Rio Bravo qWeek

Rio Bravo Family Medicine Residency Program
  • 5.0 (11)
  • MEDICINE
  • UPDATED MONTHLY

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. 1D AGO

    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

  2. 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

  3. 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

  4. 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

  5. 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

  6. 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

  7. 11/21/2025

    Episode 206: Street Medicine and Harm Reduction

    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 fentanyl Dr. Singh: Also: -providing condoms to prevent sexually transmitted infections -providing wound care to prevent further spread of infection Wase: 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 backpacks of supplies. They might start with wound care, blood pressure checks, or even medication refills. But what’s just as important is the relationship-building. Sometimes, the first visit isn’t about medicine at all — it’s about showing up consistently. Over time, that trust opens the door for conversations about addiction treatment, mental health, and preventive care. For example, in some California Street Medicine programs, teams are treating chronic conditions like hypertension, diabetes, and hepatitis C, right where patients live with the same evidence-based care we’d give in a clinic. One of my favorite quotes from Street Medicine teams is: “We’re not bringing people to healthcare; we’re bringing healthcare to people.” Challenges in Street Medicine: Wase: The populations that you will encounter include many people who will often downplay their own health concerns and prior diagnoses. Unfortunately, this is usually from countless months or years of feeling neglected by our healthcare system. Some may even express distrust in our healthcare system and healthcare providers. Patient will, at times, be apprehensive to receive care or trust you enough to tell their story.  Dr. Singh: Interviewing patients is a critical aspect of providing equitable care on the streets. It is always important to offer support and medical care, even if the patient denies it, always reassure that your street medicine clinic will be around every week and ready for them when they would like to seek care.  Wase: Respecting patient autonomy is an utmost concern as well. Another element of interviewing to consider is to invite new ideas and information; instead of lecturing patients about taking medications on time or telling them they need to stop doing drugs—simply asking a patient “would you like to know more about how we can help you stop using opioids?” respects their choice but can also spark new ideas for them to consider.  Singh: Adaptability is another key component to exceling patient care in street medicine. Like, performing physical exams on park benches or in the back of a minivan. Always doing good with our care but also respecting their autonomy is crucial in building a trust that these patients once lost with our system.  Wase: Each patient has their own timeline, but we as providers should always assure them that our door is always open for them when they are ready to seek care.  Conclusion. Wase: So, to wrap up — Street Medicine and harm reduction remind us that healthcare isn’t just about hospitals and clinics. It’s about relationships, trust, and dignity. Every patient deserves care, no matter where they sleep at night. If you’re a resident or student listening, I encourage you to seek out these experiences — volunteer with Street Medicine teams, learn from harm reduction workers, and let it shape how you practice medicine. Thank you for listening to this episode of the Rio Bravo qWeek podcast. I’m Mohammed — and I hope this conversation inspires you to meet patients where they are and walk with them on their journey to health. Dr. Singh: If you liked this episode, share it with a friend or a colleague. This is Dr. Singh, signing off. 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: Doohan, N.C. “Street Medicine: Creating a ‘Classroom Without Walls’ for People Experiencing Homelessness.” PMC – National Library of Medicine, 2019.Hawk, M., et al. “Harm Reduction Principles for Healthcare Settings.” Harm Reduction Journal, vol. 14, no. 1, 2017.Withers, J.S. “Bringing Health Professions Education to Patients on the Streets.” Journal of Ethics, AMA, vol. 23, no. 11, Nov. 2021.“Our Story.” Street Medicine Institute, 2025, www.streetmedicine.org/our-story.“Principles of Harm Reduction.” National Harm Reduction Coalition, 2024, https://harmreduction.org/about-us/principles-of-harm-reduction/.Salisbury-Afshar, Elizabeth, Bryan Gale, and Sarah Mossburg. “Harm Reduction Strategies to Improve Safety for People Who Use Substances.” PSNet, Agency for Healthcare Research & Quality, 30 Oct. 2024.Douglass, A.R. “Exploring the Harm Reduction Paradigm: The Role of Boards in Drug Policy and Practice.” PMC – National Library of Medicine, 2024.Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

    21 min

  8. 10/31/2025

    Episode 205: Atopic Dermatitis

    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.  Pathophysiology Atopic 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 Diagnosis Atopic 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 should never be applied to sensitive skin like the face. With short-term use of lower-potency steroids, there is a low likelihood of skin atrophy but use for more than 6 months is linked with greater levels of skin thinning  -Wet wrap therapy: Wet wrap therapy improves absorption of topic steroid. Apply a topical steroid, then layer a wet dressing and then a dry dressing over the top of that. This can be beneficial in providing  both relief of symptoms and prevention of itching. In pediatric patients it is called “daddy’s socks therapy” because large socks may be used to cover the arms of kids. -Topical calcineurin inhibitors — like tacrolimus — are great alternatives for sensitive areas or for maintenance once inflammation is under control. They may burn upon application which can scare patients away from their use. -PO antihistamines can help with itching, especially at night, but they don’t treat inflammation itself. -Systemic therapies, like dupilumab (Dupixent®), an IL-4 receptor antagonist, are reserved for moderate to severe cases unresponsive to topical therapy. This is a great time to refer to your local dermatologist for management! Many of the newer treatments are highly effective but can require more frequent monitoring. Recent Research  One recent study is the 2024 Cochrane network meta-analysis comparing effectiveness of topical anti-inflammatory treatments for eczema that was recently published in the AFP Journal in July of 2025. Here are the highlights: -Over 291 RCTs with ~45,846 participants were included.  -The analysis ranked potent topical corticosteroids, JAK inhibitors (for example ruxolitinib (Opzelura® 1.5 %), and tacrolimus 0.1 % among the most effective for reducing signs and symptoms of eczema.  -In contrast, PDE-4 inhibitors [like crisaborole (Eucrisa®) 2 %] were among the least effective in this comparison.  -Regarding side effects: tacrolimus and crisaborole were more likely to cause burning or stinging at the application site; corticosteroids were less likely in the short term to cause local irritation. -Long-term outcomes regarding effectiveness or safety of treatments for eczema were not addressed by the review because they are rarely reported.” -Another insight from this study is considering cost when initiating treatment. Most topical steroids are significantly more cost effective than JAK inhibitors or calcineurin inhibitors so it may be best to start with a cheaper solution in an uninsured patient considering their relative effectiveness.  Additional Tips & Lifestyle  -Keep baths and showers short and in lukewarm water. -Avoid harsh soaps and detergents — use gentle, fragrance-free cleansers. -Wear soft cotton clothing instead of wool or synthetics. -Identify and avoid triggers — common ones include stress, sweating, allergens, and certain foods (especially in kids). -Ice packs can help reduce itching and relieve any burning sensation. -Keep fingernails short, especially in children, help cause less trauma to the skin from repeated itching.  Living with eczema  Many celebrities like Kerry Washington, Jessica Simpson, Kelly Rowland, Brad Pitt and Kristen Bell have spoken out about their lives with eczema. They have shared personal stories about how they were diagnosed, what treatment works for them, and the general impact it has had on their lives and mental health. I feel like it can be so important for celebrities to speak out about their lives with certain conditions because it helps to normalize the condition, raise awareness of the struggles, and encourages more open dialogue. It is important to remember that for patients living with eczema, the persistent itch-scratch cycle can be very distressing, causing patients to struggle with their sleep and day-to-day activities. Anxiety and depression are common in patients with eczema so as physicians it is vital to monitor for signs of distress. Support groups can be incredibly helpful for patients [National Eczema Association] If you are interested in providing additional information to your patients or getting this for yourself, you can find more resources on altogethereczema.org or nationaleczema.org.  Key Takeaways  Atopic dermatitis is chronic but manageable. Moisturizers are the foundation of treatment. Topical steroids and calcineurin inhibitors control inflammation. Bleach baths help reduce bacterial load and flare severity. Always rule out other skin conditions to ensure appropriate management. Atopic dermatitis can be managed by the primary care physician but in certain cases (cases refractory to standard topical treatment, recurrent infections, etc.), a referral to dermatology can be especially helpful. 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 vi

    24 min
See All (212)

5
out of 5
11 Ratings

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
    212
  • Rating
    Explicit
  • Copyright
    © 2020 Rio Bravo Family Medicine Residency Program
  • Show Website
    Rio Bravo qWeek

You Might Also Like