Rio Bravo qWeek

Rio Bravo Family Medicine Residency Program
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  • MEDICINE
  • UPDATED BIWEEKLY

qWeek is the official podcast of the Rio Bravo Family Medicine Residency Program. Residents and faculty routinely present key topics and relevant discussions, coupled with medical jokes and Spanish medical terminology.

  1. Episode 214: Valley Fever Complications

    12H AGO

    Episode 214: Valley Fever Complications

    Episode 214: Valley Fever Complications. Dr. Arreaza:
Welcome back to the podcast. I’m Dr. Arreaza, and today we’re talking about a topic that’s very relevant here in the Central Valley but often not well known in the rest of the country, it is called ValleyFever, or coccidioidomycosis. For more info about the Valley Fever diagnosis and initial treatment, please go to our previous podcast on the subject! Episode 143, recorded by wonderful Dr. Lovedip Kooner.  To help us walk through this, I’m joined by Jordan, a medical student. Jordan, welcome back and Dr. Schlaerth, please introduce yourself.  Jordan:
Thanks, Dr. Arreaza. This is such an important topic, especially in endemic areas like where we live, the Central Valley of California, and Arizona. The public may think of Valley Fever as a mild pneumonia that just goes away eventually. But that’s not always the case. Some patients develop serious, life-altering complications, and a small but important number develop disseminated disease. Dr. Arreaza:
Exactly. So today, we’re going to break this down systematically: pulmonary complications, dissemination to other organs, CNS disease, musculoskeletal involvement, systemic symptoms, and then we’ll touch on treatment principles and why follow-up matters so much. Dr. Schlaerth: Valley Fever can be missed in areas where it is not as common as in the Valley. 1989, earthquake in LA.Pneumonias that is not responding to treatment can be pulmonary cocci. Dr. Arreaza:
Before we dive into specific complications, let’s zoom out. What percentage of patients get a complicated disease? Jordan:
So, most infections are self-limited, but about 5–10% of patients develop chronic or progressive pulmonary disease, and 1% develop extrapulmonary disseminated disease. That sounds small, but given how common Valley Fever is in endemic areas, that’s still a lot of people. Dr. Arreaza:
And the complications can be devastating, and they are not always in primary infection. Dr. Schlaerth: Dissemination can be silent. We don’t know exactly why dissemination happens; some ethnicities are more susceptible or other groups. Dr. Arreaza:
Let’s start where Valley Fever usually begins: the lungs. What are the major pulmonary complications clinicians should know about? Jordan:
The most common long-term complications are chronic pulmonary sequelae. These include: cavitary disease, pulmonary nodules, bronchiectasis, pulmonary fibrosis, and pleural complications like effusions, empyema, or pneumothorax. Dr. Arreaza:
Cavitary disease comes up a lot. What does that look like clinically? Jordan:
Cavities form in about 5–15% of cases. Many are asymptomatic, but symptomatic cavities can cause fever, fatigue, cough, sputum production, dyspnea, and hemoptysis. The tricky part is that symptoms often wax and wane, and even with treatment, current antifungals don’t eradicate the organism from chronic cavities. Dr. Arreaza:
That’s very unfortunate, and sometimes those cavities remain and patients might not know that they have them, and those cavitary lesions may rupture. Jordan:
Yes, rupture can lead to pyopneumothorax, which is a surgical emergency requiring prompt intervention. Dr. Kooner: Hello everyone, this is Dr. Kooner, and today I want to talk about one of my favorite topics: coccidioidal cavitary disease—because nothing says “fun lung pathology” like a hole in the lung that refuses to leave. Coccidioidal cavitary disease is a chronic pulmonary manifestation of infection. Many times, it’s found incidentally on imaging. Sometimes patients are being evaluated for respiratory symptoms, sometimes for systemic complaints, and sometimes for something completely unrelated—like when a chest X-ray was ordered for a pre-op clearance and suddenly… surprise cavity. Pulmonary cavities develop in about 5-10% of patients with Valley Fever. Most of the time, they appear as thin-walled residual lesions. They can be solitary or multiple, and they can range from a few centimeters to much larger. And while textbooks love to show the “classic look,” in real life they can be a little more… creative. These cavities can persist for years. Some patients feel completely fine and never know they have one. Others develop chronic symptoms or complications like rupture into the pleural space, secondary infection, or bleeding, which is when everyone suddenly becomes very interested in that cavity. Here’s an important teaching point: about 20% of patients with cavitary disease also have disseminated infection, most commonly involving bone. This challenges the old-school teaching that cavitary lung disease and dissemination rarely happen together.  One major risk factor for cavitary disease—and for more severe or complicated infection overall—is diabetes mellitus. So how do patients usually present? Symptoms often overlap with classic Valley Fever symptoms. The most common presenting symptoms for cavitary disease that usually trigger evaluation are cough, hemoptysis, fever, and shortness of breath. Diagnosis and monitoring rely heavily on chest imaging. Plain chest X-rays are usually enough for stable disease. CT scans are typically saved for when you’re worried about complications. Serologic testing is also key, especially complement fixation titers. In general, higher titers correlate with more severe disease and higher relapse risk. Management depends on symptoms and host factors.If the patient is asymptomatic and immunocompetent, they often don’t need antifungal therapy. These patients can usually be followed with periodic clinical and imaging monitoring watch closely and don’t panic. Symptomatic patients are typically treated with oral triazoles, most commonly fluconazole or itraconazole. Treatment is long—usually at least 6 to 12 months, and often longer—because symptoms love to come back once therapy stops. These medications are usually suppressive rather than curative, although newer data suggests triazoles may help with cavity closure in some patients. Relapses happen in about 25 to 33% of immunocompetent patients, and even more often in immunocompromised patients or transplant recipients. Many of these patients end up needing long-term or even indefinite therapy. Not ideal—but still better than uncontrolled disease. Surgery still has a role, but it’s more selective now. It’s usually reserved for complications like life-threatening hemoptysis or rupture into the pleural space. Early ruptures might be managed with chest tube drainage. More complicated or delayed cases may need decortication or lung resection. So, the big picture: symptomatic coccidioidal cavitary disease can be a chronic management challenge. It requires individualized treatment decisions, prolonged therapy for many patients, and long-term follow-up with imaging and serologic monitoring to catch relapses early and prevent complications. And if there’s one takeaway, it’s this: if you find a stable cavity in someone known to have Valley Fever, sometimes the best move is careful monitoring—not chasing it with endless tests that make everyone nervous, including the patient. Thanks for listening—and remember, sometimes the lung keeps souvenirs from infections… and sometimes those souvenirs stick around for years. Now, let’s continue with the discussion about pulmonary nodules. This is Dr. Kooner, signing off.

    24 min
  2. Episode 213: HIV PrEP Review

    FEB 20

    Episode 213: HIV PrEP Review

    Episode 213: HIV PrEP Review H. Nicole Magaña, medical student, reviews the history of PrEP and outlines the currently FDA-approved medications used for HIV prevention. Dr. Arreaza provides additional perspective on long-acting injectable options, including how quickly they begin to protect patients after initiation.   Written by Nicole Magana, MSIV, American University of the Caribbean. Comments and 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. Pre-exposure prophylaxis for HIV. Previous episodes related to HIV:  -Episode 67, HIV history (September 2021) -Episode 68, HIV transmissibility (October 2021) -Episode 70 (October 2021), HIV prevention (including HIV Prep with oral medications) -Episode 98 (June 2022), we introduced Apretude, the first injectable for HIV PrEP. Apretude was approved in December 2021.  What is Pre-Exposure prophylaxis (PrEP)? Pre-exposure prophylaxis, or PrEP, is the use of antiretroviral medications taken by individuals who are HIV-negative to prevent HIV acquisition. There are 30,000 new HIV infections annually in the US.  How effective is it? When taken as prescribed, PrEP is highly effective at reducing the risk of HIV transmission through sexual exposure and injection drug use. Patients who are adherent to PrEP can lower their risk of contracting HIV by 99%. The effectiveness of oral PrEP is highly adherence dependent. In trials with 70% adherence, the relative risk of HIV acquisition was 0.27, compared to 0.51 with 40-70% adherence and no significant benefit with adherence ≤40%. How does PrEP work? PrEP works by maintaining therapeutic drug levels in the bloodstream and in target tissues. If HIV exposure occurs, viral replication is inhibited, preventing the establishment of infection. Brief History of PrEP. The concept of PrEP originated from early animal studies demonstrating that antiretroviral medications could prevent retroviral transmission when administered before exposure. In 2010, the iPrEx trial showed that daily oral tenofovir disoproxil fumarate (known as Truvada) with emtricitabine significantly reduced HIV acquisition among men who have sex with men and transgender women. This was the first large clinical trial to demonstrate the effectiveness of PrEP. In 2012, the FDA approved oral Truvada, which is TDF/FTC (tenofovir disoproxil and emtricitabine) for HIV prevention. Since then, additional studies have expanded indications and introduced new formulations, including long-acting injectable options. Who Should Be Offered PrEP? PrEP should be considered for any HIV-negative individual at increased risk of HIV acquisition, including Men who have sex with men, transgender individuals, heterosexual men and women with an HIV-positive partner, individuals with recent bacterial sexually transmitted infections, people who inject drugs, individuals engaging in condomless sex with partners of unknown HIV status. Remember that PrEP should be offered in a nonjudgmental, patient-centered manner, make it a safe space to talk openly about prevention of HIV.  Available HIV PrEP Options. Daily Oral PrEP: There are 2 formulations of Tenofovir. There is Tenofovir disoproxil fumarate (TDF)/ Truvada and Tenofovir alafenamide (TAF)/ Descovy. Each is available in a tablet combined with Emtricitabine a nucleoside reverse transcriptase inhibitor. Truvada: It is approved for all populations at risk through sexual exposure or injection drug use. Something to look out for before starting this medication is for pre-existing CKD. Do not give to patients who have an estimated glomerular filtration rate of less than 60 mL/min. (6) Descovy: This option is approved for men who have sex with men and transgender women but is not approved for individuals at risk through receptive vaginal sex. It has less impact on renal function and bone mineral density compared to Truvada. It can be used in moderately reduced kidney function (GFR between 30-60 mL/min). Truvada and Descovy are taken orally once a day.  After patients start taking these medications, when are they considered to be protected?  Nicole: With daily oral PrEP, guidelines differ with WHO and International Aids Society-USA stating it takes about 7 days, while CDC states 21 days to allow for adequate concentration in tissues (1). Adherence is critical for efficacy. Injectable HIV PrEP. In 2021, the FDA approved the first Injectable PrEP option Long-acting cabotegravir (CAB-LA)- known on the market as Apretude. Cabotegravir is an integrase strand transfer inhibitor administered as an intramuscular injection.Dosing consists of an initial injection, a second injection one month later, and then maintenance injections every two months (1). Another option is Lenacapavir (Yeztugo). The Yeztugo as a pre-exposure prophylaxis (PrEP) for HIV in Oct 2024. Yeztugo is the first and only FDA-approved HIV prevention treatment that requires just two injections per year, offering a long-acting option for people who weigh at least 35kg. It is given as 2 injections every 6 months. First dose is given with 2 tablets on Day 1 and Day 2, then every 6 months 2 injections on the same day. Clinical trials, including HPTN 083 and HPTN 084, demonstrated that injectable cabotegravir is superior to daily oral PrEP in preventing HIV infection. This advantage is largely due to improved adherence rather than differences in intrinsic drug potency. There have been no head-to-head comparisons between Yeztugo and Apretude, but they are both very effective. Apretude starts protecting 7 days after the first dose, and Yeztugo starts protecting 2 hours after Day 2 (if patient takes the oral loading dose) or 3-4 weeks if no oral load is taken. Injectable PrEP is particularly beneficial for patients who struggle with daily pill adherence, have trouble swallowing pills, prefer a discreet option, have difficulty storing their medication or have renal or bone disease that limits the use of tenofovir-based regimens like Truvada and Descovy (6). In one unpublished report by Medline, patients who received Apretude had an increase in bone mineral density compared to those who received Truvada (1). Tests prior to starting PrEP. Before initiating PrEP, patients must be confirmed to be HIV-negative. Baseline evaluation includes HIV testing with a fourth-generation antigen/antibody assay, HIV RNA testing if acute infection is suspected, renal function testing for oral PrEP, Hepatitis B screening, sexually transmitted infection screening, and pregnancy testing when appropriate. PrEP should not be started in individuals with known or suspected acute HIV infection. Monitoring for patients on HIV PrEP. Monitoring typically includes HIV testing every 2 to 3 months, STI screening every 3 to 6 months, renal function monitoring for those on oral PrEP (tenofovir- based), ongoing adherence and risk-reduction counseling. And for injectable PrEP, adherence to the injection schedule is essential, as delayed dosing may increase the risk of resistance if HIV infection occurs. HIV PrEP is not a prevention for other STIs. Screening for STIs and counseling about prevention is essential. Breakthrough HIV infections on PrEP are rare and most often associated with poor adherence or delayed diagnosis. Truvada is more studied in all populations and is considered safe during pregnancy and breastfeeding. There is less data regarding the injectable option in patients who are pregnant, may become pregnant, or whose primary risk factor is injection drug use (1). Injectable PrEP provides an important alternative for patients with chronic kidney disease and bone disease (1). Key Takeaway Pre-exposure prophylaxis is a safe, effective, and evidence-based strategy for HIV prevention. With both daily oral and long-acting injectable options available, PrEP can be individualized to meet patient needs. Normalizing PrEP discussions in clinical practice is essential to reducing new HIV infections and advancing public health goals.  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: Antiretroviral Drugs for Treatment and Prevention of HIV in Adults: 2024 Recommendations of the International Antiviral Society–USA Panel. The Journal of the American Medical Association. 2025. Gandhi RT, Landovitz RJ, Sax PE, et al. Long-Acting Lenacapavir Acts as an Effective Preexposure Prophylaxis in a Rectal SHIV Challenge Macaque Model. The Journal of Clinical Investigation. 2023. Bekerman E, Yant SR, VanderVeen L, et al. Pharmacokinetics and Safety of Once-Yearly Lenacapavir: A Phase 1, Open-Label Study. Lancet. 2025. Jogiraju V, Pawar P, Yager J, et al.

    20 min
  3. Episode 212: Managing HFpEF

    FEB 13

    Episode 212: Managing HFpEF

    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 HFpEF Arreaza: 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 consensu

    13 min
  4. Episode 211: Understanding HFpEF

    FEB 6

    Episode 211: Understanding HFpEF

    Episode 211: Understanding HFpEF.  Hyo Mun and Jordan Redden (medical students) explain the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and how it differentiates from HFrEF. Dr. Arreaza asks insightful questions and summarizes some key elements of HFpEF.  Written by Hyo Mun, MS4, American University of the Caribbean; and Jordan Redden, MS4, Ross University School of Medicine. Comments and 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. What is EF? Just imagine, the heart is a pump, blood gets into the heart through the veins, the ventricles fill up and then squeeze the blood out. So, the percent of blood that is pumped out is the EF. Let’s start at the beginning.  What is HFpEF? Mike: HFpEF stands for heart failure with preserved ejection fraction. Basically, these patients squeeze normally—their ejection fraction is 50% or higher—but here's the thing: the heart can't relax and fill the way it should. The muscle gets stiff, almost like a thick leather boot that just won't stretch. And because the ventricle can't fill properly, pressure starts backing up into the lungs and the rest of the body. That's when patients start experiencing shortness of breath, leg swelling, fatigue—all those classic symptoms. Dr. Arreaza: And this is where people get fooled by the ejection fraction. Mike: Exactly. The ejectionfraction tells you total left ventricular emptying, not just forward flow. Jordan: The classic example is severe mitral regurgitation. You can eject 60% of your blood volume and still be in cardiogenic shock because most of that blood is leaking backward into the left atrium instead of going into the aorta. So, you get pulmonary edema, hypotension, fatigue, all with a “normal” EF. Which is honestly terrifying if you’re over-relying on echo reports without thinking clinically. Dr. Arreaza: And in HFpEF, functional mitral regurgitation often shows up later in the disease. It’s not usually the primary cause; it’s more of a marker of advanced disease. Moderate to severe MR in HFpEF independently predicts worse outcomes, including a higher risk of mortality or heart failure hospitalization. So, let’s contrast this with HFrEF. How are these two different? Mike: HFrEF—heart failure with reduced ejection fraction—is a pumping problem. The heart muscle is weak and can't contracteffectively. Ejection fraction drops below 40%, and this is your classic systolic dysfunction. Jordan: HFpEF, on the other hand, is diastolic dysfunction. The heart muscle is thick, fibrotic, and noncompliant. It squeezes fine, but it just doesn’t relax, even though the EF looks reassuring on paper. Mike: I like to explain it this way: HFrEF is a weak heart that can't squeeze. HFpEF is a stiff heart that can't relax. Totally different problems. Dr. Arreaza: And then there’s the gray zone: heart failure with mildly reduced EF, or HFmrEF. That’s an EF between 41 and 49% with evidence of elevated filling pressures. It really shares the features of both worlds. So, what actually causes HFpEF versus HFrEF? Jordan: HFpEF is basically what happens when all the problems of modern living catch up with you. You've got chronic hypertension, obesity, diabetes, metabolic syndrome, aging, systemic inflammation—all of these things slowly remodel the heart over years. The muscle gets thick and stiff, and eventually the ventricle just loses its ability to relax. So, HFpEF is really a disease of metabolic dysfunction and chronic stress in the heart.  Mike: HFrEF is more about direct injury. Think about myocardial infarctions, ischemic cardiomyopathy, viral myocarditis, alcohol toxicity, chemotherapy like doxorubicin, genetic cardiomyopathies, or chronic uncontrolled tachycardia. These insults actually damage or kill heart muscle cells, leading to a dilated, weak ventricle that can’t pump effectively. Dr. Arreaza: So the short version: HFpEF is caused by chronic metabolic and hypertensive stress, while HFrEF is caused mainly by myocardial damage. A question we get a lot: does HFpEF eventually turn into HFrEF? What do you guys think? Mike: In most cases, no. HFpEF patients usually stay HFpEF throughout their disease course. They don’t just “burn out” and turn into HFrEF. Jordan: They’re generally separate disease entities with different pathophysiology. A patient with HFpEF can develop HFrEF if they have a big myocardial infarction or ongoing ischemia that damages the muscle, but that’s not the natural progression. Mike: Interestingly though, the opposite can happen. Some HFrEF patients actually improve their ejection fraction with good medical therapy—that's called HF with improved EF—and it's a great sign that treatment is working. Dr. Arreaza: Another question. How do HFpEF and HFrEF compare to restrictive cardiomyopathy and constrictive pericarditis? Jordan: Clinically, they can all look very similar: dyspnea, edema, fatigue, but the underlying mechanisms are completely different. Mike: In HFpEF, the myocardium itself is stiff from hypertrophy and fibrosis. The problem is intrinsic to the heart muscle, and EF stays preserved. Echoshows diastolic dysfunction with elevated filling pressures. Jordan: In HFrEF, the myocardium is weak. The ventricle is often dilated and contracts poorly, with a reduced EF. Mike: Restrictive cardiomyopathy is different. Here, the myocardium gets infiltrated by abnormal stuff—amyloid, iron, sarcoid—and that makes it extremely stiff. It can look like HFpEF on the surface, but it's usually more severe. On Echo You'll see biatrial enlargement, small ventricles, and preserved EF. And importantly, it's a pathologic diagnosis, so you need advanced imaging or biopsy to confirm it. Jordan:  Constrictive pericarditis is another mimic, but here the myocardium is usually normal. The problem is that the pericardium is thickened, calcified, and rigid. This will physically prevent the heart from being filled. Imaging shows pericardial thickening, septal bounce, and respiratory variation in flow, and cath shows equalization of diastolic pressures, which is the hallmark of constrictive pericarditis. Dr. Arreaza: So the takeaway is: HFpEF is a clinical syndrome driven by common metabolic and hypertensive causes, while restrictive and constrictive diseases are specific pathologic entities. If “HFpEF” is unusually severe or not responding to treatment, you need to think beyond HFpEF. Which type of heart failure is more common right now? Mike: Good question, the answer is: HFpEF. It now accounts for up to 60% of all heart failure cases, and it’s still rising. Dr. Arreaza: Why is that? Jordan: Because people are living longer, gaining weight, and developing more metabolic syndrome. HFpEF thrives in older, or people with obesity, hypertension, or diabetes: basically, the modern American population. At the same time, better treatment of acute MIs means fewer people are developing HFrEF from massive heart attacks. Mike: HFpEF is the heart failure epidemic of the 21st century. It’s honestly the cardiology equivalent of type 2 diabetes. Dr. Arreaza: Let’s talk aboutCOVID-19. (2025 and still talking about it) Does it actually increase heart failure risk? Mike: Yes, absolutely. COVID increases both acute and long-term heart failure risk. Jordan: During acute infection, COVID can cause myocarditis, trigger massive inflammation, and precipitate acute decompensated heart failure, especially in patients with pre-existing disease. It also causes microthrombi, which can injure the myocardium. Mike: And after infection, even mild cases are linked to a significantly higher risk of developing new heart failure within the following year. Both HFpEF and HFrEF rates go up. Dr. Arreaza: I remember seeing this in 2021, we had a patient with acute COVID and HFrEF, her EF was about 10%, I lost contact with the patient and at the end I don’t know what happened to her. What’s the pathophysiology of COVID and heart failure? Mike: COVID causes direct viral injury through ACE2 receptors, triggers massive inflammation that damages the endothelium and heart muscle, leads to microvascular clotting and fibrosis—all mechanisms that promote HFpEF. Jordan: Add autonomic dysfunction, persistent low-grade inflammation, and worsening metabolic syndrome, and you’ve got a perfect storm for heart failure. Dr. Arreaza: Bottom line: COVID is a cardiovascular disease as much as a respiratory one. If someone had COVID and now has unexplained dyspnea or fatigue, think about heart failure. Get an echo, get a BNP, start treatment. Last big question: why did we have so many therapies for HFrEF but essentially none for HFpEF for years? Mike: HFrEF is mechanistically straightforward. You've got a weak heart with excessive neurohormonal activation going on — so you block RAAS, block the sympathetic system, drop the afterload. The drugs make sense. Jordan: HFpEF is messy. It’s not one disease. It’s stiffness, fibrosis, inflammation, microvascular dysfunction, metabolic disease, atrial fibrillation, all overlapping. One drug can’t fix all of that. Mike: And some drugs that worked beautifully in HFrEF actually made HFpEF worse. Take Beta blockers, for example.  They slow heart rate, which is a problem because HFpEF patients rely on heart rate to maintain their cardiac output. Jordan: The breakthrough came with SGLT-2 inhibitors: diabetes drugs that unexpectedly addressed multiple HFpEF mechanisms at once: volume, metabolism, inflammation, and myocardial energetics. Dr. Arreaza: The miracle drug

    15 min
  5. Episode 210: Heat Stroke Basics

    JAN 2

    Episode 210: Heat Stroke Basics

    Episode 210: Heat Stroke Basics Written by Jacob Dunn, MS4, American University of the Caribbean. Edits and 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.   Definition: Heat stroke represents the most severe form of heat-related illness, characterized by a core body temperature exceeding 40°C (104°F) accompanied by central nervous system (CNS) dysfunction.  Arreaza: Key element is the body temperature and altered mental status.  Jacob: This life-threatening condition arises from the body's failure to dissipate heat effectively, often in the context of excessive environmental heat load or strenuous physical activity.  Arreaza: You mentioned, it is a spectrum. What is the difference between heat exhaustion and heat stroke?  Jacob: Unlike milder heat illnesses such as heat exhaustion, heat stroke involves multisystem organ dysfunction driven by direct thermal injury, systemic inflammation, and cytokine release. You can think of it as the body's thermostat breaking under extreme stress — leading to rapid, cascading failures if not addressed immediately.  Arreaza: Tell us what you found out about the pathophysiology of heat stroke? Jacob: Pathophysiology:  Under normal conditions, the body keeps its core temperature tightly controlled through sweating, vasodilation of skin blood vessels, and behavioral responses like seeking shade or drinking water. But in extreme heat or prolonged exertion, those mechanisms get overwhelmed. Once core temperature rises above about 40°C (104°F), the hypothalamus—the brain’s thermostat—can’t keep up. The body shifts from controlled thermoregulation to uncontrolled, passive heating. Heat stroke isn’t just someone getting too hot—it’s a full-blown failure of the body’s heat-regulating system.  Arreaza: So, it’s interesting. the cell functions get affected at this point, several dangerous processes start happening at the same time. Jacob: Yes:  Cellular Heat Injury High temperatures disrupt proteins, enzymes, and cell membranes. Mitochondria start to fail, ATP production drops, and cells become leaky. This leads to direct tissue injury in vital organs like the brain, liver, kidneys, and heart.Arreaza: Yikes. Cytokines play a big role in the pathophysiology of heat stroke too.  Jacob:  Systemic Inflammatory Response Heat damages the gut barrier, allowing endotoxins to enter the bloodstream. This triggers a massive cytokine release—similar to sepsis. The result is widespread inflammation, endothelial injury, and microvascular collapse.Arreaza: What other systems are affected? Coagulation Abnormalities Endothelial damage activates the clotting cascade. Patients may develop a DIC-like picture: microthrombi forming in some areas while clotting factors get consumed in others. This contributes to organ dysfunction and bleeding.Circulatory Collapse As the body shunts blood to the skin for cooling, perfusion to vital organs drops. Combine that with dehydration from sweating and fluid loss, and you get hypotension, decreased cardiac output, and worsening ischemia.Arreaza: And one of the key features is neurologic dysfunction. Jacob:  Neurologic Dysfunction The brain is extremely sensitive to heat. Encephalopathy, confusion, seizures, and coma occur because neurons malfunction at high temperatures. This is why altered mental status is the hallmark of true heat stroke.Arreaza: Cell injury, inflammation, coagulopathy, circulatory collapse and neurologic dysfunction.  Jacob: Ultimately, heat stroke is a multisystem catastrophic event—a combination of thermal injury, inflammatory storm, coagulopathy, and circulatory collapse. Without rapid cooling and aggressive supportive care, these processes spiral into irreversible organ failure. Background and Types: Arreaza: Heat stroke is part of a spectrum of heat-related disorders—it is a true medical emergency. Mortality rate reaches 30%, even with optimal treatment. This mortality correlates directly with the duration of core hyperthermia. I’m reminded of the first time I heard about heat stroke in a baby who was left inside a car in the summer 2005.  Jacob: There are two primary types:  -nonexertional (classic) heat stroke, which develops insidiously over days and predominantly affects vulnerable populations like children, the elderly, and those with chronic illnesses during heat waves;  -exertional heat stroke, which strikes rapidly in young, otherwise healthy individuals, often during intense exercise in hot, humid conditions.  Arreaza: In our community, farm workers are especially at risk of heat stroke, but any person living in the Central Valley is basically at risk. Jacob: Risk factors amplify vulnerability across both types, including dehydration, cardiovascular disease, medications that impair sweating (e.g., anticholinergics), and acclimatization deficits. Notably, anhidrosis (lack of sweating) is common but not required for diagnosis. Hot, dry skin can signal the shift from heat exhaustion to stroke.  Arreaza: What other conditions look like heat stroke? Differential Diagnosis: Jacob: Presenting with altered mental status and hyperthermia, heat stroke demands a broad differential to avoid missing mimics.  -Environmental: heat exhaustion, syncope, or cramps.  -Infectious etiologies like sepsis or meningitis must be ruled out.  -Endocrine emergencies such as thyroid storm, pheochromocytoma, or diabetic ketoacidosis (DKA) can overlap.  -Neurologic insults include cerebrovascular accident (CVA), hypothalamic lesions (bleeding or infarct), or status epilepticus.  -Toxicologic culprits are plentiful—sympathomimetic or anticholinergic toxidromes, salicylate poisoning, serotonin syndrome, malignant hyperthermia, neuroleptic malignant syndrome (NMS), or even alcohol/benzodiazepine withdrawal.  When it comes to differentials, it is always best to cast a wide net and think about what we could be missing if this is not heat stroke.  Arreaza: Let’s say we have a patient with hyperthermia and we have to assess him in the ER. What should we do to diagnose it? Jacob: Workup: Diagnosis is primarily clinical, hinging on documented hyperthermia (>40°C) plus CNS changes (e.g., confusion, delirium, seizures, coma) in a hot environment.  Arreaza: No single lab confirms it, but targeted testing allows us to detect complications and rule out alternative diagnosis.  Jacob:  -Start with ECG to assess for dysrhythmias or ischemic changes (sinus tachycardia is classic; ST depressions or T-wave inversions may hint at myocardial strain).  -Labs include complete blood count (CBC), comprehensive metabolic panel (electrolytes, renal function, liver enzymes), glucose, arterial blood gas, lactate (elevated in shock), coagulation studies (for disseminated intravascular coagulation, or DIC), creatine kinase (CK) and myoglobin (for rhabdomyolysis), and urinalysis. Toxicology screen if history suggests.  Arreaza: I can imagine doing all this while trying to cool down the patient. What about imaging? -Imaging: chest X-ray for pulmonary issues, non-contrast head CT if neurologic concerns suggest edema or bleed (consider lumbar puncture if infection suspected).  It is important to note that continuous core temperature monitoring—via rectal, esophageal, or bladder probe—is essential, not just peripheral skin checks.  Arreaza: Treatment Management: Time is tissue here—initiate cooling en route, if possible, as delays skyrocket morbidity. ABCs first: secure airway (intubate if needed, favoring rocuronium over succinylcholine to avoid hyperkalemia risk), support breathing, and stabilize circulation.  -Remove the patient from the heat source, strip clothing, and launch aggressive cooling to target 38-39°C (102-102°F) before halting to prevent rebound hypothermia.  -For exertional cases, ice-water immersion reigns supreme—it's the fastest method, with immersion in cold water resulting in near-100% survival if started within 30 minutes.  -Nonexertional benefits from evaporative cooling: mist with tepid water (15-25°C) plus fans for convective airflow.  -Adjuncts include ice packs to neck, axillae, and groin;  -room-temperature IV fluids (avoid cold initially to prevent shivering);  -refractory cases, invasive options like peritoneal lavage, endovascular cooling catheters, or even ECMO.  -Fluid resuscitation with lactated Ringer's or normal saline (250-500 mL boluses) protects kidneys and counters rhabdomyolysis—aim for urine output of 2-3 mL/kg/hour.  Arreaza: What about medications? Jacob: Benzodiazepines (e.g., lorazepam) control agitation, seizures, or shivering; propofol or fentanyl if intubated. Avoid antipyretics like acetaminophen. For intubation, etomidate or ketamine as induction agents. Hypotension often resolves with cooling and fluids; if not, use dopamine or dobutamine over norepinephrine to avoid vasoconstriction.  Jacob: What IV fluid is recommended/best for patients with heat stroke? Both lactated Ringer’s solution and normal saline are recommended as initial IV fluids for rehydration, but balanced crystalloids such as LR are increasingly favored due to their lower risk of hyperchloremic metabolic acidosis and AKI. However, direct evidence comparing the two specifically in the setting of heat stroke is limited.  Arreaza: Are cold IV fluids better/preferred over room temperature fluids? Cold IV fluids are recommended as an adjunctive therapy to help lower core temperature in heat stroke, but they should not delay or replace primary cooling methods such as cold-water immersion. Cold IV fluids can decrease core tempera

    23 min
  6. Episode 209: Do not Do

    12/12/2025

    Episode 209: Do not Do

    Episode 209: Do not Do Stephanie Granat (medical student) explains three screenings that are USPSTF Grade D (Do not do): Prostate cancer, genital herpes, and pancreatic cancer. Dr. Arreaza shares some insight about testing patients with lower urinary tract symptoms and genital lesions.  Written by Stephanie Granat, MSIV, Ross University School of Medicine. Edits and 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.

    22 min
  7. Episode 208: Cough Basics (Pidjin English)

    12/05/2025

    Episode 208: Cough Basics (Pidjin English)

    Episode 208: Cough Basics (Pidjin English) Written by Ebenezer Dadzie 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. Episode 201: Cough – Revised Version (Host + 1 Resident; Resident speaks Nigerian Pidgin, Host speaks regular English) [Play intro music, start loud, then lower volume under speech, fade out later] HOST 1: [Introduction] Today we're tackling one of the most common complaints in clinic: the cough. Joining me is one of our amazing residents. Doctor, please introduce yourself. RESIDENT: Na Dr. Resident from Rio Bravo. I dey here to gist about cough wey dey disturb plenty patients for area. Segment 1 – Cough Basics HOST 2: Let’s start simple. When a coughing patient walks into the exam room, what is the first step? RESIDENT: First tin na history. You gats ask whether na dry cough or cough wey dey bring sputum, whether e just start or don tey. Whether person get exposure, dust, new medicine—history dey open many doors pass Google. HOST 1: Exactly. And as we know, acute coughs are usually viral, but chronic coughs lasting more than eight weeks can point to asthma, GERD, ACE inhibitor side effects, or more. Segment 2 – Valley Fever HOST 2: And since we’re here in Kern County, we have to mention Valley Fever. We see thousands of cases every year, many of them presenting with cough. RESIDENT: True. Valley Fever fit look like pneumonia, bronchitis, or even TB. Patient go come with cough, tiredness, sometimes rash. If person dey work for outside or dey around dusty area, you suppose reason am. Segment 3 – Workup and Treatment HOST 1: So let’s talk evaluation. When you have a cough here in California’s Central Valley, what is your approach? RESIDENT: Start from basic: chest X-ray, CBC, ask good history. If e no improve, add Valley Fever blood test. If cough get phlegm, you fit send sputum. If weight dey drop or sweats dey night, you reason TB or cancer. Treatment depend on severity. Mild one fit resolve, but if no be small, na antifungals—like fluconazole—and you go monitor liver enzymes well. Segment 4 – Humor Break HOST 2: Alright—quick humor break. Got any memorable cough stories? RESIDENT: One man tell me say “doctor, my neighbor ghost na cause my cough.” We check-am finish, na allergy. Ghost no dey push fungus, sha! [Both laugh] Segment 5 – Takeaways HOST 1: Before we wrap up, give listeners top key points on cough. RESIDENT: One—ask better history. Cough dey tell story. Two—if person dey Bakersfield, reason Valley Fever, e fit sneak. Three—no dey give antibiotics anyhow. Virus and fungus no go respond like bacteria. Trivia Time HOST 2: Trivia question: In adults who don’t smoke and aren’t on ACE inhibitors, what is the most common cause of chronic cough? A) Asthma B) GERD C) Chronic bronchitis D) Postnasal drip (Upper airway cough syndrome) RESIDENT: I go choose D—postnasal drip. Na e dey cause that tickle wey no dey go. HOST 1: And that’s correct—postnasal drip is the number one cause of chronic cough. Nicely done! You win bragging rights and a cough drop. HOST 2: Thank you for joining us today on Rio Bravo QWeek. To all our listeners—stay curious, keep learning, and if someone sounds like a barking seal in the waiting room, you know it might be more than a cold. HOST & RESIDENT (together): ¡Hasta luego! [Music fades in, rises, then fades out after 10 seconds] References: Irwin, R. S., & Baumann, M. H. (2018). Chronic cough due to upper airway cough syndrome (UACS): ACCP evidence-based clinical practice guidelines. Chest, 129(1_suppl), 63S–71S. https://doi.org/10.1378/chest.129.1_suppl.63S (Guideline on postnasal drip/upper airway cough syndrome as a leading cause of chronic cough)Dicpinigaitis, P. V. (2022). Evaluation and management of chronic cough. New England Journal of Medicine, 386(16), 1532–1541. https://doi.org/10.1056/NEJMra2115321 (Comprehensive review on causes, diagnostic strategies, and treatment of chronic cough)Centers for Disease Control and Prevention. (2023). Coccidioidomycosis (Valley fever) statistics. U.S. Department of Health and Human Services. https://www.cdc.gov/fungal/diseases/coccidioidomycosis/statistics.html (Official CDC data and epidemiology of Valley Fever in the U.S., including high incidence in Kern County)California Department of Public Health. (2022). Coccidioidomycosis in California Provisional Monthly Report. https://www.cdph.ca.gov/Programs/CID/DCDC/Pages/Coccidioidomycosis.aspx (State-level surveillance data showing high incidence rates in Bakersfield and Kern County)Prasad, K. T., & LoSavio, P. S. (2023). Approach to the adult with chronic cough. In UpToDate (L. M. Leung, Ed.). Retrieved June 20, 2025, from https://www.uptodate.com (Evidence-based resource for differential diagnosis and workup of cough in primary care)Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

    14 min
  8. Episode 207: Understanding Hypertension and Diabetes (Pidjin English)

    11/28/2025

    Episode 207: Understanding Hypertension and Diabetes (Pidjin English)

    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. Hypertension Segment 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 Factors High-salt diet and low potassium intakePhysical inactivityTobacco useExcessive alcohol intakeOverweight or obesityChronic stressPoor sleep or sleep apneaNon-Modifiable Factors Family 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 Management HOST: 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-blockers Your healthcare provider will choose the best medication based on your health profile. Segment 6: What You Can Do Today HOST: 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. Summary Hypertension 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. Diabetes 1. 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. Conclusion Q: 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/.

    40 min
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About

qWeek is the official podcast of the Rio Bravo Family Medicine Residency Program. Residents and faculty routinely present key topics and relevant discussions, coupled with medical jokes and Spanish medical terminology.

Information

  • Creator
    Rio Bravo Family Medicine Residency Program
  • Years Active
    2020 - 2026
  • Episodes
    214
  • Rating
    Clean
  • Copyright
    © 2020 Rio Bravo Family Medicine Residency Program
  • Show Website
    Rio Bravo qWeek

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