymous survey here: https://pckb.org/feedback Email us at: primarycarepodcasts@gmail.com ___ This podcast has been made with the support of GP Excellence and Greater Manchester Integrated Care Board. Given that it is recorded with Greater Manchester clinicians, the information discussed may not be applicable elsewhere and it is important to consult local guidelines before making any treatment decisions.  The information presented is the personal opinion of the healthcare professional interviewed and might not be representative to all clinicians. It is based on their interpretation of current best practice and guidelines when the episode was recorded. Guidelines can change; To the best of our knowledge the information in this episode is up to date as of it's release but it is the listeners responsibility to review the information and make sure it is still up to date when they listen. Dr Lisa Adams, Dr Sara MacDermott and their interviewees are not liable for any advice, investigations, course of treatment, diagnosis or any other information, services or products listeners might pursue as a result of listening to this podcast - it is the clinicians responsibility to appraise the information given and review local and national guidelines before making treatment decisions. Reliance on information provided in this podcast is solely at the listeners risk. The podcast is designed to be used by trained healthcare professionals for education only. We do not recommend these for patients or the general public and they are not to be used as a method of diagnosis, opinion, treatment or medical advice for the general public. Do not delay seeking medical advice based on the information contained in this podcast. If you have questions regarding your health or feel you may have a medical condition then promptly seek the opinion of a trained healthcare professional.

If you've been told “it's just hard to control,” this conversation will change how you see hypertension.

In this solo episode, Dr. Mike breaks down everything you need to know about blood pressure, why it's so commonly misunderstood, how to measure it correctly, and what optimal numbers really look like. He explains why 120/80 isn't ideal for everyone, why blood pressure variability can be more dangerous than steady high readings, and how sleep, stress, and undiagnosed sleep apnea quietly drive hypertension. The episode walks through a clear, practical framework for managing blood pressure using lifestyle interventions first, followed by supplements, and medications only when necessary. Dr. Mike covers exercise, weight loss, sodium and potassium balance, magnesium, breathing techniques, sauna use, sleep optimization, and evidence-based supplements like olive leaf extract, beetroot, citrulline, and nattokinase. He also explains when medication is appropriate, why ARBs are often preferred, and which drugs can interfere with exercise performance. This is a comprehensive, no-BS guide to protecting your heart, brain, kidneys, and long-term health.     Blood Pressure & Monitoring Ambulatory Blood Pressure Monitoring (ABPM): https://www.heart.org/en/health-topics/high-blood-pressure/understanding-blood-pressure-readings/ambulatory-blood-pressure-monitoring How to Measure Blood Pressure Correctly at Home: https://www.heart.org/en/health-topics/high-blood-pressure/understanding-blood-pressure-readings/monitoring-your-blood-pressure-at-home Sleep Apnea & Blood Pressure Sleep Apnea and High Blood Pressure (AHA): https://www.heart.org/en/health-topics/high-blood-pressure/why-high-blood-pressure-is-a-silent-killer/sleep-apnea-and-high-blood-pressure Sleep Apnea Testing Overview: https://sleepeducation.org/patients/sleep-apnea/ Supplements Discussed Olive Leaf Extract (NIH): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5452224/ Magnesium and Blood Pressure (NIH): https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5452224/ Beetroot, Nitric Oxide, and Blood Pressure: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6723444/ L-Citrulline and Blood Pressure: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5368575/ Nattokinase and Cardiovascular Health: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6043915/ Medications (General Reference) Angiotensin Receptor Blockers (ARBs): https://www.ncbi.nlm.nih.gov/books/NBK459131/ Calcium Channel Blockers: https://www.ncbi.nlm.nih.gov/books/NBK482473/ Thiazide Diuretics: https://www.ncbi.nlm.nih.gov/books/NBK470415/     Show Notes 00:00 Welcome to the Hart2Heart Podcast. 02:15 Why 120/80 isn't optimal for everyone 04:15 What actually causes blood pressure to fluctuate 06:40 Why BP variability is more dangerous than steady high BP 07:30 How to measure blood pressure correctly at home 12:45 Nighttime BP, dippers vs non-dippers (and why it matters) 14:00 Sleep apnea: the hidden driver of hypertension 18:30 The lifestyle changes that lower BP the most 21:00 Electrolytes, magnesium, and nervous system control 26:00 Supplements that actually move the needle 31:25 When medication becomes necessary (and when it doesn't) 36:20 The long-term blood pressure strategy most people miss   The Hart2Heart podcast is hosted by family physician Dr. Michael Hart, who is dedicated to cutting through the noise and uncovering the most effective strategies for optimizing health, longevity, and peak performance. This podcast dives deep into evidence-based approaches to hormone balance, peptides, sleep optimization, nutrition, psychedelics, supplements, exercise protocols, leveraging sunlight, and de-prescribing pharmaceuticals — using medications only when absolutely necessary. Beyond health science, we explore the intersection of public health and politics, exposing how policy decisions shape our health landscape and what actionable steps people can take to reclaim control over their well-being. Guests range from out-of-the-box physicians and researchers to public health experts and high-profile thinkers focused on real solutions. If you're ready to take control of your health and performance, this podcast is for you.   Connect with Dr. Mike Hart Instagram: @drmikehart Twitter: @drmikehart Facebook: @drmikehart  

Aldosterone antagonists, such as spironolactone and eplerenone, are potassium-sparing diuretics that block aldosterone at the mineralocorticoid receptor in the distal nephron. By reducing sodium and water reabsorption while conserving potassium, they play a key role in heart failure, resistant hypertension, and primary hyperaldosteronism. Clinically, they improve mortality in heart failure with reduced ejection fraction, making them much more than just “add-on” diuretics. From a safety standpoint, the biggest concerns with aldosterone antagonists are hyperkalemia and renal function decline. These risks increase in patients with chronic kidney disease or when combined with ACE inhibitors, ARBs, or potassium supplements. Spironolactone can also cause endocrine-related adverse effects such as gynecomastia and menstrual irregularities, which is why eplerenone may be preferred in some patients. Direct-acting vasodilators, most notably hydralazine and minoxidil, lower blood pressure by relaxing arteriolar smooth muscle and reducing systemic vascular resistance. Hydralazine is commonly used in heart failure in combination with nitrates, particularly in select patient populations, while minoxidil is reserved for severe, refractory hypertension due to its potency. Despite their effectiveness, direct-acting vasodilators come with important clinical trade-offs. Reflex tachycardia and fluid retention are common, so they are typically prescribed alongside a beta blocker and a diuretic. Hydralazine is associated with drug-induced lupus, while minoxidil can cause significant edema and hypertrichosis, making careful patient selection and monitoring essential. Be sure to check out our free Top 200 study guide – a 31 page PDF that is yours for FREE! Support The Podcast and Check Out These Amazing Resources! NAPLEX Study Materials BCPS Study Materials BCACP Study Materials BCGP Study Materials BCMTMS Study Materials Meded101 Guide to Nursing Pharmacology (Amazon Highly Rated) Guide to Drug Food Interactions (Amazon Best Seller) Pharmacy Technician Study Guide by Meded101

This podcast is designed to help pharmacy and nursing learners cut through the noise and focus on the high-yield concepts that matter most when it comes to angiotensin receptor blockers (ARBs) and thiazide diuretics. These two medication classes show up constantly on exams and in clinical practice, yet small details about their mechanisms, adverse effects, and monitoring parameters are often where test questions try to trip you up. Each episode is built to reinforce those key points in a clear, practical way. We'll break down how ARBs and thiazide diuretics work, why they are commonly used in hypertension and other disease states, and how to quickly differentiate them from similar drug classes. Special attention is given to classic exam “gotchas,” such as electrolyte changes, renal considerations, and patient populations where these medications are especially beneficial or should be used with caution. Beyond test prep, this podcast emphasizes real-world practice pearls that translate directly to patient care. You'll hear concise explanations of what to monitor, what side effects matter most clinically, and how to recognize problems early. These insights are especially helpful for nurses, pharmacy students, and new clinicians who want to feel confident applying pharmacology knowledge at the bedside or in clinic. Whether you're studying for boards, preparing for a pharmacology exam, or just looking to sharpen your clinical skills, this podcast delivers focused, high-yield content in an easy-to-follow format. By the end of each episode, you'll walk away with practical takeaways that improve both your test performance and your day-to-day medication management. Be sure to check out our free Top 200 study guide – a 31 page PDF that is yours for FREE! Support The Podcast and Check Out These Amazing Resources! NAPLEX Study Materials BCPS Study Materials BCACP Study Materials BCGP Study Materials BCMTMS Study Materials Meded101 Guide to Nursing Pharmacology (Amazon Highly Rated) Guide to Drug Food Interactions (Amazon Best Seller) Pharmacy Technician Study Guide by Meded101

Episode 207: Understanding Hypertension and Diabetes (Pidjin English)Written by Michael Ozoemena, MD.You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.HypertensionSegment 1: What Is Hypertension?HOST:Let's start with the basics. Blood pressure is the force of blood pushing against the walls of your arteries. Think of it like water running through a garden hose—if the pressure stays too high for too long, that hose starts to wear out.Hypertension, or high blood pressure, means this pressure is consistently elevated. It is measured using two numbers:Systolic: the pressure when the heart beatsDiastolic: the pressure when the heart relaxesNormally reading is around 120/80 mmHg. Hypertension is defined by the American College of Cardiology/American Heart Association (ACC/AHA) as 130/80 mmHg or higher.The American Academy of Family Physicians (AAFP) defines hypertension as persistent elevation of systolic and/or diastolic blood pressure, with the diagnostic threshold for office-based measurement set at 140/90 mm Hg or higher.Segment 2: Why Should We Care?HOST:Hypertension is known as “the silent killer” because most people have no symptoms. Even without symptoms, it steadily increases the risk of:Heart attackStrokeKidney diseaseThink of high blood pressure as a constant stress test on your blood vessels. The longer it goes uncontrolled, the higher the chance of complications.Segment 3: What Causes High Blood Pressure?HOST:Hypertension usually doesn't have a single cause. It often results from a combination of genetic factors, lifestyle, and underlying medical conditions.Modifiable FactorsHigh-salt diet and low potassium intakePhysical inactivityTobacco useExcessive alcohol intakeOverweight or obesityChronic stressPoor sleep or sleep apneaNon-Modifiable FactorsFamily history of hypertensionBlack race (higher prevalence and severity)Age over 65Hypertension may also be secondary to other conditions, such as kidney disease, thyroid disorders, adrenal conditions, or medications like NSAIDs or steroids.Segment 4: How Is It Diagnosed?HOST:Diagnosis requires multiple elevated blood pressure readings taken on different occasions. This includes office readings, home blood pressure monitoring, or ambulatory blood pressure monitoring.If you haven't had your blood pressure checked recently, this is your reminder. It's simple—and it could save your life.Segment 5: Treatment and ManagementHOST:Lifestyle changes are often the first line of treatment:Reduce salt intakeEat more fruits, vegetables, and whole grainsAim for 150 minutes of moderate exercise per weekManage stressMaintain a healthy weightGet enough sleepLimit alcoholQuit smokingIf these steps aren't enough, medications may be necessary. These include:Diuretics, ACE inhibitors, ARBs, Calcium channel blockers, Beta-blockersYour healthcare provider will choose the best medication based on your health profile.Segment 6: What You Can Do TodayHOST:Here are three simple, actionable steps you can take right now:Check your blood pressure—at a clinic, pharmacy, or at home.Pay attention to your salt intake—much of it is hidden in processed foods.Move more—even a 20-minute daily walk can help reduce blood pressure over time.Small steps can lead to big, lasting improvements.SummaryHypertension may be silent but understanding it gives you power. Early action can add healthy years to your life. Take charge of your blood pressure today.Diabetes1. Wetin Diabetes Be and Wetin E Go Do to Person Body?Q: Wetin diabetes mean?A: Diabetes na sickness wey make sugar (glucose) for person blood too high. E happen because the body no fit produce insulin well, or the insulin wey e get no dey work as e suppose.Q: Wetin go happen if diabetes no dey treated well?A: If diabetes no dey treated well, e fit damage the blood vessels, nerves, kidneys, eyes, and even the heart.2. Wetin Cause Diabetes and Why Black People Suffer Pass?Q: Wetin cause diabetes?A: E no be one thing wey cause diabetes. E dey happen because of mix of gene, lifestyle, environment, and society factors.Q: Why Black/African Americans get diabetes more?A: Black people for America get diabetes more because of long-standing inequality, stress, low access to healthcare, and the kind environment wey many of them dey live in. These things dey make Black people more at risk.3. Diabetes Rates for America and Black People?Q: How many people get diabetes for America?A: For America today, over 38 million people get diabetes, and the number dey rise every year.Q: Why Black people dey suffer diabetes more than White people?A: About 12% of Black adults get diabetes, compared to just 7% for White adults. Black people also dey get the sickness earlier and e dey more severe.4. Signs and Symptoms of Diabetes?Q: Wetin be the early signs of diabetes?A: The early signs no too strong, but when e show, e fit include:Too much urine (polyuria)Thirst (polydipsia)Hunger, tiredness, and blurred visionWounds no dey heal fastTingling for hand or legSometimes weight loss5. How Doctor Go Diagnose Diabetes?Q: How doctor fit confirm say person get diabetes?A: Doctor go do some lab tests to confirm:Fasting Plasma Glucose (FPG): 126 mg/dL (7.0 mmol/L) or higherHbA1c: 6.5% or higher2-hour Oral Glucose Tolerance Test (OGTT): 200 mg/dL (11.1 mmol/L) or higher after person drink glucose.Random Blood Glucose: 200 mg/dL (11.1 mmol/L) or higher plus classic symptoms like too much urination, thirst, or weight loss.Q: Wetin happen if HbA1c test no match the person?A: If HbA1c result no match person symptoms, doctor fit repeat test or try other tests like FPG or OGTT.6. Wetin Screening and Early Diagnosis Fit Do?Q: Why screening for diabetes dey important?A: Screening dey important because early detection fit prevent serious complications from diabetes.Q: How often person go do diabetes test?A: Adults wey get overweight or obesity, between 35–70 years, suppose do diabetes screening every three years. But because Black adults get higher risk, doctors dey start screening earlier and more often.7. How Person Fit Manage Diabetes?Q: Wetin be the best way to manage diabetes?A: The two main ways to manage diabetes be:Lifestyle changes: Eat better food (vegetables, fruits, whole grain, beans, fish, chicken) and exercise regularly.Medicine: If person sugar still high, doctor fit give drugs like metformin, SGLT-2 inhibitors, or GLP-1 receptor agonists.Q: Wetin be SGLT-2 inhibitors and GLP-1 drugs?A: SGLT-2 inhibitors dey help with kidney and heart problems, while GLP-1 drugs dey help with weight loss and prevent stroke.Q: Wetin be first-line treatment for diabetes?A: First-line treatment for diabetes be metformin, unless person no fit tolerate am.Q: How much exercise a person suppose do?A: Person suppose do at least 150 minutes of moderate exercise per week. This fit include things like brisk walking, swimming, or cycling. E also good to add muscle-strength training two or three times weekly to help control sugar.Q: When insulin therapy go be needed?A: Insulin therapy go be needed if person A1c is higher than 10%, or if person dey hospitalized and their glucose dey above the 140-180 range. This go help bring the blood sugar down quickly.8. Wetin Be the Complications of Diabetes?Q: Wetin fit happen if diabetes no dey well-managed?A: Complications fit include kidney disease, blindness, nerve damage, leg ulcers, heart attack, stroke, and emotional issues like depression.Q: Why Black adults get more complications?A: Black people get higher risk of these complications because of inequality, stress, and poor access to healthcare.9. Wetin Dey Affect Access to Diabetes Treatment?Q: Wetin make Black people struggle to get treatment for diabetes?A: Many Black people no dey get new effective treatments like GLP-1 and SGLT-2 inhibitors because of price, insurance issues, and lack of access. COVID-19 also worsen things.Q: Wetin government and doctors fit do?A: Policymakers dey work on improving access to drugs, better community programs, and screening for social issues wey fit affect diabetes care.10. ConclusionQ: Wetin be the solution to reduce diabetes impact?A: The solution go need medical treatment, early screening, lifestyle support, and policy changes. With proper treatment and community support, e possible to reduce the impact of diabetes, especially for Black communities.Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! _____________________References: Whelton PK, Carey RM. Overview of hypertension in adults. UpToDate. 2024.Carey RM, Moran AE. Evaluation of hypertension. UpToDate. 2024.Mann SJ, Forman JP. Lifestyle modification in the management of hypertension. UpToDate. 2024.Giles TD, Weber MA. Initial pharmacologic therapy of hypertension. UpToDate. 2024.American Heart Association. Understanding Blood Pressure Readings. Accessed 2025.American Heart Association. AHA Dietary and Lifestyle Recommendations. Accessed 2025.Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Doctors Lisa and Sara talk to Consultant Nephrologist Dr Darren Green about patients with Type 2 Diabetes who also have Chronic Kidney Disease and Heart Failure.  We go through a hypothetical case to illustrate some of the finer points of management that can commonly get missed or might not be appreciated. A really detailed talk full of useful practice enhancing tips for this complex group of patients.  Disclaimer: This episode was supported by Greater Manchester NHS who received support from Boehringer.  You can use these podcasts as part of your CPD - we don't do certificates but they still count :) Resources: Dr Kevin Fernando counselling diabetic patients starting an SGLT2 Inhibitors like Dapagliflozin or Empagliflozin: https://www.youtube.com/watch?v=pc99SdtlsyU Diabetes UK counselling sheets on SGLT2 inhibitors: https://www.diabetes.org.uk/about-diabetes/looking-after-diabetes/treatments/tablets-and-medication/sglt2-inhibitors Kidney Care UK Patient Booklets: https://kidneycareuk.org/get-support/free-resources/patient-information-booklets/ Pumping Marvellous Heart Failure Charity with patient resources: https://pumpingmarvellous.org/ International Society for Nephrology Toolkit for Initiating or Changing RAASi - Renin Angiotensin Aldosterone System Inhibitors (like ACEis such as Lisinopril or Ramipril, or ARBs like Candesartan on Losartan): https://www.theisn.org/initiatives/toolkits/raasi-toolkit/ Royal College of General Practitioners Acute Renal Failure Toolkit: https://elearning.rcgp.org.uk/course/info.php?id=899 CONFIDENCE trial: Finerenone with Empagliflozin in Chronic Kidney Disease and Type 2 Diabetes | New England Journal of Medicine: https://www.nejm.org/doi/full/10.1056/NEJMoa2410659 ATLAS trial: Efficacy and safety of high-dose lisinopril in chronic heart failure patients at high cardiovascular risk, including those with diabetes mellitus: https://pubmed.ncbi.nlm.nih.gov/11071803/ Metformin lactic acidosis Metformin in Patients With Type 2 Diabetes and Kidney Disease: A Systematic Review: https://jamanetwork.com/journals/jama/article-abstract/2084896 UK AKI Summit report UKKA AKI Summit Report + Recommendations: https://share.google/7uw1GPQ5sV2riJtiV RCGP AKI follow up  post discharge recommendations: https://bjgpopen.org/content/early/2020/06/15/bjgpopen20X101054/tab-figures-data?versioned=true ___ We really want to make these episodes relevant and helpful: if you have any questions or want any particular areas covered then contact us on Twitter @PCKBpodcast, or leave a comment on our quick anonymous survey here: https://pckb.org/feedback Email us at: primarycarepodcasts@gmail.com ___ This podcast has been made with the support of GP Excellence and Greater Manchester Integrated Care Board. Given that it is recorded with Greater Manchester clinicians, the information discussed may not be applicable elsewhere and it is important to consult local guidelines before making any treatment decisions.  The information presented is the personal opinion of the healthcare professional interviewed and might not be representative to all clinicians. It is based on their interpretation of current best practice and guidelines when the episode was recorded. Guidelines can change; To the best of our knowledge the information in this episode is up to date as of it's release but it is the listeners responsibility to review the information and make sure it is still up to date when they listen. Dr Lisa Adams, Dr Sara MacDermott and their interviewees are not liable for any advice, investigations, course of treatment, diagnosis or any other information, services or products listeners might pursue as a result of listening to this podcast - it is the clinicians responsibility to appraise the information given and review local and national guidelines before making treatment decisions. Reliance on information provided in this podcast is solely at the listeners risk. The podcast is designed to be used by trained healthcare professionals for education only. We do not recommend these for patients or the general public and they are not to be used as a method of diagnosis, opinion, treatment or medical advice for the general public. Do not delay seeking medical advice based on the information contained in this podcast. If you have questions regarding your health or feel you may have a medical condition then promptly seek the opinion of a trained healthcare professional.

Angioedema – Recognition and Management in the ED Hosts: Maria Mulligan-Buckmiller, MD Brian Gilberti, MD https://media.blubrry.com/coreem/content.blubrry.com/coreem/Angioedema.mp3 Download Leave a Comment Tags: Airway Show Notes Definition & Pathophysiology Angioedema = localized swelling of mucous membranes and subcutaneous tissues due to increased vascular permeability. Triggers increased vascular permeability → fluid shifts into tissues. Etiologies Histamine-mediated (anaphylaxis) Associated with urticaria/hives, pruritus, and redness. Triggered by allergens (foods, insect stings, medications). Rapid onset (minutes to hours). Bradykinin-mediated Hereditary angioedema (HAE): C1 esterase inhibitor deficiency (autosomal dominant). Acquired angioedema: Associated with B-cell lymphoma, autoimmune disease, MGUS. Medication-induced: Most commonly ACE inhibitors; rarely ARBs. Typically lacks urticaria and itching. Gradual onset, can last days if untreated. Idiopathic angioedema Unknown cause; diagnosis of exclusion. Clinical Presentations Swelling Asymmetric, non-pitting, usually non-painful. May involve lips, tongue, face, extremities, GI tract. Respiratory compromise Upper airway swelling → stridor, dyspnea, sensation of throat closure. Airway obstruction is the most feared complication. Abdominal manifestations

If you've ever felt overwhelmed trying to piece together how blood pressure, fluid balance, and heart failure meds all connect, this episode is for you. In this lesson, we're diving into the RAAS pathway, also known as the renin-angiotensin-aldosterone system, and how this one system plays a major role in so many things you'll encounter in nursing school and beyond. You'll learn how RAAS helps regulate systemic vascular resistance and fluid volume, which ultimately impact cardiac output and blood pressure. I'll walk you through the three main components—renin, angiotensin, and aldosterone—and show you exactly how they interact to keep the body in balance. We'll also cover the medications that disrupt this pathway, including ACE inhibitors, ARBs, and aldosterone receptor blockers. These are foundational drugs used to treat hypertension and heart failure, and understanding the pathway gives you a deeper understanding of why and how they work. Plus, we touch on the role of pharmacologic angiotensin II in hypotension and septic shock. This episode highlights how mastering one system—just one!—can give you a big-picture view of multiple conditions and treatments. It's a perfect example of what I teach in my free class, How to Thrive in Nursing School Without It Taking Over Your Life. And if you're ready to keep building that strong foundation, I'll also tell you how to join me inside Crucial Concepts Bootcamp. Ready to make the RAAS system finally click? Let's do it! ___________________ Full Transcript - Read the article and view references FREE CLASS - If all you've heard are nursing school horror stories, then you need this class! Join me in this on-demand session where I dispel all those nursing school myths and show you that YES...you can thrive in nursing school without it taking over your life! Crucial Concepts Bootcamp - Start nursing school ahead of the game, or reset after a difficult first semester with my nursing school prep course, Crucial Concepts Bootcamp. Learn key foundation concepts, organization and time management, dosage calculations, and so much more. Straight A Nursing App - Study on-the-go with the Straight A Nursing app! Review more than 5,000 flashcards covering a wide range of subjects including Fundamentals, Pediatrics, Med Surg, Mental Health, Maternal Newborn, and more! Available for free in the Apple App Store and Google Play Store. Pharmacology Success Pack - Want to get a head start on pharmacology? Download the FREE Pharmacology Success Pack.  Nursing School Thrive Guide - Get the book that many nursing students consider the ultimate survival guide for nursing school! Available in paperback, Kindle and audio formats.

NSAIDs can reduce the effectiveness of antihypertensive medications such as ACE inhibitors, ARBs, beta-blockers, and diuretics by promoting sodium and water retention and decreasing renal blood flow. Combining NSAIDs with anticoagulants or antiplatelet agents like warfarin or aspirin significantly increases the risk of gastrointestinal bleeding, due to additive effects on platelet inhibition and mucosal irritation. NSAIDs can elevate lithium levels and increase the risk of toxicity, as they reduce renal clearance of lithium by decreasing renal perfusion. Co-administration of NSAIDs with methotrexate can impair methotrexate elimination, leading to elevated levels and potential toxicity, especially at high methotrexate doses. When NSAIDs are used with corticosteroids, the risk of gastrointestinal ulcers and bleeding is greatly amplified due to synergistic impairment of gastric mucosal protection.

THE LANCET 2003;362:772-776Background: Angiotensin converting enzyme inhibitors (ACEi) reduce mortality and morbidity in patients with systolic heart failure (see CONSENSUS and SOLVD trials). However, registry data showed that up to 20% of patients with systolic heart failure were not taking ACEi. One of the frequent causes for intolerance to ACEi is cough. Angiotensin converting enzyme inhibitors work by blocking the conversion of angiotensin I to angiotensin II, a key step in the renin–angiotensin–aldosterone system (RAAS). Angiotensin II receptor blockers were tolerated in patients with systolic heart failure who were intolerant to ACEi. However, data on long term effectives as an alternative to ACEi were lacking.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.The Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM)-Alternative trial sough to assess if the angiotensin-receptor blocker (ARB) candesartan, could improve outcomes in patients with systolic heart failure who are intolerant to ACEi.Patients: Eligible patients had left ventricular ejection fraction of 40% or less and NYHA class II, III or IV symptoms of at least 4 weeks duration. Patients had also to be intolerant to ACEi.Exclusion criteria were not provided in the main manuscript.Baseline characteristics: Patients were recruited from 618 centers in 26 countries. The trial randomized 2,028 patients – 1,013 randomized to receive candesartan and 1,015 to receive placebo.The average age of patients was 67 years and 68% were men. The average left ventricular ejection fraction was 30%. Cardiomyopathy was ischemic in 68% of the patients. The NYHA class was II in 48% of the patients, III in 49% and IV in 4%.Approximately 50% had hypertension, 27% had diabetes, 61% had prior myocardial infarction, 9% had stroke, 25% had atrial fibrillation and 14% were current smokers.At the time of enrollment, 85% were taking a diuretic, 46% were taking digoxin, 55% were taking beta-blockers and 24% were taking spironolactone.The most common reasons for ACEi intolerance were cough in 72% of the patients, hypotension in 13%, renal dysfunction in 12% and angioedema or anaphylaxis in 4%.Procedures: The trial was double-blinded. Patients were assigned in a 1:1 ratio to receive candesartan starting at 4 or 8mg once daily or placebo. The treatment was doubled every two weeks to a target dose of 32mg once daily.After randomization, follow up occurred at 2, 4, and 6 weeks, 6 months and every 4 months thereafter.Endpoints: The primary outcome was a composite of cardiovascular death or heart failure hospitalizations. All deaths were classified as cardiovascular unless there was a clear non-cardiac cause.Analysis was performed based on the intention-to-treat principle. The estimated sample size to have 80% power at 5% alpha was 2,000 patients. The sample size calculation assumed 18% relative risk reduction in the primary outcome with candesartan assuming a 15% annual event rate in the placebo arm.Results: The median follow up time was 34 months. The mean candesartan daily dose was 23mg at 6 months.Candesartan reduced the primary endpoint of cardiovascular death or heart failure hospitalizations (33.0% vs 40.0%, adjusted HR: 0.70, 95% CI: 0.60 – 0.81; p< 0.001). Candesartan reduced the individual components of the primary outcome - (21.6% vs 24.8%; p= 0.02) for cardiovascular death and (20.4% vs 28.2%; p< 0.001) for heart failure hospitalizations. All-cause death was also lower with candesartan (26.2% vs 29.2%, adjusted HR: 0.83, 95% CI: 0.70–0.99; p= 0.033). The number of patients who had any hospitalization as well as the total number of hospitalizations were numerically but not statistically significantly lower with candesartan (60.2% with candesartan vs 63.3%; p= 0.16) and (1,718 vs 1,835; p= 0.06).Candesartan was associated with more hypotension (3.7% vs 0.9%), more increase in creatinine (6.1% vs 2.7%) and more hyperkalemia (1.9% vs 0.3%). Angioedema occurred in three patients in the candesartan group and none in the placebo group. Cough occurred in two patients taking candesartan and four taking placebo.Authors reported no significant subgroup interactions, however, a corresponding graph was not provided.Conclusion: In patients with systolic heart failure who are intolerant to ACEi, candesartan reduced the primary composite outcome of cardiovascular death or heart failure hospitalizations with a number needed to treat of approximately of 14 patients over 34 months of follow up. Candesartan also reduced all-cause death with a number needed to treat of approximately 33 patients. Adverse events including hypotension, increase in creatinine and hyperkalemia were more common with candesartan.The reduction in the primary endpoint with candesartan was significant and offers an alternative for patients who are unable to tolerate ACEi. Of note, 72% of the patients enrolled in the trial were intolerant to ACEi due to cough. This trial did not include a head-to-head comparison between ARBs and ACEi, and therefore does not address which agent should be preferred as first-line therapy. Only 24% of participants were receiving spironolactone. The combination of ARBs with spironolactone, may increase the risk of adverse events, particularly hyperkalemia and kidney injury.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

In this episode, we review the pharmacology, indications, adverse effects, monitoring, and unique drug characteristics of angiotensin receptor blockers (ARBs).  Key Concepts ARBs are equally efficacious as ACE inhibitors when used for hypertension, heart failure with reduced ejection fraction (HFrEF), chronic kidney disease (CKD) with proteinuria, and post-MI care. Some limited evidence suggests that they might be better in reducing albuminuria in patients with diabetes. ARBs are generally better tolerated than ACEi due to a lower risk of angioedema and dry cough.  While most ARBs are comparable to each other, small differences exists regarding hepatic metabolism (CYP metabolism for losartan, telmisartan, and azilsartan), degree of blood pressure lowering (generally better with azilsartan, olmesartan, valsartan, and candesartan), and additional pharmacological effects (telmisartan with PPAR-Y agonism, losartan with uricosuric effect). ARBs are contraindicated in pregnancy, those with bilateral renal artery stenosis, and those with previous angioedema to ARBs. The most common adverse effects include hypotension and hyperkalemia, but in rare cases acute renal impairment can also occur. Baseline serum creatinine and potassium should be monitored in patients taking ARBs. After initiation or dose adjustment, blood pressure, serum creatinine, and potassium should be repeated in 1-2 weeks. Signs and symptoms of hypotension as well as angioedema should be monitored throughout the treatment period.

THE LANCET 2003;362:767-771Background: Angiotensin II which plays a role in ventricular remodeling and progression of heart failure can be produced by pathways independent of angiotensin convening enzyme. Preliminary studies showed that the combination of angiotensin II blockers with angiotensin-converting enzyme inhibitors (ACEi) improves hemodynamics and reduces ventricular remodeling.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.The Candesartan in Heart failure: Assessment of Reduction in Mortality and morbidity (CHARM)-Added trial sough to assess if adding the angiotensin-receptor blocker (ARB), candesartan, to ACEi could improve outcomes in patients with systolic heart failure.Patients: Eligible patients had left ventricular ejection fraction of 40% or less within the previous 6 months, and NYHA class II, III or IV symptoms. Patients with NYHA class II symptoms had to have cardiac-related hospitalization within 6 months. Patients also had to have treatment with ACEi at a constant dose for at least 30 days.Exclusion criteria were not provided in the main manuscript.Baseline characteristics: Patients were recruited from 618 centers in 26 countries. The trial randomized 2,548 patients – 1,276 randomized to receive candesartan and 1,272 to receive placebo.The average age of patients was 64 years and 79% were men. The average left ventricular ejection fraction was 28%. Cardiomyopathy was ischemic in 62% of the patients. The NYHA class was II in 24% of the patients, III in 73% and IV in 3%.Approximately 48% had hypertension, 30% had diabetes, 56% had prior myocardial infarction, 9% had stroke, 27% had atrial fibrillation and 17% were current smokers.At the time of enrollment, 90% were taking a diuretic, 58% were taking digoxin, 55% were taking beta-blockers, 17% were taking spironolactone and all but two patients were taking ACEi.Procedures: The trial was double-blinded. Patients were assigned in a 1:1 ratio to receive candesartan starting at 4 or 8mg once daily or placebo. The treatment was doubled every two weeks to a target dose of 32mg once daily.After randomization, follow up occurred at 2, 4, and 6 weeks, 6 months and every 4 months thereafter.Endpoints: The primary outcome was a composite of cardiovascular death or heart failure hospitalizations. All deaths were classified as cardiovascular unless there was a clear non-cardiac cause.Analysis was performed based on the intention-to-treat principle. The estimated sample size to have 80% power at 5% alpha was 2,300 patients. The sample size calculation assumed 16% relative risk reduction in the primary outcome with candesartan assuming an 18% annual event rate in the placebo arm.Results: The median follow up time was 41 months. The mean candesartan daily dose was 24mg at 6 months.Candesartan reduced the primary endpoint of cardiovascular death or heart failure hospitalizations (37.9% vs 42.3%, adjusted HR: 0.85, 95% CI: 0.75 – 0.96; p= 0.01). Candesartan reduced the individual components of the primary outcome - (23.7% vs 27.3%; p= 0.021) for cardiovascular death and (24.2% vs 28.0%; p= 0.018) for heart failure hospitalizations. There was no significant reduction in all-cause death (29.5% with candesartan vs 32.4%; p= 0.105). The number of patients who had any hospitalization was similar in both groups (66.8% with candesartan vs 67.5%; p= 0.7), however, the total number of hospitalizations was lower with candesartan (2,462 vs 2,798; p= 0.023).Serum creatinine at least doubled in 7% of the patients in the candesartan group vs 6% in the placebo group. In the subset of patients taking spironolactone, serum creatinine at least double in 11% of the patients taking candesartan compared to 4% of the patients taking placebo.Hyperkalemia, defined as serum potassium of 6 mmol/L or higher, occurred in 3% of the patients in the candesartan group vs 1% in the placebo group. In the subset of patients taking spironolactone, hyperkalemia occurred in 4% of the patients taking candesartan compared to 1% of the patients taking placebo.There were two cases of angioedema in the candesartan group and three in the placebo group. All patients were taking an ACEi.There were no significant subgroup interactions, including in patients taking both beta-blockers and ACEi at baseline.Conclusion: In patients with systolic heart failure, adding candesartan to an ACEi reduced the primary composite outcome of cardiovascular death or heart failure hospitalizations with a number needed to treat of approximately of 23 patients over 41 months of follow up. The total number of all-cause hospitalizations was reduced by 336 with candesartan. All-cause death was not significantly reduced with candesartan.While the results of the trial appear impressive, the high number of adverse outcomes with candesartan in patients taking spironolactone is concerning. Spironolactone led to significant reduction in all-cause mortality in patients with systolic heart failure, as seen in the RALES trial, and should be prioritized over adding candesartan. Notably, fewer than 20% of patients in the trial were on spironolactone at baseline; if more had been, the incremental benefit of candesartan would likely have been reduced due to an increased risk of adverse effects from triple neurohormonal blockade (ACEi, ARBs, and mineralocorticoid receptor antagonists). Furthermore, spironolactone acts by blocking the aldosterone receptor, which is downstream in the renin–angiotensin–aldosterone system. Since candesartan blocks angiotensin II upstream in the same pathway, simultaneous inhibition at multiple points may lead to diminishing benefit.Finally, the differences observed in the subgroup of patients on beta-blockers between this trial and Val-HeFT remain unclear and may simply reflect the play of chance. As we previously discussed, patients receiving both an ACEi and beta-blockers had worse outcomes with valsartan in the Val-HeFT trial.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

In this episode of PT Snacks podcast, host Kasey explores the importance of understanding common hypertension and cholesterol medications encountered in outpatient orthopedic settings. Kasey discusses the effects of beta blockers, ACE inhibitors, ARBs, calcium channel blockers, diuretics, and statins on patients' response to exercise. The episode covers potential side effects, red flags, and practical tips for physical therapists, highlighting the significance of a holistic approach to patient care. Additional resources and special offers through MedBridge are also mentioned.00:00 Welcome to PT Snacks Podcast00:56 Importance of Pharmacology in PT02:09 Understanding Blood Pressure Medications04:31 Cholesterol Medications and Their Effects05:34 Red Flags and Patient Management Tips06:51 Additional Resources and ConclusionRelevant MedBridge Courses1. Exercise and Drug Interactions by Kenneth L. Miller - Overview: Understand how various medications interact with exercise. Covers physiology, drug metabolism, and exercise prescription. 2. Pharmacology for Rehabilitation: Considerations for the Aging Adult by Andrew Opett - Overview: Explores the effects of drugs like antihypertensives and statins, especially in older adults.Support the showWhy PT Snacks Podcast?This podcast is your go-to for bite-sized, practical info designed for busy, overwhelmed Physical Therapists and students who want to build confidence in their foundational knowledge without sacrificing life's other priorities. Stay Connected! Never miss an episode—hit follow now! Got questions? Email me at ptsnackspodcast@gmail.com or leave feedback HERE. Join the email list HERE On Instagram? Find unique content at @dr.kasey.hankins! Need CEUs Fast?Time and resources short? Medbridge has you covered: Get over $100 off a subscription with code PTSNACKSPODCAST: Medbridge Students: Save $75 off a student subscription with code PTSNACKSPODCASTSTUDENT—a full year of unlimited access for less!(These are affiliate links, but I only recommend Medbridge because it's genuinely valuable.) Optimize Your Patient Care with Tindeq Looking for a reliable dynamometer to enhance your clinical measurements? Tindeq ...

Darshan H. Brahmbhatt, Podcast Editor of JACC: Advances, discusses a recently published original research paper on Sacubitril/Valsartan vs ACE Inhibitors or ARBs: A Systematic Review and Meta-Analysis of Randomized Trials

Learn more about becoming an Insider on our website: https://www.benbikman.comThis week in The Metabolic Classroom lecture, Ben focuses on the relationship between hypertension medications and metabolic health, providing a critical examination of their mechanisms and metabolic implications.He begins by highlighting the role of insulin resistance as a common root cause of both hypertension and metabolic disorders. Ben explains that while hypertension medications such as diuretics, beta blockers, ACE inhibitors, ARBs, and calcium channel blockers are often prescribed, they each have unique effects on insulin sensitivity and glucose metabolism, which can either mitigate or exacerbate metabolic dysfunction. Notably, some classes of these medications, like ARBs, may improve insulin sensitivity, while others, like beta blockers and diuretics, can impair it, leading to heightened risks for type 2 diabetes.Ben underscores the importance of addressing the root causes of hypertension—namely, insulin resistance—through lifestyle interventions like low-carbohydrate diets and fasting, which improve both blood pressure and metabolic health. He emphasizes the need for personalized treatment plans that consider the metabolic side effects of medications, advocating for strategies that tackle insulin resistance as a primary approach to improving overall health.Show Notes/References:For complete show notes and references referred to in this episode, we invite you to become a Ben Bikman “Insider” subscriber. As a subscriber, you'll enjoy real-time, livestream Metabolic Classroom access which includes live Q&A with Ben, ad-free Metabolic Classroom Podcast episodes, show notes and references, Ben's Research Reviews Podcast, and a searchable archive that includes all Metabolic Classroom episodes and Research Reviews. Learn more about becoming an Insider on our website: https://www.benbikman.comBen's favorite yerba maté and fiber supplement: https://ufeelgreat.com/usa/en/c/InsulinIQBen's favorite meal-replacement shake: https://gethlth.com (discount: BEN10)Ben's favorite electrolytes (and more): https://redmond.life (discount: BEN15)Ben's favorite allulose source: https://rxsugar.com (discount: BEN20)Ben's favorite health check-up for women: https://choosejoi.co/drben15 (discount: DRBEN15)Ben's favorite health check-up for men: https://blokes.co/drben15 (discount: DRBEN15)Ben's favorite exogenous ketone: https://www.americanketone.com (discount: Ben10)Other products Ben likes: https://www.amazon.com/shop/benbikmanphd#MetabolicHealth #Hypertension #BloodPressure #DrBenBikman #InsulinResistance #MetabolicScience #FatCellBiology #Diuretics #BetaBlockers #ACEInhibitors #CalciumChannelBlockers #BloodPressureMedications #HealthTips #DASHDiet #InsulinSensitivity #FatCells #KetogenicDiet #LowCarbLiving #HealthyLifestyle #HeartHealth Hosted on Acast. See acast.com/privacy for more information.

$5 Q-BANK: https://patreon.com/highyieldfamilymedicine Intro 0:30, Hypertension classifications 1:45, Lifestyle modifications 3:00, Thiazide diuretics 4:16, ACE Inhibitors and ARBs 5:59 Calcium channel blockers 8:15, Beta blockers 9:36, Mineralocorticoid receptor antagonists 10:49, Goal-directed medical therapy 12:49, Resistent hypertension 15:37, Other antihypertensives 16:38, Hypertensive emergency 20:33, Hypertension in pregnancy 23:00, Primary hyperaldosteronism 24:38, Renal artery stenosis 26:24, Cushing syndrome 27:22 Pheochromocytoma 28:53, Obstructive sleep apnea 30:26, Coarctation of the aorta 31:30, Practice questions 32:30

Sounds like a nifty musical group, but "Crochet and the White Sox Arbs" is the focus right now for this front office. The price for the All-Star pitcher is set, and only some teams can provide the ask. We'll explain why Chris Getz is in his element with this move. Meanwhile the team is already dropping arbitration eligible players, and the salary clearing makes sense at this stage of the offseason. Chris Lanuti and his buddy Ed Siebert sit at his 9-foot homemade oak bar in a basement on the South Side of Chicago to discuss their favorite team - The Chicago White Sox in a podcast "For Fans, By Fans!" Listen. Subscribe. Share. Call 708-459-8406 and leave your comments and questions for the next episode! SUBSCRIBE NOW​ on Apple Podcasts, Spotify, everywhere podcasts can be found and always at SoxInTheBasement.com!

Busking has long been a way for musicians to gain performance experience and garner a following. Busking in the streets of Melbourne CBD with their heartfelt performance is a new group of Filipino musicians (Birch, Zyra and Arbs) who call themselves “After Hours”. - Ang busking ay matagal nang naging paraan para sa mga musikero na magkaroon ng karanasan sa pagganap at makakuha ng mga followers. Makikita ang bagong grupong "After Hours" na sina Birch, Zyra at Arbs na nagtatanghal sa mga kalye ng Melbourne CBD.

Episode 49 – Abnormal Repetitive Behaviours in Dogs – What You Need To Know!   Abnormal Repetitive Behaviours in dogs are challenging to diagnose and treat. Their genetic and heritable nature, the large number of physical medical differential diagnoses and their ritualistic and invariant nature can make them difficult to live with and their treatment really requires the help and support of an expert!   In this episode you will learn: 1.      The definition of Abnormal Repetitive Behaviours 2.      The big 5 groups of ARBs 3.      What we need to think about when it comes to physical medical rule outs 4.      What breeds are predisposed 5.      How to treat these patients   Here are some of the resources Dr Katrin mentions in this episode: 1.      Moon-Fanelli, A. A., Dodman, N. H., & Cottam, N. (2007). Blanket and flank sucking in Doberman Pinschers. Journal of the American Veterinary Medical Association, 231(6), 907–912. https://doi.org/10.2460/javma.231.6.907   2.      Dodman, N. H., Karlsson, E. K., Moon-Fanelli, A., Galdzicka, M., Perloski, M., Shuster, L., Lindblad-Toh, K., & Ginns, E. I. (2010). A canine chromosome 7 locus confers compulsive disorder susceptibility. Molecular Psychiatry, 15(1), 8–10. https://doi.org/10.1038/mp.2009.111 We really hope you enjoy this episode; it is packed with so much information!   If you liked this episode of the show, The Pet Behaviour Chat, please LEAVE A 5-STAR REVIEW, like, share, and subscribe!   Facebook Group: Join The Pet Behaviour Community on Facebook   You can CONNECT with me: Website: Visit my website Trinity Veterinary Behaviour Instagram: Follow Trinity Veterinary Behaviour on Instagram Trinity Veterinary Behaviour Facebook: Join us on Trinity Veterinary Behaviour's Facebook page Trinity Veterinary Behaviour YouTube: Subscribe to Trinity Veterinary Behaviour on YouTube LinkedIn Profile: Connect with me on LinkedIn   Thank you for tuning in!

Guideline evolution is driven by ongoing research; recent studies like PeriOperative ISchemic Evaluation-3 Trial (POISE-3) and trials such as OPtimisation of Peri-operaTive CardIovascular Management to Improve Surgical outcomE II (OPTIMISE II) trial may influence recommendations on hemodynamic management and the use of tranexamic acid. Future guidelines are expected to integrate machine learning models for risk prediction, addressing complex patient phenotypes and interactions. Discontinuation vs. continuation of renin–angiotensin system inhibition before non-cardiac surgery: the SPACE trial has challenged existing practices regarding the discontinuation of ACE inhibitors or ARBs, highlighting the dynamic nature of medical guidelines and the continuous incorporation of new evidence to enhance patient care. Presented by Andy Cumpstey and Joff Lacey with Mark Edwards, Consultant in Anaesthesia and Perioperative Medicine, University Hospital Southampton Honorary Senior Clinical Lecturer, University of Southampton and John Whittle, Clinical Academic working in Perioperative Translational Medicine at UCL and Honorary Consultant in Perioperative Medicine, Anaesthesia and Critical Care at University College Hospitals London. -- More on POISE-3 here: https://clinicaltrials.gov/study/NCT03505723 More on OPTIMISE II here: https://optimiseii.org/ More on the SPACE trial here: https://doi.org/10.1093/eurheartj/ehad716  

We're taking a short summer break, but we'll be back at the end of August with brand new episodes.  Lose your heart to NephMadness 2022! Dr. Joel Topf (@kidney_boy) and Dr. Sadiya Khan (@HeartDocSadiya) tackle the NephMadness 2022 Cardiorenal Syndrome region, leading us through the pathophysiology of cardiorenal syndrome, how to approach the creatinine “bump” with diuresis, managing patients with diuretic resistance, and more. Claim CME for this episode at curbsiders.vcuhealth.org! Episodes | Subscribe | Spotify | Swag! | Top Picks | Mailing List | thecurbsiders@gmail.com | Free CME! Show Segments Intro, disclaimer, guest bios Guest one-liners, Introduction to Nephmadness 2022 Case #1 from Kashlak: acute decompensated heart failure with elevated creatinine Definition and pathophysiology of cardiorenal syndrome Use of home ACE-is/ARBs and SGLT-2 inhibitors in cardiorenal syndrome Case #2 from Kashlak: the creatinine bump with diuresis Approach to the creatinine bump with diuresis Tips for the volume exam Interpreting cardiac biomarkers in patients with chronic kidney disease Case #3 from Kashlak: diuretic resistance Maximizing loop diuretic efficacy Sequential nephron blockade Use of hypertonic saline Outro Credits Producer, Writer, Show Notes, Infographics: Malini Gandhi Cover Art:  Beth Garbitelli Hosts: Matthew Watto MD, FACP; Paul Williams MD, FACP    Reviewer: Emi Okamoto MD, FACP Executive Producer: Beth Garbitelli Showrunner: Matthew Watto MD, FACP Editor: Clair Morgan of nodderly.com Guest: Dr. Joel Topf MD, Dr. Sadiya Khan MD Sponsor: Beginly Health Ready to take control of your job search? Visit beginlyhealth.com/curbsiders to get started.  Sponsor: Locumstory Tune in to The Locumstory Podcast on Spotify, Apple, or Google podcasts. Sponsor: Freed You can try Freed for free right now by going to freed.ai. And listeners of Curbsiders can use code CURB50 for $50 off their first month.

CardioNerds Dr. Rick Ferraro, Dr. Gurleen Kaur, and Dr. Maryam Barkhordarian discuss the evidence and data supporting SGLT inhibition for cardiovascular and kidney health outcomes with expert faculty Dr. Muthu Vaduganathan. They discuss the role of SGLT inhibitors in different populations, including those with diabetes mellitus, heart failure, CKD, and myocardial infarction. Show notes and audio editing by CardioNerds Academy Fellow Dr. Maryam Barkhordarian. This episode was produced in collaboration with the American Society of Preventive Cardiology (ASPC) with independent medical education grant support from Lexicon Pharmaceuticals. CardioNerds Prevention PageCardioNerds Episode PageCardioNerds AcademyCardionerds Healy Honor Roll CardioNerds Journal ClubSubscribe to The Heartbeat Newsletter!Check out CardioNerds SWAG!Become a CardioNerds Patron! Pearls - The Data Supporting SGLT Inhibition with Dr. Muthiah Vaduganathan The benefit of SGLT inhibition extends beyond diabetes, and improves cardiovascular and kidney health outcomes independent of diabetes in appropriate patient populations. SGLT inhibition decreases cardiovascular mortality and heart failure hospitalization independent of left ventricular ejection fraction. SGLT inhibitors reduce clinically relevant events such as dialysis and transplantation in CKD patients irrespective of etiology and are now a cornerstone for the prevention of CKD progression. The introduction of polypills in heart failure can simplify GDMT implementation. Show notes - The Data Supporting SGLT Inhibition with Dr. Muthiah Vaduganathan How did SGLT inhibitors transition from “diabetes medication” to guideline-directed cardiovascular medicine? Most therapies in cardiology were developed for a particular purpose and ended up being indicated for a vastly different reason. The SGLT-2 inhibitors are no different. Cardiovascular safety concerns about diabetes medications led to a mandate to conduct cardiovascular outcomes trials for all novel diabetes medications. This federal requirement shed light on the cardiovascular benefits of SGLT inhibitors in patients with diabetes. These initial trials showed that not only are these medications safe but also, surprisingly, proved their role in preventing heart failure and delaying progression of chronic kidney disease. What are the mechanisms of action of SGLT-2 and SGLT-1/2 inhibitors? The central mechanism(s) of how these medications confer health outcomes benefits patients is/are not well understood. The main organ involved in the action of SGLT-2 inhibitors is the kidney at the level of the proximal tubule, impacting the cardiovascular system by handling salt and water and improving kidney efficiency. Conversely, SGLT-1/2 inhibitors also act at the level of the gut, the predominant location of the SGLT-1 cotransporter. Their effects on the cardiovascular system are secondary, given there is no SGLT-1 or -2 cotransporters in the myocardium. These secondary effects can be impacted through blood pressure reduction, volume regulation, improved glycemic control, etc. to overall improve cardiovascular status. Whatever the underlying mechanisms, the empirical data for their use is strong and growing. What is the role of SGLT inhibitors in preventing CKD progression? RAAS inhibitors (ACE inhibitors and ARBs) have been the cornerstone of CKD management for the past two to three decades. SGLT inhibitors have been the first add-on to this background therapy. Four trials, DAPA-CKD, EMPA-CKD, CREDENCE, and the SCORED, investigated the effects of SGLT-2 and SGLT-1/2 inhibitors in patients with CKD with or without diabetes. The outcomes of these trials include modifying the course of CKD and reducing events such as dialysis initiation and transplantation. These effects were regardless of participants' diabetic status, CKD etiology, or individual patient profile.

We're taking a short summer break, but we'll be back at the end of August with brand new episodes. Master common hypertension scenarios in the clinic! Our guest Dr. Jordy Cohen (@jordy_bc) will lead us through the FAQs of outpatient hypertension management, including making a diagnosis of hypertension, managing blood pressure in patients with chronic kidney disease, working up refractory hypertension, and more. Claim CME for this episode at curbsiders.vcuhealth.org! Credits ● Writer: Matthew Watto, MD, FACP ● Producers: Matthew Watto, MD, FACP and Malini Gandhi ● Show Notes, Infographic, and Cover Art: Malini Gandhi ● Hosts: Matthew Watto MD, FACP; Paul Williams MD, FACP ● Reviewer: Emi Okamoto MD ● Executive Producer: Beth Garbitelli ● Showrunner: Matthew Watto MD, FACP ● Editor: Clair Morgan of nodderly.com ● Guest: Jordy Cohen MD Show Segments ● Intro, disclaimer, guest bio ● Guest one-liner, Picks of the Week* ● Case from Kashlak: New diagnosis of hypertension ● How to make a diagnosis of hypertension ● When to start anti-hypertensive medication ● Initial blood pressure regimen ● Case from Kashlak: White coat hypertension ● Case from Kashlak: Hypertension in chronic kidney disease ● ACEis and ARBs in chronic kidney disease ● Diuretics in chronic kidney disease ● Case from Kashlak: Refractory hypertension ● History and initial workup for refractory hypertension ● Treatment of primary hyperaldosteronism ● Outro

N Engl J Med 2024;390:1372-1381Background: Beta-blockers are prescribed to the majority of patients with acute myocardial infarction. The bulk of evidence supporting this practice comes from trials published in the 1980s - BHAT and ISIS-I. Since the publication of these seminal trials, the care of patients with acute myocardial infarction has significantly changed with improvement in antiplatelet therapy, the addition of high-intensity statins and renin–angiotensin–aldosterone system antagonists in addition to early revascularization for STEMI patients. Furthermore, myocardial injury is now detected based on high-sensitivity troponin assays which can detect smaller myocardial infarctions. Therefore, there is a lack of evidence whether beta-blockers provide benefit for patients with acute myocardial infarction in the current era.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber.The Randomized Evaluation of Decreased Usage of Beta-Blockers after Acute Myocardial Infarction (REDUCE-AMI) trial sought to assess whether long-term oral beta-blocker treatment improves outcomes in patients with acute myocardial infarction and preserved left ventricular ejection fraction.Patients: Eligible patients were adults, 1 to 7 days after myocardial infarction who underwent coronary angiography and echocardiography. Patients were required to have obstructive coronary artery disease on coronary angiography defined as stenosis of ≥50%, a fractional flow reserve of ≤0.80, or an instantaneous wave-free ratio of ≤0.89 at any time point before randomization. Left ventricular Ejection fraction on echocardiogram had to be ≥50%. Patients were excluded if they had contraindications to beta-blockers or if the treating physician determined that treatment with beta-blockers is indicated for other conditions.Baseline characteristics: The trial randomized 2,508 patients to the beta-blockers group and 2,512 patients to the control group. The average age of patients was 65 years with 78% being men. About 20% were current smokers, 46% had hypertension, 14% had diabetes, 7% had prior myocardial infarction and < 1% had prior heart failure.The index event was STEMI in 35% of the patients. About 96% underwent percutaneous coronary intervention. The median heart rate was 74 bpm and the median systolic blood pressure was 151 mm Hg.Medications at discharge included aspirin in 97% of the patients, P2Y12 inhibitors in 96%, ACEi or ARBs in 80% and statins in 99%.Procedures: Patients were randomized 1:1 to receive metoprolol succinate (first choice), bisoprolol (second choice) or no beta-blockers. The target doses were at least 100 mg daily for metoprolol succinate and at least 5 mg daily for bisoprolol. Patients in the control group were discouraged from using beta-blockers; they did not receive placebo. If a patient was on beta-blocker therapy at the time of enrollment and was randomly assigned to the no–beta-blocker group, the beta-blocker had to tapered off over a period of 2 to 4 weeks.Endpoints: The primary end point was a composite of death from any cause or new myocardial infarction. Secondary end points were death from any cause, death from cardiovascular causes, myocardial infarction, hospitalization for atrial fibrillation as primary diagnosis, and heart failure hospitalization. There were three safety endpoints: 1- Hospitalization for bradycardia, second- or third-degree atrioventricular block, hypotension, syncope, or implantation of a pacemaker, 2- hospitalization for asthma or chronic obstructive pulmonary disease as a primary diagnosis and 3- hospitalization for stroke.Data on clinical end points were not centrally adjudicated but rather obtained from the SWEDEHEART registry and the Swedish Population Registry.Statistical analysis was performed based on the intention-to-treat principle. Before trial initiation, the estimated event rate in the control group was 7.2%/ year and at least 16.7% lower event rate in the beta-blocker group was considered clinically meaningful. During the trial, the actual event rate in control group was 3%/ year. Given this event rate, a 25% lower event rate in the beta-blocker group was considered clinically meaningful. A total of 379 primary end point events were needed in order to have 80% power at a two-sided alpha of 0.05, to detect the 25% lower event rate with beta-blockers. The estimated number of patients needed was about 5,000.Results: Among the patients who attended the SWEDEHEART registry, 1500/1831 (81.9%) of the beta-blocker group were still taking beta-blockers after 11 to 13 months; compared to 269/ 1886 (14.3%) in the no beta-blocker group.After a median follow up time of 3.5 years, beta-blockers did not the reduce the composite primary endpoint compared to no beta-blockers (7.9% vs 8.3%, HR: 0.96; 95% CI, 0.79 - 1.16; p= 0.64). There were no significant differences in death from any cause (3.9% vs 4.1%), death from cardiovascular causes (1.5% vs 1.3%), myocardial infarction (4.5% vs 4.7%), hospitalization for atrial fibrillation (1.1% vs 1.4%) or hospitalization for heart failure (0.8% vs 0.9%).Safety endpoints were also not significantly different between both groups; 3.4% vs 3.2% for the bradyarrhythmia, syncope or hypotension endpoint, 0.6% in both groups for the hospitalization for asthma or COPD endpoint and 1.4% vs 1.8% for hospitalization for stroke.There were no significant subgroup interactions.Conclusion: In patients with acute myocardial infarction who underwent coronary angiography and had preserved left ventricular systolic function, treatment with beta-blockers did not improve outcomes over a 3.5-year follow-up. Events were infrequent in the trial; 1.4% for cardiovascular death, 4.6% for recurrent myocardial infarction and 0.8% for hospitalization for heart failure. The low event rate in this population in the current era makes it difficult to demonstrate additional benefit with more therapies.The open-label design of the study may have introduced performance bias; however, this bias is expected to favor beta-blockers given the superiority design of the study. Another limitation, as noted by the authors, is that outcomes were obtained from the SWEDEHEART registry and the Swedish Population Registry and were not centrally adjudicated. However, this is expected to affect both groups equally.We believe the divergent results between this trial and older beta-blocker trials in myocardial infarction patients such as BHAT and ISIS-1 which were published in the 1980s, is due to the significant improvement in the management of acute myocardial infarction over time including improved medical therapy in addition to early revascularization for STEMI patients. This improved patient care has led to significantly lower mortality rates over time. For instance, all-cause death in the control arm of REDUCE-AMI is significantly lower than that of BHAT and ISIS-1, at 4.1% vs 9.8% and 11.9%, respectively. This is despite REDUCE-AMI having a longer follow-up period of 3.5 years compared to 2.1 years and 1 year in the earlier trials.In conclusion, this study does not provide evidence that beta-blockers improve outcomes for patients with acute myocardial infarction and preserved ejection fraction in the contemporary era.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support my work, consider becoming a free or paid subscriber. Get full access to Cardiology Trial's Substack at cardiologytrials.substack.com/subscribe

NEJM 2021:385:1845-55.Background Over two decades had passed since the publications of the seminal trials comparing ACE inhibitors with placebo in post-MI patients with LV dysfunction and congestive heart failure (SAVE, AIRE and TRACE). The VALIANT trial, published in 2003, found that the ARB drug Valsartan was as effective as Captopril in improving survival and reducing cardiovascular morbidity in this patient population. Thus, for many years, a cornerstone of managing post-MI patients with LV dysfunction and heart failure involved afterload reduction with ACE inhibitors or ARBs.Then in 2014, the landscape of heart failure management changed with the publication of the PARADIGM-HF trial which found that Entresto, a drug combining the ARB Valsartan and the neprilysin inhibitor Sacubitril, significantly reduced death and heart failure hospitalizations. We will review PARDIGM-HF later since it enrolled patients with chronic, stable heart failure and not post-MI patients. The rationale for the combination drug is that it simultaneously blocks the renin-angiotensin system and inhibits of the breakdown of several vasoactive peptides including atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP), serving to enhance vasodilation and reduce blood volume.The PARADISE-MI trial sought to test the hypothesis that early initiation of Sacubitril-Valsartan in post-MI patients with LV dysfunction and congestive heart failure would reduce cardiovascular death or incident heart failure compared to the ACE inhibitor Ramipril.Cardiology Trial's Substack is a reader-supported publication. To receive new posts and support our work, consider becoming a free or paid subscriber.Patients Adults without a history of heart failure who had a spontaneous MI within 0.5 to 7 days before presentation who had either a LVEF of /= 70 years, diabetes, previous MI, eGFR

Arbs for Blood Pressure? Favorite Foods to Carb Up, Highest Protein Per Meal? Favorite Foods For Contest Carb Up? TIME STAMPS BELOW Coaches Skip Hill, Andrew Berry, Scott McNally - Blood Sweat & Gear Coaching QA 245

In this episode, I divide losartan and Cozaar into syllables, tell you which syllables to emphasize, and share my sources. The written pronunciations can be helpful, so you can see them below and in the show notes on thepharmacistsvoice.com.   The purpose of my pronunciation episodes is to provide the intended pronunciations of drug names from reliable sources so you feel more confident saying them and less frustrated learning them.    Losartan = loe-SAR-tan, emphasize SAR (source: USP Dictionary Online)   Cozaar = CO-zar, emphasize CO (patient information on Organon's website)   If you know someone who needs to learn how to say losartan and Cozaar, please share this episode with them. Subscribe to/follow this podcast for all future episodes.    Thank you for listening to episode 272 of The Pharmacist's Voice ® Podcast!   To read the FULL show notes, visit https://www.thepharmacistsvoice.com.  Click the Podcast tab, and select episode 272.   Subscribe to or follow The Pharmacist's Voice ® Podcast to get each new episode delivered to your podcast player and YouTube every time a new one comes out!     Apple Podcasts   https://apple.co/42yqXOG  Spotify  https://spoti.fi/3qAk3uY  Amazon/Audible  https://adbl.co/43tM45P YouTube https://bit.ly/43Rnrjt   Links from this episode USP Dictionary Online (aka “USAN”)  **Subscription-based resource USP Dictionary's (USAN) pronunciation guide (Free resource on the American Medical Association's website) Patient Information for Cozaar ® via Organon's website accessed April 1, 2024 The Pharmacist's Voice Podcast Episode 269, pronunciation series episode 28 (tirzepatide) The Pharmacist's Voice Podcast Episode 267, pronunciation series episode 27 (atorvastatin)  The Pharmacist's Voice Podcast Episode 265, pronunciation series episode 26 (omeprazole) The Pharmacist's Voice Podcast Episode 263, pronunciation series episode 25 (PDE-5 inhibitors) The Pharmacist's Voice Podcast Episode 259, pronunciation series episode 24 (ketorolac) The Pharmacist's Voice ® Podcast episode 254, pronunciation series episode 23 (Paxlovid) The Pharmacist's Voice ® Podcast episode 250, pronunciation series episode 22 (metformin/Glucophage) The Pharmacist's Voice Podcast ® episode 245, pronunciation series episode 21 (naltrexone/Vivitrol) The Pharmacist's Voice ® Podcast episode 240, pronunciation series episode 20 (levalbuterol) The Pharmacist's Voice ® Podcast episode 236, pronunciation series episode 19 (phentermine)  The Pharmacist's Voice ® Podcast episode 228, pronunciation series episode 18 (ezetimibe) The Pharmacist's Voice ® Podcast episode 219, pronunciation series episode 17 (semaglutide) The Pharmacist's Voice ® Podcast episode 215, pronunciation series episode 16 (mifepristone and misoprostol) The Pharmacist's Voice ® Podcast episode 211, pronunciation series episode 15 (Humira®) The Pharmacist's Voice ® Podcast episode 202, pronunciation series episode 14 (SMZ-TMP) The Pharmacist's Voice ® Podcast episode 198, pronunciation series episode 13 (carisoprodol) The Pharmacist's Voice ® Podcast episode 194, pronunciation series episode 12 (tianeptine) The Pharmacist's Voice ® Podcast episode 188, pronunciation series episode 11 (insulin icodec)  The Pharmacist's Voice ® Podcast episode 184, pronunciation series episode 10 (phenytoin and isotretinoin) The Pharmacist's Voice ® Podcast episode 180, pronunciation series episode 9 Apretude® (cabotegravir) The Pharmacist's Voice ® Podcast episode 177, pronunciation series episode 8 (metoprolol)  The Pharmacist's Voice ® Podcast episode 164, pronunciation series episode 7 (levetiracetam) The Pharmacist's Voice ® Podcast episode 159, pronunciation series episode 6 (talimogene laherparepvec or T-VEC)  The Pharmacist's Voice ® Podcast episode 155, pronunciation series episode 5 Trulicity® (dulaglutide)  The Pharmacist's Voice ® Podcast episode 148, pronunciation series episode 4 Besponsa® (inotuzumab ozogamicin) The Pharmacist's Voice ® Podcast episode 142, pronunciation series episode 3 Zolmitriptan and Zokinvy The Pharmacist's Voice ® Podcast episode 138, pronunciation series episode 2 Molnupiravir and Taltz The Pharmacist's Voice ® Podcast episode 134, pronunciation series episode 1 Eszopiclone and Qulipta

On this podcast episode, I discuss some of the most common antihypertensive drug interactions you need to know. One major interaction I discuss is the trifecta of a diuretic, an ACE or ARB, and an NSAID. This combination significantly increases the risk for acute renal failure. Nitrates aren't classically referred to as an antihypertensive but they can definitely cause some problems when combined with PDE5 Inhibitors. Lithium can interact with 3 blood pressure medication classes. ACEIs, ARBs, and diuretics can all increase the risk for lithium toxicity.

Special guest Luke Laffin, MD, FACC, the Co-Director, Center for Blood Pressure Disorders with the Department of Cardiovascular Medicine at the Cleveland Clinic joins us to talkabout first-line meds for hypertension.Listen in as they discuss nuances regarding selection of a first-line medication for the treatment of hypertension.You'll also hear practical advice from panelists on TRC's Editorial Advisory Board:Andrea Darby Stewart, MD, Associate Director, Honor Health Family Medicine Residency Program and Clinical Professor of Family, Community & Occupational Medicine at the University of Arizona College of Medicine - PhoenixDouglas S. Paauw, MD, MACP, Professor of Medicine at the University of Washington School of MedicineFor the purposes of disclosure, Dr. Luke Laffin reports relevant financial relationships with CRISPR Therapeutics [hyperlipidemia], Eli Lilly [obesity], Medtronic [hypertension] (honorarium); Arrowhead [hyperlipidemia], AstraZeneca [hyperlipidemia], Mineralys Therapeutics [hypertension] (grants/research support).The other speakers have nothing to disclose. All relevant financial relationships have been mitigated.TRC Healthcare offers CE credit for this podcast. Log in to your Pharmacist's Letter or Prescriber Insights account and look for the title of this podcast in the list of available CE courses.The clinical resources mentioned during the podcast are part of a subscription to Pharmacist's Letter and Prescriber Insights: Chart: Treatment of HypertensionChart: Angiotensin Receptor Blockers and Angiotensin-Converting Enzyme InhibitorsChart: Comparison of Calcium Channel BlockersChart: Comparison of Commonly Used DiureticsIf you're not yet a Pharmacist's Letter or Prescriber Insights subscriber, find out more about our product offerings at trchealthcare.com. Follow or subscribe, rate, and review this show in your favorite podcast app. You can also reach out to provide feedback or make suggestions by emailing us at ContactUs@trchealthcare.com.

Episode 154: Heart Failure and GDMTDr. Malave explains the four main medications that are part of the guideline-directed medical therapy of heart failure with reduced ejection fraction. Dr. Arreaza added comments and questions.  Written by Maria Fernanda Malave, MD. Edits by Hector Arreaza, MD.  You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.Brief introduction: Heart failure (HF) is a common condition that affects about 23 million people in the world, and it is estimated that 50% of cases are due to heart failure with reduced ejection fraction (HFrEF). It is a major public health concern because of the high morbidity and mortality with a 5-year survival rate of 25% after hospitalization due to HFrEF.In recent years, the management of HFrEF has evolved due to increased evidence in favor of certain medications. Guideline-directed medical therapy (GDMT) is the foundation of medical therapy for these patients, and it is the result of multiple randomized controlled trials and reviews favoring four main drug classes: 1. renin-angiotensin system inhibitors (angiotensin-converting enzyme inhibitors -ACEi- and angiotensin receptor blockers -ARB), 2. evidence-based β-blockers, 3. mineralocorticoid inhibitors, and 4. sodium-glucose cotransporter 2 inhibitors -SGLT-2i-. The benefit of this therapy is mostly seen when these four groups of medications are used in conjunction. During this episode, we will provide some key elements about the prescription of these medications, but this is only an overview, and you are invited to continue learning from reputable sources.Definitions: HF is defined as the impairment of the heart to meet the metabolic demands of the body. It can be caused by multiple conditions that interfere with the filling up of the heart or conditions that prevent an effective ejection of blood out of the heart. Classification of HFrEF: Based on the EF by echocardiogram, heart failure can be classified as:Heart failure with preserved ejection fraction (HFpEF) when the EF is 50% or more.Heart failure with mildly reduced ejection fraction when EF ranges between 41-49%.Heart failure with reduced ejection fraction (HFrEF) when EF is 40% or less.GDMT: Once we make the diagnosis of HF, it is key to educate our patients and re-educate them every single visit about the importance of guideline-directed medical therapy (GDMT) and lifestyle modifications, because this can change the prognosis and exacerbation rates. Many patients think that since they are feeling well after starting GDMT they can stop it, but that's going to increase exacerbations, hospitalizations, and decrease quality of life. Key points to discuss with patients.First, discuss that GDMT are disease-modifying drugs that regulate the neurohormonal system to stop the progression of the disease. We should explain to our patients that medications should be taken despite feeling well. Also, patients should be educated about regular follow-ups and medication titration. We can even instruct our patients about increasing their furosemide dose if they observe signs of overload, such as a weight increase of 2-3 kgs in 3-4 days, tight rings, socks or bracelets, also Paroxysmal nocturnal dyspnea, dyspnea on exertion, and more.  Second, lifestyle modifications such as: quit smoking and alcohol. Additionally, in general, water restriction between 1.2-1.5L daily, salt restriction (there is no official recommendation about how many grams, but in general we recommend less than 2g daily). Third, it is highly recommended to do aerobic exercise that produces mild dyspnea since this improves cardiovascular capacity and decreases hospitalization risk. Patients should be encouraged to have their annual influenza vaccine and pneumococcal vaccine according to their own immunization schedule. According to the AFP journal, in September 2022, researchers found a clinically and statistically significant reduction in all-cause mortality for patients who received an influenza vaccine right after an MI, with a number needed to treat of 50, the effectivity of the vaccine may vary by season.GDMT, groups of medications:What are the basic medications any patient with HF should be on? At least, patients should be on angiotensin receptor blockers ARBs/ACEIs and Beta-blockers. Let's keep in mind that beta-blockers should be given cautiously in cases of exacerbation, but in general low doses are safe. We also have the angiotensin receptor/neprilysin inhibitors (ARNIs), a group of medications whose representative is the combination of sacubitril/valsartan, aka Entresto®. This medication should be the target once ARBs/ACEIs are tolerated. ARBs/ACEIs/ARNIs should be discontinued in the setting of advanced CKD, with a GFR of 30 or less. This applies to other medications used in HF such as SGLT-2 and mineralocorticoid receptor antagonist (MRA, such as spironolactone/eplerenone). Remember that SGLT-2 inhibitors should be started regardless diabetes status, and BB are safe in the setting of CKD. We also have other groups that are considered safe in patients with advanced CKD such as hydralazine/isosorbide dinitrate (combined or not), which are used in African Americans whose BP and HF symptoms do not improve with maximally tolerated dose of ARBs/ACEIs + BB.Ivabradine: Let's not forget about ivabradine, which is an SA node inhibitor like BB. Patients need to meet criteria such as a maximally tolerated dose of beta-blocker, heart rate of a least 70 or more and being on normal sinus rhythm to be started on this medication. Ivabradine does not improve survival as BB do, so even though they are not contraindicated in HF exacerbation, BB are still preferred since ivabradine does not decrease mortality.Titration and follow-ups in the HF management:-ARBs/ACEIs/ARNIs should be titrated approx. Q2 weeks until the maximally tolerated dose is achieved, ARNI should be titrated up Q2-4weeks. With these medications, we should monitor BP, potassium levels and Glomerular Filtration Rate (GFR). -BB can also be titrated up Q2weeks until the maximally tolerated dose is achieved. HR, BP and signs of congestion should be observed in patients on BB. Same for hydralazine/isosorbide, with BP follow-up. -MRA, such as spironolactone/eplerenone, these meds can be added in patients who remain symptomatic despite maximally tolerated doses of “ARBs or ACEIs or ARNIs” plus Beta-blockers. For MRA, potassium level, and GFR should be monitored every 2-3 days after initiation, 7 days after titration, monthly for 3 months, and then Q3 months. To start a patient on MRA, K+ must be lower than 5.Patients with HF should be followed up at least in a 2-week interval either via telephone, telemedicine, or clinic visit to assess symptoms, vital signs, bloodwork and to perform a physical exam. Monitoring EF: After 3-6 months of the patient´s stabilization, we should reorder an echo, EKG, BNP and Basic Metabolic Panel. The ejection fraction improves in all patients after GDMT initiation and compliance, and in some patients, this improvement is very significant, so we need to reassess EF after stabilization. Comorbidities: Also, let´s keep in mind that most of the patients have associated comorbidities such as Afib, diabetes, valve disease, or anemia. These comorbidities must be addressed either by starting anticoagulation, adjusting anti-diabetes medications, starting iron, or referring to cardiology if a valve replacement is needed.When to refer to Cardiology? Some patients will qualify for device therapy (ICD) as a primary prevention for ventricular arrhythmias that can degenerate either into torsades or ventricular fibrillation. These patients must be symptomatic, at least in 3 months of maximally tolerated GDMT, and EF between 30-35%. Symptomatic

On this episode, I discuss aliskiren pharmacology, adverse effects, drug interactions, and much more. Aliskiren should not be used with ACE Inhibitors or ARBs. I discuss why that is in this episode. Aliskiren has a long enough half-life at approximately 24 hours so it is recommended to only take this once daily. Hyperkalemia is a major concern with aliskiren. It is important to monitor potassium levels and renal function.

Injectable, long-acting therapy is a new frontier for hypertension management. Join host, Geoff Wall, as he evaluates zilebesiran, a hepatic angiotensinogen blocker for blood pressure control for up to six months. The GameChangerZilebesiran blocks the final production of angiotensinogen at the hepatic level making it safer from a renal perspective than the ACEis or ARBs. A single subcutaneous injection provides therapy for up to six months. HostGeoff Wall, PharmD, BCPS, FCCP, BCGPProfessor of Pharmacy Practice, Drake UniversityInternal Medicine/Critical Care, UnityPoint Health ReferenceDesai AS, Webb DJ, Taubel J, et al. Zilebesiran, an RNA Interference Therapeutic Agent for Hypertension. N Engl J Med. 2023 Jul 20;389(3):228-238. doi: 10.1056/NEJMoa2208391. PMID: 37467498.https://www.nejm.org/doi/full/10.1056/NEJMoa2208391 Pharmacist Members, REDEEM YOUR CPE HERE! Not a member? Get a Pharmacist Membership & earn CE for GameChangers Podcast episodes! (30 mins/episode)CPE Information Learning ObjectivesUpon successful completion of this knowledge-based activity, participants should be able to:1. Describe the mechanism of action of Zilebesiran2. Discuss possible advantages and disadvantages of this drug in the treatment of hypertension0.05 CEU/0.5 HrUAN: 0107-0000-23-323-H01-PInitial release date: 10/16 /2023Expiration date: 10/16/2024Additional CPE details can be found here.Follow CEimpact on Social Media:LinkedInInstagramDownload the CEimpact App for Free Continuing Education + so much more!

We're taking a short summer break, but we'll be back in September with brand-new episodes. Can't wait? Join our Kashlak family at patreon.com/curbsiders for access to twice-monthly bonus episodes… there are already 9 of them available to feed your brain hole! Yummy! Master common hypertension scenarios in the clinic! Our guest Dr. Jordy Cohen (@jordy_bc) will lead us through the FAQs of outpatient hypertension management, including making a diagnosis of hypertension, managing blood pressure in patients with chronic kidney disease, working up refractory hypertension, and more. Free CME for this episode at curbsiders.vcuhealth.org Patreon | Episodes | Subscribe | Spotify | YouTube | Newsletter | Contact | Swag! | CME Credits Writer: Matthew Watto, MD, FACP Producers: Matthew Watto, MD, FACP and Malini Gandhi Show Notes, Infographic, and Cover Art: Malini Gandhi Hosts: Matthew Watto MD, FACP; Paul Williams MD, FACP    Reviewer: Emi Okamoto MD Executive Producer: Beth Garbitelli Showrunner: Matthew Watto MD, FACP Editor: Clair Morgan of nodderly.com Guest: Jordy Cohen MD CME Partner: VCU Health CE The Curbsiders are partnering with VCU Health Continuing Education to offer FREE continuing education credits for physicians and other healthcare professionals. Visit curbsiders.vcuhealth.org and search for this episode to claim credit. See info sheet for further directions. Note: A free VCU Health CloudCME account is required in order to seek credit. Show Segments Intro, disclaimer, guest bio Guest one-liner, Picks of the Week* Case from Kashlak: New diagnosis of hypertension How to make a diagnosis of hypertension When to start anti-hypertensive medication Initial blood pressure regimen Case from Kashlak: White coat hypertension Case from Kashlak: Hypertension in chronic kidney disease ACEis and ARBs in chronic kidney disease Diuretics in chronic kidney disease Case from Kashlak: Refractory hypertension History and initial workup for refractory hypertension Treatment of primary hyperaldosteronism Outro Sponsor: Green Chef Go to GreenChef.com/60curb and use code 60curb to get 60% off plus free shipping.

Dette afsnit er en liveoptagelse fra Empire Bio, hvor vi talte om og så Barry Jenkins' prisvindende fænomenale film fra 2016, Moonlight. Dramaet 'Moonlight' er historien om den unge mand, Chiron, fortalt gennem tre definerende nedslag: barndom, ungdom og voksenliv. Fra en ludfattig barndom med grov mobning og en opvækst, hvor vold og spørgsmål om seksualitet presser sig på til et voksenliv, hvor han må genforhandle sin identitet og tage ejerskab over sit eget liv.'Moonlight' er skrevet og instrueret af Barry Jenkins. Han vandt en Oscar for bedste adapterede manuskript, og selve filmen modtog den prestigefyldt Oscar for bedste film i 2017.Til at snakke om Moonlight har vi inviteret to überseje film-professionelle og yderst kyndige typer med os i dag: Elombe brice Parfait & Kristian Arbs. Vi taler blandt andet om, hvordan Moonlight især blev fremhævet for måden den formåede at hæve sig over den stereotypiserende skildring af både tilværelsen i det amerikanske ghetto og en kærlighedsrelation mellem to sorte mænd. En skildring, der er båret af en særdeles fremragende, nærværende og levende skuespilpræstation. Har I set Moonlight, og hvad har gjort særligt indtryk hos jer?

The Kidney Disease: Improving Global Outcomes (KDIGO) guidelines were recently updated with a focus on kidney health in patients with diabetes.  The updated guidelines include recommendations on screening, prevention, and treatment of chronic kidney disease (CKD), including the use of SGLT2 inhibitors, finerenone, and ACE inhibitors or ARBs.  The written commentary posted on the iForumRx website provides a succinct summary of the Top Ten Things Every Clinician Should Know. Guest Authors:  Kara Olstad, PharmD; Gurminder Sanghera, BSc, PharmD; and Darren Grabe, PharmD Music by Good Talk

In this episode we explore ways in which the extracellular matrix can be manipulated, including the story of doxycycline, TGF-beta in Marfan syndrome and whether beta blockers can reduce vascular events in vascular EDS. ·        Intro 0:12 ·        Review of previous episode 0:28 ·        In this episode 2:26 ·        The pressure against the vessels 4:06 ·        The pressure against the wall 8:44 ·        Matrix metalloproteinases 10:16 ·        Tadpole study – collagen breakdown 10:35 ·        Tetracycline antibiotics 14:05 ·        Rat model – periodontal disease and hydroxyproline 14:24 ·        Chemically modified tetracyclines 20:14 ·        Mouse model – tetracycline use 22:00 ·        Tetracyclines and other autoimmune conditions 23:22 ·        Marfan syndrome 24:45 ·        Fibrillin and Marfan syndrome 28:48 ·        TGF-beta 29:36 ·        Mouse model – Marfan syndrome and fibrillin 31:14 ·        ARBs and TGF-beta 33:51 ·        TGF-beta and vascular EDS 37:25 ·        Back to the mouse model 38:38 ·        Protein kinase C 39:56 ·        Summary 40:26 Disclosures: Brown reports no relevant financial disclosures. We'd love to hear from you! Send your comments/questions to Dr. Brown at rheuminationspodcast@healio.com. Follow us on Twitter @HRheuminations @AdamJBrownMD @HealioRheum. References: Bowen CJ, et al. J Clin Invest. 2020;130:686-698. Brooke BS. Lancet. 2010;doi:10.1016/S0140-6736(10)61155-5 Dietz HC, et al. Am J Med Genet C Semin Med Genet. 2005;doi:10.1002/ajmg.c.30068. Dubacher N, et al. Cardiovasc Res. 2020;116:457-465. Golub LM, et al. SAGE. 1998;doi:10.1177/08959374980120010501. Gross J, et al. PNAS. 1962;doi:10.1073/pnas.48.6.1014 Habashi JP, et al. Science. 2006;312:117-121. Morissette R, et al. Circ Cardiovasc Genet. 2014;7:80-88. Mullen M, et al. Lancet. 2019;394:2263-2270. Neptune ER, et al. Nat Genet. 2003;33:407-411.

On this episode, I discuss indapamide pharmacology, adverse effects, drug interactions, and pharmacokinetics. I discuss how indapamide differs from other thiazide diuretics. Particularly, I discuss indapamide compared to hydrochlorothiazide. Frequent urination, hypokalemia, and dehydration are all possible risks with indapamide. Pay attention to medications that can increase the risk for acute renal failure when added to indapamide. NSAIDs, ACEIs, ARBs, and other diuretics can increase this risk.

On this podcast episode, I discuss valsartan pharmacology, adverse effects, drug interactions, and much more. Valsartan is a fairly common ARB. I mostly see losartan and valsartan used as the most common ARBs in hypertension management. Valsartan has a longer half-life than losartan which is why we can often get away with once daily dosing compared to losartan which sometimes requires twice daily. Hyperkalemia is a major concern with ARBs like valsartan. Trimethoprim and spironolactone are two medications that can increase this risk.

Robert Lefkowitz: A Funny Thing Happened on the Way to Stockholm Robert Lefkowitz is James B. Duke Professor of Medicine and Professor of Biochemistry and Chemistry at the Duke University Medical Center. His group spent 15 difficult years developing techniques for labeling the receptors with radioactive drugs and then purifying the four different receptors that were known and thought to exist for adrenaline. In 1986 Bob and his team transformed the understanding of what had become known as G protein coupled receptors, when he and his colleagues cloned the gene for the beta2-adrenergic receptor. Today, more than half of all prescription drug sales are of drugs that target either directly or indirectly the receptors discovered by Bob and his trainees. These include amongst many others beta blockers, angiotensin receptor blockers or ARBs and antihistamines. He has received numerous honors and awards, including the National Medal of Science, the Shaw Prize, the Albany Prize, and the 2012 Nobel Prize in Chemistry. He was elected to the National Academy of Sciences, the Institute of Medicine, and the American Academy of Arts and Sciences. He is the author with Randy Hall of A Funny Thing Happened on the Way to Stockholm: The Adrenaline Fueled Adventures of an Accidental Scientist. In this conversation, Bob and I explore the important nature of mentoring in his success — and how he has in turn utilized mentoring to support so many colleagues and students. We discuss the importance of building careers around problems versus techniques and other key principles that effective mentors adopt. Plus, we explore the key of ownership of work and using fun as an indicator to follow. Key Points Success is rarely accidental. Most people with extraordinary accomplishments had outstanding mentors along the way. Teach people to build their careers around problems, not techniques. The crucial job of a mentor is to keep things in focus for the person you are mentoring — both in their current work and their careers. People achieve the most motivation when they have ownership over their work. A key measure of striking the right guidance between ownership and guidance is whether or not everybody is having fun. Resources Mentioned A Funny Thing Happened on the Way to Stockholm: The Adrenaline Fueled Adventures of an Accidental Scientist* by Robert Lefkowitz Interview Notes Download my interview notes in PDF format (free membership required). Related Episodes What You Gain By Sponsoring People, with Julia Taylor Kennedy (episode 398) How to Know What You Don't Know, with Art Markman (episode 437) How to Lead and Retain High Performers, with Ruth Gotian (episode 567) Discover More Activate your free membership for full access to the entire library of interviews since 2011, searchable by topic.

Canagliflozin is an SGLT2 inhibitor. I discuss the pharmacology, dosing, adverse effects, and drug interactions of this medication. Canagliflozin reduces blood sugar, by facilitating its exit through the urine. This can increase the risk of genitourinary infections. A diuresis type effect can happen due to canagliflozin and this effect may be exacerbated by the use of thiazide and loop diuretics. Hyperkalemia has been reported with the use of canagliflozin; the risk for this is increased with the use of medications like ACE inhibitors, ARBs, and aldosterone antagonists.

How do you counsel patients on beta blockers? Is one beta-blocker better than the other? What is preferred: ACEi, ARBs or ARNIs? What are the pros and cons of each? How does spironolactone compare to eplerenone? When do you stop mineralocorticoid receptor antagonist? What are risks with SGLT2 inhibitors? How do you initiate GDMT? Which meds do you start first and in what order?Show notes, Transcript and References:  https://www.coreimpodcast.com/2022/05/11/5-pearls-on-guideline-directed-medical-therapy/Sponsor: https://go.amboss.com/GDMTGet CME-MOC credit with ACP: https://www.acponline.org/cme-moc/cme/internal-medicine-podcasts/core-im Time stamps:03:13 Pearl 112:14 Pearl 220:36 Pearl 326:42 Pearl 432:16 Pearl 5Tags: IM Core, CoreIM, heart failure with reduced ejection fraction, GDMT, treatment, cardiology

In this episode, we review new updates and key concepts from the 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure. This guideline is newly published (April 2022) and is a full update of the 2013 guidelines and the 2017 focused update for heart failure. Key Concepts Heart failure is classified as HFrEF (heart failure with reduced ejection fraction = 50% with increased LV filling pressures). Most drug therapy recommendations are similar for HFrEF, HFimpEF, and HFmrEF whereas HFpEF therapies are different. The 2022 AHA/ACC/HFSA heart failure guidelines now recommend SGLT2 inhibitors, such as dapagliflozin and empagliflozin, in patients with HFrEF, HFmrEF, and HFpEF. The 2022 AHA/ACC/HFSA heart failure guidelines continue to prefer ARNi, such as sacubitril/valsartan (Entresto), over ACE inhibitors and ARBs in patients with HFrEF. Based on the PARAGON-HF trial, ARNi is also recommended in those with HFpEF albeit with a weak recommendation. Avoiding excessive dietary sodium is reasonable to reduce congestive symptoms in patients with heart failure; however, guidelines do not recommend a specific maximum intake nor does data support clinical outcome benefit with dietary sodium restriction. References Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA Guideline for the Management of Heart Failure: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines [published online ahead of print, 2022 Apr 1]. Circulation. 2022;101161CIR0000000000001063. doi:10.1161/CIR.0000000000001063. https://www.ahajournals.org/doi/10.1161/CIR.0000000000001063 Ezekowitz JA, Colin-Ramirez E, Ross H, et al. Reduction of dietary sodium to less than 100 mmol in heart failure (SODIUM-HF): an international, open-label, randomised, controlled trial. Lancet. 2022;399(10333):1391-1400. doi:10.1016/S0140-6736(22)00369-5

Lose your heart to NephMadness 2022! Dr. Joel Topf (@kidney_boy) and Dr. Sadiya Khan (@HeartDocSadiya) tackle the NephMadness 2022 Cardiorenal Syndrome region, leading us through the pathophysiology of cardiorenal syndrome, how to approach the creatinine “bump” with diuresis, managing patients with diuretic resistance, and more. *Claim free CME for this episode at curbsiders.vcuhealth.org! *Available within 24 hours of release. Episodes | Subscribe | Spotify | Swag! | Top Picks | Mailing List | thecurbsiders@gmail.com | Free CME! Credits Producer, Writer, Show Notes, Infographics: Malini Gandhi Cover Art:  Beth Garbitelli Hosts: Matthew Watto MD, FACP; Paul Williams MD, FACP    Reviewer: Emi Okamoto MD, FACP Executive Producer: Beth Garbitelli Showrunner: Matthew Watto MD, FACP Editor: Clair Morgan of nodderly.com Guest: Dr. Joel Topf MD, Dr. Sadiya Khan MD Sponsor: ACP's Internal Medicine Board Review The Greater Chicago course, beginning on May 23rd  through May 27th     or Washington, D.C., on July 11th through July 15th New registrants will receive 6 months of access to the course recordings. Visit acponline.org/imbr2022 to register or learn more. Sponsor: SquareSpace Go to Squarespace.com for a free trial, and when you're ready to launch, go to squarespace.com/Curb to save 10% off your first purchase of a website or domain. Sponsor: Green Chef Go to GreenChef.com/curb130 and use code curb130 to get $130 off, plus free shipping! Sponsor: Masterworks Masterworks is giving listeners priority access to their newest offerings. Just head to masterworks.art/curbsiders  CME Partner: VCU Health CE The Curbsiders are partnering with VCU Health Continuing Education to offer FREE continuing education credits for physicians and other healthcare professionals. Visit curbsiders.vcuhealth.org and search for this episode to claim credit.  Show Segments Intro, disclaimer, guest bios Guest one-liners, Introduction to Nephmadness 2022 Case #1 from Kashlak: acute decompensated heart failure with elevated creatinine Definition and pathophysiology of cardiorenal syndrome Use of home ACE-is/ARBs and SGLT-2 inhibitors in cardiorenal syndrome Case #2 from Kashlak: the creatinine bump with diuresis Approach to the creatinine bump with diuresis Tips for the volume exam Interpreting cardiac biomarkers in patients with chronic kidney disease Case #3 from Kashlak: diuretic resistance Maximizing loop diuretic efficacy Sequential nephron blockade Use of hypertonic saline Outro