Rio Bravo qWeek

Episode 217: Testicular Cancer Dr. Arreaza: Welcome to Rio Bravo qWeek Podcast. Today we are discussing testicular cancer, a topic that may not appear frequently in primary care but is extremely important to recognize early. We are joined by Brandon Noorvash and Dr. Ebenezer Dadzie. Please introduce yourselves. Brandon: Thank you, Dr. Arreaza. My name is Brandon Noorvash. I am a third-year medical student at Western University of Health Sciences with a strong interest in urology. Ebenezer: Thank you for having us. My name is Dr. Ebenezer Dadzie, and I am a PGY-1 resident in the Clinica Sierra Vista Family Medicine Residency Program. Dr. Arreaza: Testicular cancer represents about 1-2% of cancers in men, but it is the most common cancer in men between the ages of 15 and 40. The good news is that it is also one of the most curable cancers in medicine, especially when detected early. Let’s start with a quick question for our listeners. If a 25-year-old man presents with a painless lump in his testicle, what diagnosis should immediately come to your mind? Ebenezer: Testicular cancer should always be high on the differential. While benign conditions can cause scrotal swelling, a painless testicular mass should be considered cancer until proven otherwise. Dr. Arreaza: I agree. Especially if we perform a physical exam and find that the mass is attached to the testicle. Why is this such an important diagnosis for primary care physicians to recognize, what do you think, Brandon? Brandon: Testicular cancer typically affects young, otherwise healthy men, and early detection dramatically improves outcomes. Patients may delay seeking care because the lump is painless or because they feel embarrassed discussing symptoms. However, when diagnosed early, the 5-year survival rate exceeds 95%, and in localized disease it approaches 99%. Dr. Arreaza: Exactly, the survival is incredible and it gets even better with early detection. How common is testicular cancer? Ebenezer: In the United States, approximately 10,000 new cases are diagnosed each year, with around 500 deaths annually. The relatively low mortality reflects how effective current treatments are, especially chemotherapy for germ cell tumors. Dr. Arreaza: Let’s talk about risk factors. What should clinicians know about risk factors for testicular cancer? Who is at risk? Brandon: The most important risk factor is cryptorchidism, or undescended testicle. Men with a history of cryptorchidism have about a 4-to-8-fold increased risk of developing testicular cancer. Ebenezer: Other risk factors include family history, personal history of testicular cancer, infertility, testicular atrophy, and certain genetic conditions such as Klinefelter syndrome. However, many patients who develop testicular cancer have no clear risk factors. Dr. Arreaza: Brandon, you recently saw a patient with testicular cancer during your rotation. Can you briefly tell us about that case? Protected health information is not being revealed, so patient confidentiality is being respected during this discussion. Dr. Arreaza: I think we all were pleasantly surprised to know that lung metastasis did not place the patient in a higher risk category. On the other hand, nonpulmonary visceral metastases (such as liver, bone, or brain) define poor-risk disease in nonseminoma and intermediate-risk disease in seminoma. Dr. Arreaza: And of course, if the patient presents with sudden severe pain, we should always think about testicular torsion, which is a surgical emergency. What should clinicians focus on during the physical exam? Ebenezer: Testicular tumors typically feel firm, irregular, non-tender, and located within the testicle itself. Brandon: A helpful exam pearl is transillumination. Fluid-filled structures like hydroceles will transilluminate, whereas solid tumors do not. Dr. Arreaza: I have to admit I’ve never done a transillumination in a scrotum before. Brandon/Ebenezer: I’ve done it. I had to clean my pen light afterwards. Arreaza: Once you suspect testicular cancer, what is the next step in evaluation? Ebenezer: The first diagnostic test is a scrotal ultrasound. Ultrasound is highly sensitive and can determine whether the mass is intratesticular, which is highly suspicious for malignancy. Dr. Arreaza: US and tumor markers. Let’s talk a bit more about tumor markers. Why are they useful in testicular cancer? Brandon: Tumor markers help with diagnosis, staging, and monitoring response to treatment. Ebenezer: Alpha-fetoprotein, or AFP, is typically elevated in non-seminomatous germ cell tumors, particularly yolk sac tumors. An important point is that pure seminomas do not produce AFP. Brandon: Beta-hCG can be elevated in both seminomas and non-seminomatous tumors, although the levels are often higher in the non-seminomatous types. Ebenezer: LDH is less specific but can reflect tumor burden and disease activity, so it’s useful for monitoring progression or response to treatment. Dr. Arreaza: So, tumor marker

Episode 216: Fibromyalgia Overview Reitta Wyllie and Tejasvi Ayaggari (medical students) discuss with Dr. Arreaza the presentation, diagnosis and management of fibromyalgia, a commonly unrecognized disease that may impact patient’s quality of life if left untreated. Written by Reitta Nash, MSIV, American University of the Caribbean. Additional commentary provided by Dr. Tejasvi Ayyagari. 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. Introduction Fibromyalgia is a chronic pain condition that affects millions of people worldwide, yet it remains one of the most misunderstood disorders in medicine. Patients often experience widespread pain, fatigue, sleep disturbances, cognitive difficulties, and a host of other symptoms that significantly impact daily functioning and quality of life. TJ: It’s common, but I feel it is mostly misunderstood and sometimes goes undiagnosed. Reitta: Yes, despite its prevalence, fibromyalgia has historically been met with skepticism, delayed diagnosis, and stigma. Today, we’ll break down what fibromyalgia is, what we know about its underlying mechanisms, how it’s diagnosed, and how it’s managed using evidence-based approaches. What is fibromyalgia? Fibromyalgia is a chronic pain disorder characterized by widespread musculoskeletal pain, accompanied by symptoms such as fatigue, non-restorative sleep, cognitive dysfunction often referred to as “fibro/brain fog,” and mood disturbances. TJ: Unlike inflammatory or autoimmune diseases, fibromyalgia does not cause structural damage to joints or muscles, nor does it produce objective findings on imaging or routine laboratory testing. Instead, it is considered a centralized pain disorder, meaning pain processing within the central nervous system is altered. Arreaza: Many years ago, I had a patient who had fibromyalgia in Germany. He shared how hard it was for him to get diagnosed and treated because many countries fail to recognize fibromyalgia as a disease. However, Germany is not one of them. The German Association of the Medical Scientific Societies (AWMF) has established specific diagnostic criteria for fibromyalgia syndrome (FMS). Also, the World Health Organization recognizes fibromyalgia as a chronic condition, and it is included in the International Classification of Diseases 10th edition (ICD-10). Reitta: The American College of Rheumatology (ACR) recognizes fibromyalgia as a distinct clinical diagnosis, affecting approximately 2–4% of the population, with a higher prevalence in women, though it can affect individuals of any sex or age. Historical Perspective Fibromyalgia was once referred to by terms such as fibrositis, a name that implied inflammation of connective tissue. However, as research failed to demonstrate inflammatory changes, the terminology evolved. In 1990, the American College of Rheumatology introduced the first formal diagnostic criteria, which focused heavily on tender point examination. Over time, these criteria were revised as understanding of the condition improved. Modern diagnostic criteria no longer rely on tender points and instead emphasize symptom severity and widespread pain distribution, reflecting a more patient-centered and clinically practical approach. What causes fibromyalgia? The exact cause of fibromyalgia is not fully understood, but current evidence supports a multifactorial, neurobiological model. The American Academy of Family Physicians identifies a spectrum of chronic overlapping pain conditions that frequently coexist with fibromyalgia, including IBS, TMJ pain, vulvodynia, Chronic fatigue syndrome, interstitial cystitis, endometriosis, chronic tension headaches, migraine, and chronic low back pain. These functional somatic conditions may represent a single disorder manifesting as pain in different body regions at different times over the life span. _____________________ References: Aaron RV, Ravyts SG, Carnahan ND,et al. Prevalence of depression and anxiety among adults with chronic pain: a systematic review and metaanalysis‑analysis. JAMA Netw Open. 2025;8(3):e250268. doi:10.1001/jamanetworkopen.2025.0268. PMID: 40053352. Bradley LA. Pathophysiologic mechanisms of fibromyalgia and its related disorders. J Clin Psychiatry. 2008;69(Suppl 2):6‑14. PMID: 19962493. doi:10.4088/JCP.v69s02102. Häuser W, Ablin J, Fitzcharles MA, et al. Fibromyalgia. Am Fam Physician. 2023;107(2):158‑166. Häuser W, Fitzcharles MA. Facts and myths pertaining to fibromyalgia. Nat Rev Rheumatol. 2018;14(9):525‑535. PMID: 38607678; doi:10.1038/s41584‑018‑0084‑4. Kleykamp BA, Ferguson MC, McNicol E, et al.The prevalence of psychiatric and chronic

Episode 215: Meth-associated HFrEF. Abishak and Zat (medical students) explain the cardiotoxic effect of methamphetamine and the diagnosis and treatment of heart failure with reduced ejection fraction (HFrEF). Dr. Arreaza adds insight into the reversibility of meth-associated HFrEF. Written by Abishak Govindarajan, MSIV and Zat Akbar Shaw. American University of the Caribbean. Edits and comments by Hector Arreaza, MD. Welcome Dr. Arreaza: Welcome to Rio Bravo qWeek. My name is Hector Arreaza, family physician, faculty and associate program director of the Clinica Sierra Vista/Rio Bravo Family Medicine Residency Program. Today we will explore heart failure with reduced ejection fraction, a high-yield and clinically relevant topic in medicine. We will discuss the role of methamphetamine use in the development of HFrEF. This is a pressing issue because about 0.8% of the population 12 and older in the US reported using methamphetamine within the past 12 months in 2024 (National Survey on Drug Use and Health, NSDUH), that’s about ≈2.4 million people!We are joined by two aspiring physicians who will help explore this topic. By the way, we will refer to methamphetamine in this episode as “meth”. [Abishak and Akbar introduce themselves] Abishak: [Introduce yourself] The role of meth in HFrEF Dr. Arreaza: Meth is a growing problem in many places, including Bakersfield, where we live. Meth is also known as Meth Crystal, Poor man’s cocaine, Ice, Glass, Crank, Speed, Chalk, and Tina. How does meth contribute to the development of HFrEF? Abishak: So, first, let's understand how methamphetamine works. It has a chemical structure similar to dopamine and norepinephrine, and it gets taken up through the neuron transporter proteins. Once it enters the synaptic vesicles (storage sacs for neurotransmitters), it displaces and forces the release of large amounts of dopamine, norepinephrine, and serotonin into the synapse (the space between neurons). Additionally, meth blocks the reuptake of those neurotransmitters into the neuron, ensuring they remain in the synapse for a prolonged period. All this causes a downstream effect of increased sympathetic pathways in the body. Diagnosis Dr. Arreaza: The diagnosis starts with collecting a good history and performing a complete physical exam, and then we confirm with an echocardiogram. Abishak: Yes, diagnosis requires both symptoms consistent with heart failure and objective evidence of reduced ejection fraction. Echocardiography is the primary diagnostic tool. We also measure BNP. In certain cases, cardiac MRI is used to evaluate myocardial fibrosis and exclude infiltrative or inflammatory etiologies. Coronary angiography may be performed if ischemic disease is suspected.Guideline-Directed Medical Therapy Dr. Arreaza: GDMT Guideline-Directed Medical Therapy started around 1987 when ACE inhibitors were proven to improve mortality in patients with heart failure. Then, during the following decades, many medications have been added to GDMT. Until around 2019–2022 we came out with the main 4 groups of medications that we know as GDMT. Let’s talk about GDMT. Akbar: There are four core pillars in GDMT. First, an angiotensin receptor-neprilysin inhibitor, such as sacubitril with valsartan (Entresto), is preferred over ACE inhibitors when tolerated. This medication reduces mortality and heart failure hospitalizations. Second, evidence-based beta blockers including carvedilol, metoprolol succinate, or bisoprolol are used to reduce sympathetic overactivity and improve ventricular remodeling. Third, mineralocorticoid receptor antagonists such as spironolactone or eplerenone reduce fibrosis and improve survival. The Fourth pillar is SGLT2 inhibitors such as dapagliflozin or empagliflozin, which provide significant reductions in heart failure hospitalizations and cardiovascular mortality, regardless of diabetes status. Abishak: Other main parts of the treatment are diuretics, which are used for symptom control but do not reduce long-term mortality. Dr. Arreaza: As a recap: The current 4 pillars of GDMT are: ARNI/ACEi + β-blocker + MRA + SGLT2i) Beta Blocker Considerations Dr. Arreaza: Sometimes we may be concerned about using beta blockers in active meth users. What did you read about it? Abishak: Historically, there was concern about unopposed alpha stimulation. However, in chronic heart failure, beta blockers remain essential. Carvedilol is often favored because it provides both alpha and beta blockade. Careful titration and close monitoring are critical.Reversibility and Remodeling Dr. Arreaza: Regarding meth-associated HFrEF, we have good news for meth users. Tell us about how reversible this condition is. Akbar: It can be reversible. One of the most important aspects of this condition is that significant reverse remodeling may occur if the patient stops methamphetamine use and adheres to medical therapy. The Left ventricular ejection fraction can improve substantially and, in some cases, normal

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

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 m

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

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

Episode 210: Heat Stroke BasicsWritten 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 InjuryHigh 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 ResponseHeat 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 AbnormalitiesEndothelial 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 CollapseAs 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 DysfunctionThe 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 bot

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.

Episode 208: Cough Basics (Pidjin English)Written by Ebenezer DadzieYou 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 BasicsHOST 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 FeverHOST 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 TreatmentHOST 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 BreakHOST 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 – TakeawaysHOST 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 TimeHOST 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) AsthmaB) GERDC) Chronic bronchitisD) 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 an

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

Episode 206: Street Medicine and Harm Reduction. Mohammed Wase (medical student) and Dr. Singh describe what it is like to provide health care on the streets. They share their personal experiences working in a street medicine team. They describe the practice of harm reduction and emphasize the importance of respecting autonomy and being adaptable in street medicine. Written by Mohamed Wase, MSIV, American University of the Caribbean. Editing by Hector Arreaza, MD. Hosted by Harnek Singh, 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.Introduction Dr. Singh: Welcome to another episode of our podcast, my name is Dr. Harnek Singh, faculty in the Rio Bravo Family Medicine Residency Program. Today we have prepared a great episode about street medicine, a field that has grown a lot during the last decade and continues to grow now. We are joined by a guest who is passionate about this topic. Wase, please introduce yourself.Wase: Hello everyone, my name is Mohammed, many know me as Wasé, I am a 4th year medical student from the American University of the Caribbean. Today we’re diving into a topic that sits at the intersection of medicine, compassion, and public health — Street Medicine and Harm Reduction. We’re going to step outside with this episode, literally, away from the clinic and hospital, to explore more about what care looks like in the streets. Historic background: How did street medicine start?Wase: The roots of Street Medicine in the United States go back to Dr. Jim Withers in Pittsburgh in the 1990s, who literally began by dressing as a homeless person and providing care on the streets to build trust. His efforts have shaped street medicine to what it is today. It combines primary care, mental health, and social support. Dr. Singh: For family physicians, this model aligns perfectly with our holistic approach. We don’t just treat diseases; we treat people in context — their environment, their challenges, their stories. What is the main population seen by a street medicine team?Wase: This patient population includes those struggling with homelessness, housing insecurity, food insecurity, substance use disorders; with patients being preoccupied on where they will sleep that night or when their next meal comes, they do not have the luxury of prioritizing their health. Street Medicine is a powerful outreach program to bring care to them in order to provide equitable care within our community. Dr. Singh: How is street medicine different than caring for patients in the clinic?Wase: Working on the street means we have to think differently about what healthcare looks like — and that’s whereharm reductioncomes in.What is Harm Reduction?Wase: Harm reduction is a public health philosophy that focuses on reducing the negative consequences of high-risk behaviors, rather than demanding complete abstinence.Dr. Singh: Preventive care is the backbone of family medicine. For example, we keep up with the USPSTF guidelines and make sure our patients are up to date with their screenings. But what does that look like in the street medicine setting? Wase: In practice, that might mean:-needle exchange program: Offering clean syringes to prevent HIV transmission and removing used needles-distributing naloxone to prevent overdose deaths-offering fentanyl test-strips to prevent use of substances that are unknowingly laced with fentanylDr. Singh: Also:-providing condoms to prevent sexually transmitted infections-providing wound care to prevent further spread of infectionWase: Yes, the idea is: people are going to engage in risky behaviors whether or not we approve of it, so let’s meet them with compassion, tools, and trust instead of judgment. Harm reduction also applies beyond substance use; think about safer sex education, or even diabetic foot care among people who can’t refrigerate insulin or change shoes daily. It’s all about meeting people where they areandkeeping them alive and engaged in care. Planning in Street Medicine: Wase: It takes careful disposition planning and aftercare for this population. Instead of the traditional outpatient setting where we can place referrals and expect our patients to follow through with them. On street medicine, for follow up visits it requires arranging transportation, finding a pharmacy close in proximity, educating and counseling on medication adherence and how to make it, and making sure they have some sort of shelter to get by. Dr. Singh: Let’s describe a typical street med encounter.Wase: A typical Street Medicine encounter might look like this: a small team — usually a physician, nurse, social worker, and sometimes a peer advocate — goes out with bac

Episode 205: Atopic Dermatitis Kara Willbanks (medical student) explains the definition, pathophysiology, and treatment of eczema. Dr. Arreaza adds some input about bleach baths and topical steroids. Written by Kara Willbanks, 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.October is the Eczema Awareness Month!What Is Atopic Dermatitis? Atopic dermatitis, a form of eczema, is a chronic, relapsing inflammatory skin disorder that often begins in childhood but can affect people of all ages. Other eczematous dermatoses include seborrheic dermatitis, contact dermatitis, juvenile plantar dermatosis, and stasis dermatitis. Atopic dermatitis is one of the most common skin conditions in the developed world, typically affecting up to 20% of children and 5-10% of adults. Patients usually present with severe pruritus (itchiness) and dry, inflamed patches of skin. Common sites include the face and extensor surfaces in infants, and flexural areas — like the elbows and knees — in older children and adults. Atopic dermatitis is often associated with other allergic conditions like asthma and allergic rhinitis — what we call the “atopic triad.” These conditions should also be considered when diagnosing someone with atopic dermatitis. PathophysiologyAtopic dermatitis is believed to occur due to a combination of genetic, immune, and environmental factors. A major component is a defective skin barrier, often linked to mutations in the filaggrin gene. This allows irritants, allergens, and microbes to penetrate the skin more easily, triggering inflammation.Differential DiagnosisAtopic dermatitis can sometimes mimic other skin conditions, so it’s important to keep a differential in mind: -Contact dermatitis – triggered by allergens or irritants; often limited to the area of exposure but also tends to be very itchy. -Seborrheic dermatitis – greasy scales, typically on the scalp, eyebrows, and nasolabial folds -Psoriasis – well-demarcated plaques with silvery scales; sometimes found in similar areas of the body as eczema. -Tinea (fungal infections) – ring-shaped lesions with active, scaly borders -Important to note that treatment of tinea with topical steroids can make the rash much worse. -Scabies – intense itching, especially at night, with burrows between fingers. Ruling out these conditions helps guide the right treatment and prevent chronic mismanagement. As a recap our main differential diagnosis: contact dermatitis, seborrheic dermatitis, psoriasis, tinea, and scabies.The treatment cornerstone: Moisturizers The most important daily treatment for atopic dermatitis is regular moisturizing. Moisturizers repair the skin barrier, reduce water loss, and protect against irritants. They should be applied at least twice daily, ideally right after bathing while the skin is still damp (within 3 minutes is most ideal). Use greasy ointments or thick creams rather than lotions — think products with ceramides or glycerin (hydrates and protects skin). It is best to choose ointments or creams without additives, perfumes or fragrances. Greasier ointments are the preferred vessel; however, patient compliance may be less as they may be unpleasant to some.Bleach Baths For patients with frequent skin infections or severe eczema, dilute bleach baths can be a game-changer. How to do it? Use ¼ to ½ cup of household bleach in a full standard bathtub of water (about 40 gallons) and soak for 10 minutes, twice a week. This helps reduce bacterial colonization — particularly Staphylococcus aureus — which commonly worsens eczema. After the bath, pat the skin dry and immediately apply a moisturizer (within 3 minutes). Bleach baths are endorsed by the American Academy of Pediatrics and the American Academy of Dermatology as an adjunctive treatment for atopic dermatitis, especially in patients with moderate to severe disease and frequent bacterial infections, but the evidence for their efficacy is mixed, and further well-designed studies are needed.Medical Treatments-Topical corticosteroids: When moisturizers alone aren’t enough, we move to anti-inflammatory therapy. Topical corticosteroids are the first-line treatment for flares. Some studies suggest that a short burst of a high-potency topical corticosteroid to rapidly control active disease, followed by a quick taper in potency, is most effective, whereas others use the lowest-potency agent thought to be needed and adjust upward only if this fails. Common steroids used are hydrocortisone (low potency), triamcinolone (medium potency), or betamethasone (high potency). -High-potency steroids shou

Episode 204: Adult Pneumococcal Vaccines in 2025. Luz Perez (MSIV) presents all the available pneumococcal vaccines for adults. Dr. Arreaza guides the discussion about what to do with adults who have previously received pneumococcal vaccines. Written by Luz Perez, 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.Today we’re answering a clinic classic: Which pneumococcal vaccine should my adult patient get—and when? This is an update of episode 90.Why pneumococcal vaccines matter?Pneumococcal vaccines prevent infections caused by the bacteria Streptococcus pneumonia. These bacteria can cause serious infections like pneumonia, meningitis, and bacteremia. In 2017, the CDC reports that there were more than 31,000 cases of pneumococcal infections and 3,500 deaths from invasive pneumococcal disease. Children are vaccinated in early childhood, before age 5, with PCV15 or PCV 20, at the age of 2, 4, 6 months and a last dose around 12-15 months. Why do we vaccinate adults?Adults are vaccinated because they’re at higher risk of getting pneumococcal disease or of having worse outcomes if they do. Vaccines are important because they protect these at-risk patients and reduce the spread of infections among communities. What are the available vaccines? PCV vs PPSV.There are two pneumococcal vaccines used in practice: a polysaccharide vaccine (PPSV) and a conjugate vaccine (PCV). Both protect by targeting capsular polysaccharides from pneumococcal serotypes most often responsible for invasive disease. In simple terms, these vaccines target a part of the bacteria “coating” and create antibodies or proteins that protect the body when the strep enters the body. PPSV (polysaccharide): PPSV is made from purified pieces of the pneumococcal capsule or coating. The current vaccine PPSV23 (Pneumovax®) covers 23 serotypes (or strains) that were the leading cause of pneumococcal infections in the 1980s. PCV (conjugate): Pneumococcal conjugate vaccines (PCVs) take capsular polysaccharides from the bacterium and chemically link them to a carrier protein, which changes and strengthens the immune response. Current PCVs come in four versions: PCV13 (Prevnar 13)PCV15 (Vaxneuvance)PCV20 (Prevnar 20)PCV21 (Capvaxive) The number indicates the amount of pneumococcal capsule types covered by each vaccine. PCV21 was designed around adult disease patterns and covers many serotypes currently driving invasive disease in adults. However, it does not include serotype 4, but this serotype is covered by the PCV20 and PCV15.Who should be vaccinated? In 2024, the United States Centers for Disease Control and Prevention's Advisory Committee on Immunization Practices (ACIP) updated their recommendations on Pneumococcal vaccinations for adults. Their recommendations are: Everyone 50 years or olderAdults age 19–49 with risks: chronic lung/liver disease, heart failure, diabetes; CSF leak or cochlear implant; immunocompromised states (e.g., HIV, hematologic malignancy, CKD/nephrotic syndrome); functional/anatomic asplenia.Patients with history of prior invasive pneumococcal disease: still vaccinate. What vaccine should be given for adults that have never received the Pneumococcal vaccine?For eligible adults with no prior pneumococcal vaccines, there are three choices:PCV21 oncePCV20 oncePCV15 now, followed by PPSV23 later, usually 1 year; 8 weeks if immunocompromised, CSF leak, or cochlear implant.PCV 20 or PCV21 seem more convenient. Once and done. If available, PCV21 is a great one-and-done pick for most adults because it’s tailored to current adult serotypes.Serotype 4 caveat: If your patient is at higher risk for serotype 4 disease—think Navajo Nation, or folks in the Western US/Canada with substance use disorders or experiencing homelessness—choose PCV20 (or PCV15 followed by PPSV23 if PCV20 isn’t available).What if the patient already received a Pneumococcal vaccine in the past?Plan depends on which vaccine they received and when.PPSV23 only: give PCV21 ≥1 year later (or PCV20 if serotype-4 risk or PCV21 unavailable).PCV10 or PCV13 only: give PCV21 (or PCV20 if PCV21 unavailable) ≥1 year later. If a PCV is not available, discuss PPSV23 now vs waiting until PCV is available.If patient receives PPSV23 now will need to return ≥1 year later to receive a PCV vaccine, and no more vaccines are needed after that.Is it safe to administer the Pneumococcal vaccine with other vaccines?Coadministration is fine with other non-pneumococcal vaccines, as long as we use different syringes and sites. Data support same-day administration of PPSV23 + influenza, and PCV20 wit