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Rio Bravo qWeek

Rio Bravo qWeek

223 episodes — Page 1 of 5

Episode 223: Oncogenic Viruses

May 8, 202619 min

Episode 222: Antibiotic Resistance

May 1, 202617 min

Episode 221: Insomnia Pharmacotherapy in Adults

Apr 24, 202619 min

Episode 220: Approach of Insomnia in Adults

Apr 20, 202628 min

Episode 219: Chronic Pain and Functionality in Cancer Survivors

Apr 13, 202615 min

Episode 218: Statin Therapy Fundamentals

Apr 6, 202617 min

Episode 217: Testicular Cancer

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

Mar 27, 202618 min

Episode 216: Fibromyalgia Overview

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

Mar 20, 202620 min

Episode 215: Meth-associated HFrEF

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

Mar 6, 202621 min

Episode 214: Valley Fever Complications

Episode 214: Valley Fever Complications. Dr. Arreaza: Welcome back to the podcast. I’m Dr. Arreaza, and today we’re talking about a topic that’s very relevant here in the Central Valley but often not well known in the rest of the country, it is called ValleyFever, or coccidioidomycosis. For more info about the Valley Fever diagnosis and initial treatment, please go to our previous podcast on the subject! Episode 143, recorded by wonderful Dr. Lovedip Kooner. To help us walk through this, I’m joined by Jordan, a medical student. Jordan, welcome back and Dr. Schlaerth, please introduce yourself. Jordan: Thanks, Dr. Arreaza. This is such an important topic, especially in endemic areas like where we live, the Central Valley of California, and Arizona. The public may think of Valley Fever as a mild pneumonia that just goes away eventually. But that’s not always the case. Some patients develop serious, life-altering complications, and a small but important number develop disseminated disease. Dr. Arreaza: Exactly. So today, we’re going to break this down systematically: pulmonary complications, dissemination to other organs, CNS disease, musculoskeletal involvement, systemic symptoms, and then we’ll touch on treatment principles and why follow-up matters so much. Dr. Schlaerth: Valley Fever can be missed in areas where it is not as common as in the Valley. 1989, earthquake in LA.Pneumonias that is not responding to treatment can be pulmonary cocci. Dr. Arreaza: Before we dive into specific complications, let’s zoom out. What percentage of patients get a complicated disease? Jordan: So, most infections are self-limited, but about 5–10% of patients develop chronic or progressive pulmonary disease, and 1% develop extrapulmonary disseminated disease. That sounds small, but given how common Valley Fever is in endemic areas, that’s still a lot of people. Dr. Arreaza: And the complications can be devastating, and they are not always in primary infection. Dr. Schlaerth: Dissemination can be silent. We don’t know exactly why dissemination happens; some ethnicities are more susceptible or other groups. Dr. Arreaza: Let’s start where Valley Fever usually begins: the lungs. What are the major pulmonary complications clinicians should know about? Jordan: The most common long-term complications are chronic pulmonary sequelae. These include: cavitary disease, pulmonary nodules, bronchiectasis, pulmonary fibrosis, and pleural complications like effusions, empyema, or pneumothorax. Dr. Arreaza: Cavitary disease comes up a lot. What does that look like clinically? Jordan: Cavities form in about 5–15% of cases. Many are asymptomatic, but symptomatic cavities can cause fever, fatigue, cough, sputum production, dyspnea, and hemoptysis. The tricky part is that symptoms often wax and wane, and even with treatment, current antifungals don’t eradicate the organism from chronic cavities. Dr. Arreaza: That’s very unfortunate, and sometimes those cavities remain and patients might not know that they have them, and those cavitary lesions may rupture. Jordan: Yes, rupture can lead to pyopneumothorax, which is a surgical emergency requiring prompt intervention. Dr. Kooner: Hello everyone, this is Dr. Kooner, and today I want to talk about one of my favorite topics: coccidioidal cavitary disease—because nothing says “fun lung pathology” like a hole in the lung that refuses to leave. Coccidioidal cavitary disease is a chronic pulmonary manifestation of infection. Many times, it’s found incidentally on imaging. Sometimes patients are being evaluated for respiratory symptoms, sometimes for systemic complaints, and sometimes for something completely unrelated—like when a chest X-ray was ordered for a pre-op clearance and suddenly… surprise cavity. Pulmonary cavities develop in about 5-10% of patients with Valley Fever. Most of the time, they appear as thin-walled residual lesions. They can be solitary or multiple, and they can range from a few centimeters to much larger. And while textbooks love to show the “classic look,” in real life they can be a little more… creative. These cavities can persist for years. Some patients feel completely fine and never know they have one. Others develop chronic symptoms or complications like rupture into the pleural space, secondary infection, or bleeding, which is when everyone suddenly becomes very interested in that cavity. Here’s an important teaching point: about 20% of patients with cavitary disease also have disseminated infection, most commonly involving bone. This challenges the old-school teaching that cavitary lung disease and dissemination rarely happen together. One major risk factor for cavitary disease—and for more severe or complicated infection overall—is diabetes mellitus. So how do patients usually present? Symptoms often overlap with classic Valley Fever symptoms. The most common presenting symptoms for cavitary disease that usually trigger evaluation are cough, hemoptysis, fever, and shortness

Feb 27, 202624 min

Episode 213: HIV PrEP Review

Episode 213: HIV PrEP Review H. Nicole Magaña, medical student, reviews the history of PrEP and outlines the currently FDA-approved medications used for HIV prevention. Dr. Arreaza provides additional perspective on long-acting injectable options, including how quickly they begin to protect patients after initiation. Written by Nicole Magana, MSIV, American University of the Caribbean. Comments and edits by Hector Arreaza, MD. You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice. Pre-exposure prophylaxis for HIV. Previous episodes related to HIV: -Episode 67, HIV history (September 2021) -Episode 68, HIV transmissibility (October 2021) -Episode 70 (October 2021), HIV prevention (including HIV Prep with oral medications) -Episode 98 (June 2022), we introduced Apretude, the first injectable for HIV PrEP. Apretude was approved in December 2021. What is Pre-Exposure prophylaxis (PrEP)? Pre-exposure prophylaxis, or PrEP, is the use of antiretroviral medications taken by individuals who are HIV-negative to prevent HIV acquisition. There are 30,000 new HIV infections annually in the US. How effective is it? When taken as prescribed, PrEP is highly effective at reducing the risk of HIV transmission through sexual exposure and injection drug use. Patients who are adherent to PrEP can lower their risk of contracting HIV by 99%. The effectiveness of oral PrEP is highly adherence dependent. In trials with 70% adherence, the relative risk of HIV acquisition was 0.27, compared to 0.51 with 40-70% adherence and no significant benefit with adherence ≤40%. How does PrEP work? PrEP works by maintaining therapeutic drug levels in the bloodstream and in target tissues. If HIV exposure occurs, viral replication is inhibited, preventing the establishment of infection. Brief History of PrEP. The concept of PrEP originated from early animal studies demonstrating that antiretroviral medications could prevent retroviral transmission when administered before exposure. In 2010, the iPrEx trial showed that daily oral tenofovir disoproxil fumarate (known as Truvada) with emtricitabine significantly reduced HIV acquisition among men who have sex with men and transgender women. This was the first large clinical trial to demonstrate the effectiveness of PrEP. In 2012, the FDA approved oral Truvada, which is TDF/FTC (tenofovir disoproxil and emtricitabine) for HIV prevention. Since then, additional studies have expanded indications and introduced new formulations, including long-acting injectable options. Who Should Be Offered PrEP? PrEP should be considered for any HIV-negative individual at increased risk of HIV acquisition, including Men who have sex with men, transgender individuals, heterosexual men and women with an HIV-positive partner, individuals with recent bacterial sexually transmitted infections, people who inject drugs, individuals engaging in condomless sex with partners of unknown HIV status. Remember that PrEP should be offered in a nonjudgmental, patient-centered manner, make it a safe space to talk openly about prevention of HIV. Available HIV PrEP Options. Daily Oral PrEP: There are 2 formulations of Tenofovir. There is Tenofovir disoproxil fumarate (TDF)/ Truvada and Tenofovir alafenamide (TAF)/ Descovy. Each is available in a tablet combined with Emtricitabine a nucleoside reverse transcriptase inhibitor. Truvada: It is approved for all populations at risk through sexual exposure or injection drug use. Something to look out for before starting this medication is for pre-existing CKD. Do not give to patients who have an estimated glomerular filtration rate of less than 60 mL/min. (6) Descovy: This option is approved for men who have sex with men and transgender women but is not approved for individuals at risk through receptive vaginal sex. It has less impact on renal function and bone mineral density compared to Truvada. It can be used in moderately reduced kidney function (GFR between 30-60 mL/min). Truvada and Descovy are taken orally once a day. After patients start taking these medications, when are they considered to be protected? Nicole: With daily oral PrEP, guidelines differ with WHO and International Aids Society-USA stating it takes about 7 days, while CDC states 21 days to allow for adequate concentration in tissues (1). Adherence is critical for efficacy. Injectable HIV PrEP. In 2021, the FDA approved the first Injectable PrEP option Long-acting cabotegravir (CAB-LA)- known on the market as Apretude. Cabotegravir is an integrase strand transfer inhibitor administered as an intramuscular injection.Dosing consists of an initial injection, a second injection one month later, and then m

Feb 20, 202620 min

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 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

Feb 13, 202613 min

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

Feb 6, 202615 min

Episode 210: Heat Stroke Basics

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

Jan 2, 202623 min

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.

Dec 12, 202521 min

Episode 208: Cough Basics (Pidjin English)

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

Dec 5, 202513 min

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.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

Nov 28, 202540 min

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 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

Nov 21, 202521 min

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. 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

Oct 31, 202523 min

Episode 204: Adult Pneumococcal Vaccines in 2025

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

Oct 10, 202517 min

Episode 203: Microinduction and harm reduction in OUD

Episode 203: Microinduction and harm reduction in OUD. Nathan Bui and Sanjay Reddy describe how to manage opioid use disorder (OUD) by using microinduction and harm reduction, strategies that are reshaping the way we treat opioid use disorder. Written by Sanjay Reddy, OMSIV and Nathan Bui, OMSIV. Western University of Health Sciences, College of Osteopathic Medicine of the Pacific.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.IntroWelcome to episode 203 of Rio Bravo qWeek, your weekly dose of knowledge.Today, we’re tackling one of the biggest health challenges of our time: opioid use disorder, or OUD. Nearly every community in America has been touched by it: families, friends, even healthcare providers themselves. For decades, treatment has been surrounded by barriers, painful withdrawals, stigma, and strict rules that often do more harm than good. Too many people who need help never make it past those walls. But here’s the hopeful part, new approaches are rewriting the story. They are less about rigid rules and more about meeting people where they are. Two of the most promising strategies for treatment of OUD are buprenorphine microinduction and harm reduction. Let’s learn why these two connected strategies could change the future of addiction recovery. Background information of treatment: The X-waiver (short for DATA 2000 waiver) was a special DEA requirement for prescribing buprenorphine for opioid use disorder. Doctors used to take extra training (8 hours) and apply for it. Then, they could prescribe buprenorphine to a very limited number of patients. The X-waiverhelped regulate buprenorphine but also created barriers to access treatment to OUD. It was eliminated in January 2023 and now all clinicians with a standard DEA registration no longer need a waiver to prescribe buprenorphine for OUD. Why buprenorphine?Buprenorphine is one of the safest and most effective medications for opioid use disorder. It has some key attributes that make it both therapeutic and extremely safe: 1) As a partial agonist at mu-opioid receptors, it binds and provides enough partial stimulation to prevent cravings and withdrawal symptoms without producing strong euphoria associated with full agonists. 2) Because it has a strong binding affinity compared to full agonists, it easily displaces other opioids that may be occupying the receptor. 3) As an antagonist at kappa-opioid receptors, it contributes to improved mood and reduced stress-induced cravings. 4) The “ceiling effect”: increasing the dosage past a certain point does not produce a stronger opioid effect. This ceiling effect reduces the risk of respiratory depression and overdose, making it a safer option than full agonists. 5) It also had mild analgesic effects, reducing pain. 6) Long duration of action: The strong binding affinity and slow dissociation from the mu-opioid receptor are responsible for buprenorphine's long half-life of 24–60 hours. This prolonged action allows for once-daily dosing in medication-assisted treatment for OUD. Induction vs microinduction:The problem is, starting it—what’s called “induction”—can be really tough. Patients usually need to stop opioids and go through a period of withdrawal first. Drugs like fentanyl, which can cause precipitated withdrawal —a sudden, severe crash may push people back to using opioids. Because buprenorphine binds so tightly to the mu-opioid receptor, it can displace other opioids, such as heroin or methadone. If buprenorphine is taken while a person still has other opioids in their system, it can trigger sudden and severe withdrawal symptoms.Opioid withdrawal sign sand symptoms:Opioid withdrawal symptoms are very uncomfortable; patients may even get aggressive during withdrawals. As a provider, once you meet one of these patients you never forget how uncomfortable and nasty they can be. The symptoms are lacrimation or rhinorrhea, piloerection "goose flesh," myalgia, diarrhea, nausea/vomiting, pupillary dilation, photophobia, insomnia, autonomic hyperactivity (tachypnea, hyperreflexia, tachycardia, sweating, hypertension, hyperthermia), and yawning. Think about all the symptoms you run for COWS (Clinical Opiate Withdrawal Scale). It is estimated 85 % of opioid-using patients who inject drugs (PWID) reported opioid withdrawal. Fortunately, even though opioid withdrawal is very uncomfortable, it is not life-threatening (unlike alcohol or benzodiazepine withdrawal, which can be fatal).Many patients who start the journey treating opioid use disorder experience “bumps in the road” --they avoid treatment or drop out early. What is Microinduction? Microinduction is a fairly new strategy sta

Sep 19, 202512 min

Episode 202: BPA Overview

Episode 202: BPA OverviewWritten by Cameron Carlisle, 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._____________________Arr: Welcome to another episode of Rio Bravo qWeek. My name is Hector Arreaza, I’m an associate program director and faculty in the Rio Bravo Family Medicine Residency Program. Today my co-host is Cameron Carlisle, who is a 4th-year medical student finishing his last rotation of med school. Welcome, Cameron, please introduce yourself.Arreaza: What are we talking about today, Cameron?Cam: Dr. Arreaza, did you know you’re probably carrying around a chemical in your body that mimics estrogen? In fact, a 2004 CDC study found over 92% of Americans had detectable levels of Bisphenol A (BPA) in their urine. Today’s topic is BPA.BPA is everywhere: receipts, water bottles, canned foods, baby bottles, and even our dental fillings. It’s one of the most ubiquitous endocrine-disrupting chemicals (EDCs), which interferes with the body’s hormone systems. That’s why today’s episode is about making the invisible visible. Our goals for today’s podcast:Break down what BPA isShow how it affects the human bodyExplain how you and your patients can limit exposureEmpower both clinicians and the public with real, practical informationArreaza: Thanks for clarifying BPA today. It seems like we always have to learn about a new carcinogen or toxic substance that we are exposed to. I remember when I was a child, Yellow #5 became very concerning for the general public but it is still being used in our foods. So, it’s good you are talking about this. What Is BPA?Cam: Bisphenol A (BPA) is an industrial chemical used since the 1950s, primarily in polycarbonate plastics and epoxy resins. It makes plastic clear, and is often found in:Water bottlesCanned food liningsBaby bottles (pre-2012)Takeout containersCash register receiptsDental sealantsArreaza: So, I’ve seen the “BPA-free” labels many times, and today I’m glad you are going to shed some light about it.Cam: What’s alarming is that BPA leaches out of these products, especially when exposed to heat, acidity, or repeated use. A Harvard study found that people who drank from plastic bottles for just one week had a 69% increase in urinary BPA levels (Carwile & Michels, 2009).Arreaza: That’s a lot of people 69%. Section 3: What happens when BPA gets into our body? How BPA Works in the BodyCam: BPA is classified as an endocrine disruptor, meaning it can bind to estrogen receptors and mimic or block natural hormone functions.It affects:Reproductive systems (both male and female)NeurodevelopmentThyroid signalingPancreatic β-cell functionMetabolism and fat storageEven low-dose exposure can disrupt cellular function. BPA acts as a xenoestrogen (foreign estrogen) and has been shown to alter DNA methylation, leading to epigenetic changes that persist across generations (Manikkam et al., 2013).Arreaza: So, BPA can cause epigenetic changes that can be inherited. BPA can persist for generations in your offspring.BPA’s Health Impacts – What the Research SaysHere’s where it gets serious. Let’s go system-by-system:1. Reproductive HealthFemales: Linked to PCOS, infertility, and early puberty (Peretz et al., 2014).Males: Reduced sperm count and motility; altered testosterone levels.2. Pregnancy and Birth OutcomesIncreased risk of preterm birth, gestational diabetes, and low birth weight (Snijder et al., 2013).Studies show BPA crosses the placenta, directly affecting the fetus.3. Neurological DevelopmentAssociated with ADHD, anxiety, and impaired executive function in children exposed in utero (Mustieles et al., 2015).4. Metabolism and DiabetesBPA exposure is linked to insulin resistance, obesity, and type 2 diabetes, even at low doses (Lang et al., 2008).5. CancerAnimal and human data link BPA to increased risk of breast and prostate cancer via estrogenic mechanisms.6. MortalityA 2020 JAMA study found individuals with higher BPA levels had a 49% increased risk of all-cause mortality compared to those with lower levels (Gao et al., 2020).Arreaza: You are scaring me. I wonder what my BPA level is in my blood. Actually, BPA can be detected in urine. This is the most common approach for population-level biomonitoring, because BPA and its metabolites are mostly excreted in urine. Studies have found that BPA is present in most people, even up to 85–99% in large cohorts. Cam: That’s literally everyone. Sources of BPA ExposureLet’s talk about things we use every day:Thermal receipts (like from Target or Starbucks): BPA can transfer onto your skin and be absorbed, especially if your hands are we

Sep 5, 202522 min

Episode 201: AKI Roadmap

Episode 201: AKI Roadmap. Future Dr. Ayyagari describes the different types of acute kidney injury and shares some elements of management for each category. Dr. Arreaza shares some input about statistics and the importance of drinking water during summer.Written by Tejasvi Ayyagari, 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.INTRODUCTION:Dr. Arreaza: Hello everyone, and welcome back to Rio Bravo qWeek — your weekly dose of knowledge. I’m Dr. Arreaza, I am a faculty member and associate program director of the Rio Bravo FM residency program. In Episode 126, we briefly introduced the topic of Acute Kidney Injury (AKI), but today, we’re taking a deep dive into the matter. I have here alongside my cohost, future Dr. Ayyagari, AKA TJ. Please, TJ, introduce yourself.TJ: Hey everyone, good to be back on the podcast. My name is TJ Ayyagari, and I am currently finishing my last rotation of medical school with Rio Bravo CSV outpatient. I hope everyone is doing well and staying safe.Dr. Arreaza: So, TJ prepared this discussion about acute kidney injury, also known as AKI. This is a critical topic for our Kern community, especially during the summer months when the risk of AKI increases. You will face many patients with AKI on the wards, in the clinic, and especially on your future board exam. Hopefully, by the end of this episode, you all will have more information on AKI, but also the three different types: prerenal, intrinsic, and postrenal. TJ: Without further ado, let’s get started, Dr. Arreaza.SECTION 1 – What is AKI?Dr Arreaza: Let’s start with the definition. Let’s explain what AKI is. TJ: Absolutely. So, an AKI is not just a bump in the patient’s creatinine. According to the Kidney Disease Improving Global Outcomes (KDIGO) definition, an AKI embodies any of the following criteria:Increase in serum creatinine by ≥0.3 mg/dL within 48 hours, ORIncrease in serum creatinine to ≥1.5 times baseline within the prior 7 days, ORUrine volume Dr. Arreaza: The numbers show that AKI is increasing in our hospitals. According to the CDC, the incidence rate of newly diagnosed AKI has increased from 80 per 1,000 patient-years in 2007 to 242 per 1,000 patient-years in 2022. We must be vigilant and diagnose AKI appropriately because time is gold. We need to correct it and prevent further kidney damage, if possible. A critical step in the treatment is determining why the AKI is happening. Let’s start by discussing prerenal AKI. SECTION 2 – Prerenal AKIDr. Arreaza: Let’s remember our Latin language, “pre” means before, and “renal” means kidney. So, when you say pre-renal, it sounds like you’re referring to an event that happens before the kidneys.TJ: You’re right.A prerenal AKI is the most common type, and it refers to a problem that occurs before the kidney. The keyword here is perfusion — the kidneys are fine structurally, but they’re not getting enough blood flow.Common causes:Hypovolemia: vomiting, diarrhea, bleeding, and overdiuresis (surreptitious diuretic use).Low cardiac output: heart failure, MI (if the heart cannot pump blood effectively across the body, the kidneys suffer)Systemic vasodilation: sepsis, cirrhosis (with widespread vasodilation and increased capillary permeability, resulting in more fluids shifting across the vasculature to tissues, which means less is available for the kidneys).Dr. Arreaza: So, less perfusion means less oxygen, less nutrients and more damage to the kidney.TJ: However, the good news is that it’s often reversible if you fix the underlying cause quickly. Dr. Arreaza: What would we expect to see on lab values?TJ: As a result of low kidney perfusion, the kidneys do their best to conserve sodium and water, and urea reabsorption is increased in the proximal tubule. Subsequently, BUN rises disproportionately compared to creatinine (BUN: Cr ratio > 20:1). There is also a lab value called the Fractional excretion of sodium, otherwise known as FeNa, which will appear as Dr. Arreaza: Let’s talk about correction of prerenal AKI. If there is no perfusion, let’s improve renal perfusion!TJ: Of course! The treatment is to restore volume — fluids if hypovolemic, improve cardiac output if heart-related, and treat infection if septic. But remember, in CHF or cirrhosis, fluids can be tricky.SECTION 3 – Intrinsic AKIDr. Arreaza: Excellent explanation, TJ. So, let’s talk about the second type of AKI: intrinsic. Intrinsic AKI means the problem is inside the kidney itself. If you’re comparing it to simple terms, the plumbing and water pressure are fine (perfusion is normal), the drains are fine (no

Aug 29, 202526 min

Episode 200: All About Ascites

Episode 200: All About Ascites. Jesica Mendoza explains the pathophysiology, diagnosis and management of ascites. Dr. Arreaza adds input about early detection and prevention of spontaneous bacterial peritonitis. Written by Jesica Mendoza, OMS IV, Western University, College of Osteopathic Medicine of the Pacific. 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.Welcome to our episode 200! It is an honor to welcome back a wonderful medical student, her name is Jesica, and she has prepared this topic, and she is excited to share this information with us. Jesica presented in June this year an episode about gestational diabetes (episode 193) and today she will talk about ascites. Jesica, please tell us who you are again. What is ascites?Ascites is the buildup of fluid in between the visceral peritoneum and the parietal peritoneum in the abdomen. This is often caused by cirrhosis of the liver due to the increased portal HTN which leads to increased nitrous oxide (NO) and prostaglandins which then causes splanchnic vasodilation and decreased effective arterial volume. The decrease in arterial volume then causes an increase in the renin–angiotensin–aldosterone system (RAAS) and antidiuretic hormone (ADH) from the renal system which leads to sodium and water retention. This then causes a net reabsorption of fluids and ascites.Evaluation of ascites.Once someone has been found to have ascites the next step will be a diagnostic paracentesis. This includes removing fluid from the peritoneal cavity in order to determine the SAAG (Serum Ascites Albumin Gradient) score. SAAG : (serum albumin) − (albumin level of ascitic fluid). The two values should be measured at the same time.This score helps determine the cause of the ascites with a score >1.1 g/dL indicating portal hypertension usually due to liver disease such as cirrhosis. A SAAG score of A paracentesis can be done for diagnostic purposes in a new-onset ascites or if a patient with known ascites has clinical deterioration (such as fever, abdominal pain, hepatic encephalopathy, renal dysfunction, or leukocytosis). In cases of tense or refractory ascites, the paracentesis can be done for both diagnostic and therapeutic purposes. Tell us more about the serum ascites albumin gradient (SAAG).If the SAAG is greater than 1.1 (portal hypertension) you then use the serum protein levels for further management. For a low serum protein (Budd-Chiari syndrome is caused by obstruction of the hepatic venous outflow tract, most commonly the hepatic veins or the intra-/suprahepatic inferior vena cava, in the absence of cardiac or pericardial disease. This causes hepatic congestion, which can present with acute or chronic abdominal pain, hepatomegaly, ascites, and, in some cases, progressive liver dysfunction or portal hypertension; but up to 20% of cases may be asymptomatic. The most frequent underlying cause is a prothrombotic state, particularly cancer (Jes: myeloproliferative neoplasm). That’s why you mention the treatment: anticoagulation.A SAAG greater than 1.1 with a high serum protein level (>2.5) the cause points towards right sided heart failure or constrictive pericarditis. In both cases a referral to cardiology should be placed for management of the underlying cause of the ascites. Another cause of elevated protein levels is portal or splenic vein thrombosis. If this is the case, the patient is managed with anticoagulation again. Treating the underlying cause.Patients with cirrhosis causing ascites will need treatment for the underlying cause. If that cause is Hepatitis C or Hepatitis B, then starting antiviral therapy is crucial to reduce the liver’s inflammation. Diuresis is also very important to help with decreasing the ascites and in turn all the symptoms of ascites. Usually Furosemide and/or spironolactone can be used. In cases of mild ascites spironolactone is usually first line treatment. If the patient has recurrent ascites, they often are given a combination of spironolactone and loop diuretics like furosemide. The recommended ratio of furosemide (Lasix) to spironolactone for the treatment of ascites is 40 mg of furosemide to 100 mg of spironolactone (a 1:2.5 ratio). Recommended max dose: 160 mg furosemide and 400 mg spironolactone daily. Dose adjustments can be made every 72 hours to minimize electrolyte disturbances. Once the patient has ascites under control the diuretic dose is adjusted to the lowest effective dose to minimize side effects.Medications to avoid, sodium and water restriction.In conjunction with medical management, it is ideal that the patient stops alcohol if the patient has

Aug 15, 202517 min

Episode 199: Essential Screenings for Young Adults

Episode 199: Essential Screenings for Young AdultsDr. Lopez presents the most important screening tests for young adults. Dr. Arreaza adds some input on screening for depression and anxiety. Written by Alejandra Lopez, MD. Edits by Hector Arreaza, MD. Rio Bravo Family Medicine Residency Program. 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.Dr. Lopez: Screening is testing done to help identify disease in a person or population that typically appears healthy. Our goal as clinicians is to see which children are at increased risk of disease and will merit additional testing. For clinicians, testing should be both easy to perform and interpret. Now let’s talk about prevention in young adults.Dr. Arreaza: I can see it is important to talk about young adults because that population may be very hesitant to go to the doctor, in general. Tell us more about it.Dr. Lopez: We all know that early detection and prevention are key, but many young adults skip routine check-ups. Why is that? Sometimes it’s lack of awareness, fear, or just not knowing where to start. That’s why today, we’ll focus on four key screenings that every adolescent and young adult should know about.The Annual Physical ExamDr. Arreaza: I’m excited to talk about it. Many young adults only see a doctor when they’re sick, but screenings help catch issues early, sometimes before symptoms even appear. Tell us about the annual wellness exams and why they matter.Dr. Lopez: Let’s start with the basics—annual wellness exams. Many young people don’t feel the need to see a doctor if they’re feeling fine. So, these check-ups are important because many serious health conditions start silently, meaning no symptoms at first. Dr. Arreaza: What do we look for in an annual exam?Dr. Lopez: An annual check-up:· It is important to track growth and development (especially important for adolescents)It also helps monitor blood pressure, weight, and BMI to help find out who is at risk for elevated or low BP, underweight or overweight/obesity, by analyzing both weight and body mass index.· Discuss lifestyle habits like diet, exercise, and sleep· Evaluate whether you are up to date on vaccinations or due for age-appropriate vaccines.· Address any mental health concernsIt’s also a great opportunity for young people to establish a relationship with a provider they trust. This makes it easier to discuss sensitive topics like sexual health or mental health.Dr. Arreaza: So, you say that the annual physical exam helps identify all these issues early, and at the same time, you establish a relationship of trust with a doctor who you may need at any time. STI ScreeningDr. Arreaza: That brings us to our second key screening: testing for sexually transmitted infections (STIs). There are many STIs. Let’s focus on gonorrhea, chlamydia, syphilis, and HIV. Dr. Lopez, can you breakit down for us? Who needs STI screening, and why is it so important?Dr. Lopez: Absolutely. The CDC recommends that ALL sexually active women under age 25 get screened for chlamydia and gonorrhea annually. HIV testing should also be done at least once for all young adults and annually for those at higher risk. Why is this the case? Because Many STIs have no symptoms, but untreated infections can lead to serious complications like infertility or pelvic inflammatory disease (PID) in women. The good news is that these infections are easily treatable if caught early. If caught later in life, then women and men alike are at risk for worse conditions. Dr. Arreaza: Let's talk about how do we do it?Dr. Lopez: STI screening is simple:· For chlamydia and gonorrhea, it’s usually a urine test or a vaginal/cervical/oral swab.· For HIV, it’s a quick blood test or even an oral swab.Many young adults avoid testing because of fear, stigma, or concerns about privacy, but most clinics offer confidential or even anonymous testing. Doctors do not share any information regarding the minor or young adult or any patient for that matter. AND if we are requested to share any information with others- then it is our obligation as doctors to ALWAYS ASK THE PATIENT before sharing ANY health information with third parties/other entitiesDr. Arreaza: And that includes parents of minors. Doctors are not allowed to discuss STI test results with parents of minors unless they are authorized by the patient or if the patient is in danger, for example, if this is a result of sexual abuse.Mental Health ScreeningsDr. Arreaza: Now, let’s talk about something that’s just as important as physical health—mental health. Depression and anxiety are very common in young people, but many don’t seek help. How do doctors screen for depre

Jul 25, 202516 min

Episode 198: Fatigue

Episode 198: Fatigue. Future doctors Redden and Ibrahim discuss with Dr. Arreaza the different causes of fatigue, including physical and mental illnesses. Dr. Arreaza describes the steps to evaluate fatigue. Some common misconceptions are explained, such as vitamin D deficiency and “chronic Lyme disease”. Written by Michael Ibrahim, MSIV, and Jordan Redden, MSIV, Ross University School of Medicine. Edits and comments by Hector Arreaza, MDYou 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.Dr. Arreaza: Today is a great day to talk about fatigue. It is one of the most common and most complex complaints we see in primary care. It involves physical, mental, and emotional health. So today, we’re walking through a case, breaking down causes, red flags, and how to work it up without ordering the entire lab catalog.Michael:Case: This is a 34-year-old female who comes in saying, "I’ve been feeling drained for the past 3 months." She says she’s been sleeping 8 hours a night but still wakes up tired. No recent illnesses, no weight loss, fever, or night sweats. She denies depression or anxiety but does report a lot of work stress and taking care of her two little ones at home. She drinks 2 cups of coffee a day, doesn’t drink alcohol, and doesn’t use drugs. No medications, just a multivitamin. Regular menstrual cycles—but she’s noticed they’ve been heavier recently.Jordan:Fatigue is a persistent sense of exhaustion that isn’t relieved by rest. It’s different from sleepiness or muscle weakness.Classification based on timeline: • Acute fatigue: less than 1 month • Subacute: 1 to 6 months • Chronic: more than 6 monthsThis patient’s case is subacute—going on 3 months now.Dr. Arreaza:And we can think about fatigue in types: • Physical fatigue: like muscle tiredness after activity • Mental fatigue: trouble concentrating or thinking clearly (physical + mental when you are a medical student or resident) • Pathological fatigue: which isn’t proportional to effort and doesn’t get better with restAnd of course, there’s chronic fatigue syndrome, also called myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), which is a diagnosis of exclusion after 6 months of disabling fatigue with other symptoms.Michael:The differential is massive. So, we can also group it by systems.Jordan:Let’s run through the big ones.Endocrine / Metabolic Causes • Hypothyroidism: A classic cause of fatigue. Often associated with cold intolerance, weight gain, dry skin, and constipation. May be subtle and underdiagnosed, especially in women. • Diabetes Mellitus: Both hyperglycemia and hypoglycemia can cause fatigue. Look for polyuria, polydipsia, weight loss, or blurry vision in undiagnosed diabetes. • Adrenal Insufficiency: Think of this when fatigue is paired with hypotension, weight loss, salt craving, or hyperpigmentation. Can be primary (Addison's) or secondary (e.g., due to long-term steroid use).Michael: Hematologic Causes • Anemia (especially iron deficiency): Very common, especially in menstruating women. Look for fatigue with pallor, shortness of breath on exertion, and sometimes pica (craving non-food items). • Vitamin B12 or Folate Deficiency: B12 deficiency may present with fatigue plus neurologic symptoms like numbness, tingling, or gait issues. Folate deficiency tends to present with megaloblastic anemia and fatigue. • Anemia of Chronic Disease: Seen in patients with chronic inflammatory conditions like RA, infections, or CKD. Typically mild, normocytic, and improves when the underlying disease is treated.Michael: Psychiatric Causes • Depression: A major driver of fatigue, often underreported. May include anhedonia, sleep disturbance, appetite changes, or guilt. Sometimes presents with only somatic complaints. • Anxiety Disorders: Mental fatigue, poor sleep quality, and hypervigilance can leave patients feeling constantly drained. • Burnout Syndrome: Especially common in caregivers, healthcare workers, and educators. Emotional exhaustion, depersonalization, and reduced personal accomplishment are key features.Jordan: Infectious Causes • Epstein-Barr Virus (EBV):Mononucleosis is a well-known cause of fatigue, sometimes lasting weeks. May also have sore throat, lymphadenopathy, and splenomegaly. • HIV:Consider it in high-risk individuals. Fatigue can be an early sign, along with weight loss, recurrent infections, or night sweats. • Hepatitis (B or C):Can present with chronic fatigue, especially if liver enzymes are elevated. Screen at-risk individuals. • Post-viral Syndromes / Long COVID:Fatigue that lingers for weeks or months after viral infection. Often, it includes brain fog, muscle aches, and post-exertional m

Jul 18, 202531 min

Episode 197: Continuous Glucose Monitoring

Episode 197: Continuous Glucose MonitoringWritten by William Zeng, MSIII, and Chris Kim, MSIII. University of Southern California.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.Will: IntroToday we’re exploring Continuous Glucose Monitoring, or CGM. We’ll break down what CGM is, who benefits, how to access it, options available for our patients, the pros and cons, and a few final reflections on where this technology is heading. Chris, So what is CGM?Chris:Continuous glucose monitoring refers to the use of a small wearable sensor placed just under the skin to track glucose levels in real time throughout the day and night. These sensors measure glucose in the interstitial fluid and transmit readings to a receiver or smartphone at regular intervals, allowing for 24/7 glucose trend tracking. Will:CGM has been shown to improve glycemic control, increase “time in range,” and reduce hypoglycemia. Let’s review some evidence.Chris:A 2023 meta-analysis published in Diabetes Technology & Therapeutics reported a mean Hemoglobin A1c reduction of 0.43% across multiple trials. Will:In people with Type 1 diabetes, the IMPACT and DIAMOND studies showed sustained improvement in Hemoglobin A1c and hypoglycemia reduction over 6–12 months. CGM use in insulin-treated Type 2 diabetes patients also resulted in significant benefits, including reduced variability and fewer severe glucose excursions. Chris:Clinically and economically, CGMs help prevent long-term complications such as cardiovascular disease, nephropathy, and retinopathy. Chris, What patients specifically benefit the most from CGM?Will: CGMs are most commonly indicated for people with Type 1 diabetes and for those with Type 2 diabetes who are using intensive insulin regimens—typically defined as multiple daily injections or insulin pump therapy. Chris:And what are the qualifications in order to be covered by insurance?Will:In the United States, Medicare covers CGM as durable medical equipment for qualifying patients, and coverage requires a prescription, documentation of insulin use, and regular follow-up. Most major private insurers—including Blue Cross, Aetna, UnitedHealthcare, Cigna, and Kaiser—follow similar guidelines. Coverage is generally granted for patients with Type 1 diabetes or insulin-requiring Type 2 diabetes who monitor glucose at least four times daily or use an insulin pump. Chris:Some plans require demonstration of hypoglycemia unawareness or frequent glucose variability. For patients not on insulin, OTC CGMs may be an option, but coverage is typically not provided. That said, new FDA decisions are allowing over-the-counter access to CGMs like Abbott’s FreeStyle Libre and Dexcom’s Stelo, expanding availability for lifestyle or preventive purposes.Will:[There are a lot of products on the market. Which are the main products and how are they different?]Chris:The three main players in the CGM space are Dexcom, Abbott (FreeStyle Libre), and Senseonics (Eversense), each with unique offerings.Let’s start with Dexcom. Dexcom G7 is a real-time CGM system approved for both Type 1 and Type 2 diabetes. It combines a sensor and transmitter into one compact wearable patch worn on the abdomen or upper arm for up to 10 days. It updates glucose readings every 5 minutes and connects directly to a smartphone or Apple Watch via Bluetooth. Dexcom also integrates with insulin pumps like Tandem’s t:slim and the Omnipod 5. Data can be shared with providers through Dexcom Clarity, which integrates into electronic medical records (EMRs) like Epic. OTC access is not yet available for DEXCOM G7, but a new non-prescription product called Dexcom Stelo is being rolled out in 2025, targeting non-insulin-using Type 2 patients. Dexcom Stelo will also offer 15-day wear, smartphone integration, and factory calibration. The estimated OTC cost for Dexcom Stelo is expected to be around $99 for a 15-day sensor, or about $198/month.Will:$200! Abbott FreeStyle Libre comes in several versions. The Libre 2 offers 14-day wear and requires users to scan the sensor with their smartphone or reader to retrieve a glucose value. It has optional real-time alarms for high and low readings and transmits data to LibreView, which can integrate with most EMRs. Libre 3 is a real-time CGM with 1-minute interval updates, Bluetooth transmission, and a slimmer profile. Libre sensors are widely used in primary care and available OTC for non-insulin users. Libre 2 sensors cost approximately $70–$85 for a 14-day sensor, while Libre 3 is slightly higher, around $85–$100 per sensor—totaling about $140–$200/month out of pocket without insurance.Chris:Senseonics Eversense E3 is the only im

Jul 11, 202521 min

Episode 196: Bipolar Disorder

Episode 196: Bipolar Disorder. Learn about the diagnosis and management of bipolar disorder, presented by medical students Jennifer, Targol, and Tyler. Written by Jennifer Burnham, OMS III; Targol Mehrazar, OMS III; and Tyler Richins, OMS III. Western University of Health Sciences. Comments and editing 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.

Jun 27, 202515 min

Episode 195: Case of headache

Episode 195: Case of headache. Future doctors Ibrahim and Redden explain the most common causes of headaches and explain the features of a serious cause of headache. Dr. Arreaza highlights the importance of diagnosis migraines. Written by Michael Ibrahim, MSIV, and Jordan Redden, 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.Dr. Arreaza: Our topic today is one every doctor will commonly see in their practice: headaches. Headache is one of the most common neurological complaints encountered in clinical practice and affects people of all ages and backgrounds. I have learned that a headache can be “the noise of a working brain” or it can be a cue to a more serious condition. So, let’s start at the beginning: Michael, give us the big picture: how should clinicians think about headaches?Michael:Sure thing, Dr. Arreaza. So, at its core, a headache is pain that’s felt in the head, scalp, or neck. But that’s just the surface. Clinically, we break headaches into two broad categories: primary and secondary. Primary headaches are their own condition: things like migraines, tension-type headaches, or cluster headaches. Secondary headaches, on the other hand, are a symptom of something else: an infection, trauma, vascular event, or even a brain tumor.The challenge for us as clinicians is distinguishing between the two. Because while most headaches are benign, some can signal something much more serious. That’s why a detailed clinical history and a careful neurologic exam are absolutely essential.Jordan:Exactly. We were taught that while not every headache needs imaging, every headache needs a detailed history. Understanding the timeline, triggers, and associated symptoms can really point you in the right direction.Dr. Arreaza:Great points. Let's move into a real-world scenario. Michael, tell us about the patient case you brought to the podcast.Michael:Right. Our patient is a 32-year-old woman, Ms. A., who’s had six months of intermittent, throbbing headaches. They’re mostly on the right side, and they come with nausea, sensitivity to light and sound. She notices they’re often triggered by stress, poor sleep, or skipping meals. Her neuro exam is normal, but she’s anxious; she fears it might be a brain tumor.Jordan:That’s such a common scenario. Even when the clinical picture strongly suggests migraine, patients often fear the worst. And honestly, given how disabling migraine attacks can be, their concern is totally valid.Dr. Arreaza: Exactly. We should never downplay the patient’s fear. And in Ms. A’s case, the symptoms: unilateral throbbing, photophobia, nausea; these really do fit the classic migraine profile. Let’s review the major types of headaches.Michael:So, we break headaches down into primary and secondary. Under primary headaches, you’ve got migraines (with or without aura), tension-type headaches, which are the most common, and cluster headaches, which are rarer but incredibly distinctive.Jordan:When it comes to secondary headaches, we must think broadly. There are infectious causes like meningitis or encephalitis, vascular emergencies like subarachnoid hemorrhage, temporal arteritis in older adults, tumors, trauma, and even medication overuse.Dr. Arreaza:Let’s pause on that one: medication overuse. That’s a headache many patients don’t expect. They’re trying to manage their pain, but if they use analgesics too frequently (especially things like triptans, combination pain meds, or opioids) they can actually perpetuate the cycle of pain.Michael:It’s a vicious loop. Patients take more meds to control their headaches, but the rebound from those meds keeps the headache going. That’s why we always ask, how often are you taking something for your headache?Dr. Arreaza:That’s right. What are the clinical clues that would help us figure out the type of headache we’re dealing with?Michael:Well, migraines typically present with a combination of features: moderate to severe pain, often unilateral and throbbing, worsened by activity, and associated with nausea or vomiting and light or sound sensitivity. If there's an aura: visual changes, sensory symptoms, or speech disturbance, that can help confirm the diagnosis.Dr. Arreaza: Let’s remember the POUND mnemonics. Pulsating, throbbing, or varying the heartbeat. One to three days (4-72 h in duration). Unilateral location, usually frontotemporal. In children, it is often bilateral and switches to unilateral in adolescence. Nausea/Vomiting AND/OR Photophobia/Phonophobia. Disabling intensity: moderate to severe in intensity and it get worse with movement. Migraines

Jun 27, 202521 min

Episode 194: Acute Low Back Pain

Episode 194: Acute low back pain. Future Dr. Ibrahim presents a clinical case to explain the essential points in the evaluation of back pain. Future Dr. Redden adds information about differentiating between a back strain and more serious diseases such as cancer, and Dr. Arreaza shares information about returning to work after back strain.Written by Michael Ibrahim, MSIV. Editing and comments by Jordan Redden, MSIV, and 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.Dr. Arreaza:Welcome back, everyone. Today’s topic is one that every primary care provider, emergency doctor, and even specialist sees routinely: low back pain. It's so common that studies estimate up to 80% of adults will experience it at some point in their lives. But despite how frequent it is, the challenge is to identify which cases are benign and which demand urgent attention.Jordan:Exactly. Low back pain is usually self-limiting and mechanical in nature, but we always need to keep an eye out for the rare but serious causes: things like infection, malignancy, or neurological compromise. That’s why a good history and physical exam are our best tools right out of the gate.Michael:And to ground this in a real example, let me introduce a patient we saw recently. John is a 45-year-old warehouse worker who came in with two weeks of lower back pain that started after lifting a 50-lb box. He describes it as a dull, aching pain that radiates from his lower back down the posterior left thigh into the calf. He says it gets worse with bending or coughing, but he feels better when lying flat. He also mentioned some numbness in his left foot, but he denies any bowel or bladder issues. His vitals are completely normal. On exam, he had lumbar paraspinal tenderness, a positive straight leg-raise at 40 degrees on the left and decreased sensation in the L5 dermatome, though reflexes were still intact.Dr. Arreaza:That’s a great case. Let’s take a minute and talk about the straight leg raise test. This is a bedside tool we use to assess for lumbar nerve root irritation often caused by a herniated disc. ***Here's how it works: the patient lies supine, and you slowly raise their straight leg. If pain radiates below the knee between 30° and 70°, that suggests radiculopathy, especially involving the L5 or S1 nerve roots. Pain at higher angles is more likely due to hamstring tightness or mechanical strain.Michael:Right. So, stepping back: what do we mean by "low back pain"? Broadly, it's any pain localized to the lumbar spine, but it’s often classified by type or cause:Mechanical (like muscle strain or degenerative disc disease), Radicular (nerve root involvement), Referred pain (like from pelvic or abdominal organs), Inflammatory (AS), and Systemic or serious causes like infection or malignancy. Jordan:In John’s case, we’re thinking radicular pain, most likely from a herniated disc compressing the L5 nerve root. That’s supported by the dermatomal numbness, the leg pain, and that positive straight leg test.Dr. Arreaza:Good reasoning. Now, anytime we see back pain, our brains should run a checklist for red flags. These help us pick up more serious causes that require urgent attention. Let’s run through the red flags.Michael:Sure. For fracture, we think about major trauma or even minor trauma in the elderly, especially those with osteoporosis or on chronic steroids. Also, anyone over 70 years old.Jordan:Then we have infections, which could include things like discitis, vertebral osteomyelitis, or epidural abscess. Red flags include fever, IV drug use, recent surgery, or immunosuppression.Michael:Malignancy is another critical one, especially if there’s a history of breast, prostate, lung, kidney, or thyroid cancer. Clues include unexplained weight loss, night pain, or constant pain not relieved by rest.Jordan:And don’t forget about inflammatory back pain, like ankylosing spondylitis, which is often seen in younger patients with morning stiffness that lasts more than 30 minutes and improves with activity.Dr. Arreaza:And of course, we always rule out cauda equina syndrome: a surgical emergency. That’s urinary retention or incontinence, saddle anesthesia, bilateral leg weakness, or fecal incontinence. Missing this diagnosis can be catastrophic.Michael:Thankfully, in John's case, we don’t see any red flags. His presentation is classic for uncomplicated lumbar radiculopathy. But we must stay vigilant, because sometimes patients don’t offer up key symptoms unless we ask directly.Jordan:And that’s where associated symptoms help guide us. For example:Radicular symptoms like numbness or weakness follow dermatomal patterns. Const

Jun 20, 202518 min

Episode 193: Gestational Diabetes Intro

Episode 193: Gestational Diabetes IntroJesica Mendoza (OMSIII) describes the pathophysiology of gestational diabetes and the right timing and method of screening for it. Dr. Arreaza adds insight into the need for culturally-appropriate foods, such as vegetables in Mexican cuisine. Written by Jesica Mendoza, OMSIII, Western University of Health Sciences, College of Osteopathic Medicine of the Pacific. Editing 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.DefinitionGestational diabetes mellitus (GDM) is a condition that occurs to previously non-diabetic pregnant women, caused by glucose intolerance at around the 24th week of gestation. PathophysiologyGDM arises due to an underlying pancreatic beta cell dysfunction in the mother which leads to a decrease in the amount of insulin produced and thus leads to higher blood sugar levels during pregnancy. The placenta of the fetus will produce hPL (human placental lactogen) to ensure a steady supply of sugars to the fetus, creating an anti-insulin effect. However, hPL readily crosses the placental barrier causing the mothers insulin requirement to increase, when the mother’s pancreas cannot increase production of insulin to that level needed to counter the effect of hPL they become diabetic, and this leads to gestational diabetes. So, basically the placenta is asking for more glucose for the baby and the mother’s pancreas struggles to keep the glucose level within normal limits in the body of the mother. If left untreated, high levels of glucose in the mother can cause glucotoxicity in the mother.“Glucotoxicity” refers to the toxic effect of glucose. Glucose is the main fuel for cell functions, but when it is high in the bloodstream, it causes toxicity to organs. Prevalence of GDM.The CDC reports mean prevenance of GDM is 6.9%. In U.S. mothers the prevenance increased from 6.0% in 2016 to 8.3% in 2021. Many different factors have played a role in increasing gestational diabetes in American mothers, some of those being the ongoing obesity epidemic with excess body weight being a known risk factor for insulin resistance. Another being advanced maternal age (AMA) as more American women have children later in life their body becomes less sensitive to insulin and requires a higher insulin output on top of the insulin that is required for the fetus. The “American diet” is also something that has a big effect in diabetes development. With the increase of high-carb foods that are readily available, the diet of Americans has declined and is affecting the metabolic health of mothers as they carry and deliver their children. Despite ongoing awareness of GDM, 6% to 9% of pregnant women in the United States are diagnosed with gestational diabetes, and the prevalence continues to increase worldwide. It is estimated that in 2017 18.4 million pregnancies were affected by GDM in the world, which then continued to increase to 1 in 6 births to women with GDM in 2019. It was also found that women living in low-income communities were disproportionately affected due to limited healthcare access. Additionally, women with GDM had a 1.4-fold increase in likelihood of undergoing a c-section, with 15% increase in risk of requiring blood transfusion. Screening for GDMGestational diabetes is screened between the 24th to 28th week of gestation in all women without known pregestational diabetes. In women who have high-risk for GDM the screening occurs during the first trimester, these women usually have at least one of the following: BMI > 30, prior history of GDM, known impaired glucose metabolism, and/or a strong family history of diabetes. The screening during the first trimester is to detect “pregestational diabetes” because we have to keep a good glycemic control to improve outcomes of pregnancy. So, if it’s positive, you start treatment immediately. If these women are found to have a normal glucose, they repeat the testing again as done normally, at 24-28 weeks of gestation. How do we screen?The screening itself consists of two types of approaches. The two-step approach includes a 50-gram oral glucose tolerance test (OGTT), where blood glucose is measured in an hour and if it is below 140 they are considered to not have GDM, however if the reading is greater than 140 they must then do a 3-hour, 100g oral glucose tolerance test. The 3-hour OGTT includes measuring the blood sugars at Fasting which should be less than 95, at 1 hour at less than 180, at 2 hours at less than 155, and at 3 hours at less than 140. If 2 or more of these values exceed the threshold the patient is diagnosed with gestational diabetes mellitus. The one-step approach

Jun 6, 202524 min

Episode 192: ADHD Treatment

Episode 192: ADHD Treatment. Jordan Redden (MSIV) explains the treatment of ADHD. Dr. Bustamante adds input about pharmacologic and non-pharmacologic treatments. Dr. Arreaza shares the how stimulants were discovered as the treatment for ADHD. Written by Jordan Redden, MSIV, Ross University School of Medicine. Comments and edits by Isabelo Bustamante, MD, and 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.ADHD is a chronic neurodevelopmental condition characterized by inattention, impulsivity, and/or hyperactivity. While it’s often diagnosed in childhood, symptoms can persist well in adulthood. The treatment for ADHD is multifaceted. It often includes medication, behavioral therapy, environmental modifications, and sometimes educational interventions which are especially effective in younger patients. Ongoing evaluation is needed during treatment. Treatment needs adjustments over time.Starting with medications: Stimulants are the most well-studied and effective pharmacologic treatment for ADHD. These include methylphenidate-based medications such as Ritalin, Concerta, and Focalin, and amphetamine-based options, like Adderall, Vyvanse, and Dexedrine. Discovery of stimulants for ADHD> Dr. Charles Bradley discovered stimulants as the treatment for ADHD around 1937. ADHD did not have a name at that time, but it was known that some children had behavioral problems related to poor attention and inability to control their impulses, but they were still intelligent. Dr. Bradley was a psychiatrist who was working in the Bradley Hospital (Rhode Island), he was studying these children and, as part of his experiments, they developed severe headaches. He gave “Benzedrine” (a decongestant) to his pediatric patients to treat severe headaches, and he discovered that Benzedrine improved academic performance and interest in school and improved disruptive behavior in some children.How do stimulants work.Stimulants work primarily by increasing dopamine and norepinephrine levels in the brain, which helps improve focus, attention span, and impulse control. They typically show a rapid onset of action and can lead to noticeable improvements within the first few days of use. Dosing is individualized and should start low with gradual titration. Side effects can include reduced appetite, insomnia, headaches, increased heart rate, and emotional lability.Types of stimulants. Stimulants come as short acting and long acting. They can come as a tablet, liquid, patch, or orally disintegrating tablet. After the discovery of Benzedrine as a possible treatment for ADHD, more research was done over the years, and Ritalin became the first FDA-approved medication for ADHD (1955). The list of medications may seem overwhelming, but there are only two types of stimulants used to treat ADHD: methylphenidate and amphetamine. Long-acting stimulant medications are often preferred for their consistent symptom control and lower potential for misuse. Vyvanse (lis-dexa-mfetamine) is a widely used long-acting amphetamine-based option. As a prodrug, it remains inactive until metabolized in the body, which results in a smoother onset and offset of action and may reduce the risk of abuse. This extended duration of effect can help patients maintain focus and regulate impulses throughout the day without the peaks and crashes sometimes seen with shorter-acting formulations. Of note, Vyvanse is also approved for Binge Eating Disorder. Many of these medications are Schedule II controlled substances, so to prescribe them you need a DEA license. Other long-acting options include Concerta, an extended-release methylphenidate, as well as extended-release versions of Adderall and Focalin. These are especially helpful for school-aged children who benefit from once-daily dosing, and for adults who need sustained attention during work or academic activities. The choice between short- and long-acting stimulants depends on individual response, side effect tolerance, and daily routine.For patients who cannot tolerate stimulants, or for those with contraindications such as a history of substance misuse or certain cardiac conditions, non-stimulant medications are an alternative. One of the most used is atomoxetine, which inhibits the presynaptic norepinephrine transporter (NET). This leads to increased levels of norepinephrine (and to a lesser extent dopamine). Guanfacine or clonidine are alpha-2A adrenergic receptor agonists that lead to reduced sympathetic outflow and enhanced prefrontal cortical function, improving attention and impulse control. These alpha agonists are particularly useful in younger children with

May 30, 202519 min

Episode 191: Diagnosis of ADHD

Episode 191: Diagnosis of ADHDFuture Dr. Granat explains how to diagnose Attention Deficit Hyperactivity Disorder. She explained the influence of social media in increasing awareness of ADHD. Dr. Arreaza added input about the validated tools for ADHD diagnosis and highlighted the importance of expert evaluation for the diagnosis of this disorder. Written by Yen Stephanie Granat, MSIV. Ross University School of Medicine. Comments and editing 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.Steph: I love podcasts—many of us do—and if you, like me, spend any amount of your leisure time listening to podcasts, perusing the news, or scrolling social media; you’ve likely noticed an alarming trend in the number of discussions we seem to be having about ADHD. It has grown into a very hot topic over the past couple of years, and for some of us, it seems to have even begun sneaking into our “recommended videos” and across our news feeds! Naturally, for the average person this can spur questions like:“Do I have ADHD? Do we all have it? How can I be certain either way, and what do I do if I find myself relating to most of the symptoms that I’m seeing discussed?”Granted that there is a whirlpool of information circulating around this hot topic, I was hoping to spend a bit of time clearly outlining the disorder for anyone finding themselves curious. I believe that can best be achieved through outlining a clear, concise, and easy-to-understand definition of what ADHD is; outlining what it is not; and helping people sift through the fact and the fiction. As with many important things we see discussed on the internet, we’re seeing is that there is much more fiction than fact. Arreaza: I’m so glad you chose this topic! I think it is challenging to find reliable information about complex topics like ADHD. Tik Tok, Instagram and Facebook are great social media platforms, but we have to admit that fake news have spread like a fire in recent years. So, if you, listener, are looking for reliable information about ADHD, you are in the right place. With ADHD, there aren’t any obvious indicators, or rapid tests someone can take at home to give themselves a reliable “yes” or “no” test result. People’s concerns with ADHD are valid, and important to address, so we will discuss the steps to identify some of signs and symptoms they are seeing on TikTok or their favorite podcaster. Steph: Healthcare anxiety is a vital factor to consider when it comes to large cultural conversations around our minds and bodies; so, I hope to sweep away some of the misconceptions and misinformation floating around about ADHD. In doing so, I want to help alleviate any stress or confusion for anyone finding themselves wondering if ADHD is impacting their lives! We might even be able to more accurately navigate these kinds of “viral topics” (for lack of a better term) next time we see them popping up on our news feeds.Arreaza: The first thing I want to say about ADHD is “the crumpled paper sign.”Steph: What is that?Arreaza: It is an undescribed sign of ADHD, I have noticed it, and it is anecdotal, not evidence based. When I walk into a room to see a pediatric patient, I have noticed that when the paper that covers the examination table is crumpled, most of the times it is because the pediatric patient is very active. Then I proceed to ask questions about ADHD and I have been right many times about the diagnosis. So, just an anecdote, remember the crumpled paper sign. Steph: When you have patients coming to you asking for stimulants because they think they have ADHD, hopefully, after today, you can be better prepared to help those patients. So, for the average person—anyone wanting to be sure if this diagnosis applies to them—how can we really know?”Arreaza: So, let’s talk about diagnosis.Steph: Yes, the clearest information we have is the DSM-5, which defines these disorders, as well as outlines the specific criteria (or “checkpoints”) one needs to meet to be able to have a formal diagnosis. However, this manual is best utilized by a trained professional—in this case, a physician—who can properly assess your signs and symptoms and give you a clear answer. Steph: ADHD stands for Attention Deficit Hyperactivity Disorder. It is among the most common neurodevelopmental disorders of childhood. That is not to say it does not affect adult—it does—and because it can be easy to miss, it’s very possible for someone to have ADHD without knowing. Arreaza: I recently learned that ADD is an outdated term. Some people with ADHD do not have hyperactivity but the term still applies to them. Steph: Yes, there are multiple types

May 16, 202525 min

Episode 190: Measles Basics

Episode 190: Measles BasicsFuture Dr. Kapur explained the basics of measles, including the pathophysiology, diagnosis and management of this disease. Dr. Schlaerth added information about SPPE and told interesting stories of measles. Dr. Arreaza explained some statistics and histed the episode. Written by Ashna Kapur MS4 Ross University School of Medicine. Comments by Katherine Schlaerth, MD, and 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.According to the CDC, as of April 24, 2025, a total of 884 confirmed measles cases were reported by 30 states, including California, and notably Texas. This is already three times more cases than 2024. There are 3 confirmed deaths so far in the US. What is measles?Measles is a disease that’s been around for centuries, nearly eradicated, yet still lingers in parts of the world due to declining vaccination rates. Let's refresh our knowledge about its epidemiology, clinical features, diagnosis, management, and most importantly — prevention.Definition.Measles, also known as rubeola, is an acute viral respiratory illness caused by the measles virus. It’s a single-stranded, negative-sense RNA virus belonging to the Paramyxoviridae family. It’s extremely contagious with a transmission rate of up to 90% among non-immune individuals when exposed to an infected person.EpidemiologyBefore the introduction of the measles vaccine in 1963, nearly every child got measles by the time they were 15 years old. With the introduction of vaccination, cases and deaths caused by measles significantly declined. For example, in 2018, over 140,000 deaths were reported in the whole world, mostly among children under the age of 5.Measles is still a common disease in many countries, including in Europe, the Middle East, Asia, and Africa. Measles outbreaks have been reported recently in the UK, Israel, India, Thailand, Vietnam, Japan, Ukraine, the Philippines, and more recently in the US. So, let’s take prevention seriously to avoid the spread of this disease here at home and abroad. How do we get measles, Ashna?Mode of Transmission:● Air: Spread primarily through respiratory droplets.● Surfaces: The virus remains viable on surfaces or in the air for up to 2 hours. (so, if a person with measles was in a room and you enter the same room within 2 hours, you may still get measles)● Other people: Patients are contagious from 4 days before until 4 days after the rash appears.PathophysiologyThe measles virus first infects the respiratory epithelium, replicates, and then disseminates to the lymphatic system.It leads to transient but profound immunosuppression, which is why secondary infections are common. It affects the skin, respiratory tract, and sometimes the brain, leading to complications like pneumonia or encephalitis.Clinical PresentationThe classic presentation of measles can be remembered in three C’s:● Cough● Coryza (runny nose)● ConjunctivitisCourse of Disease (3 Phases):1. Prodromal Phase (2-4 days)○ High fever (can peak at 104°F or 40°C)○ The 3 C’s○ Koplik spots: Small white lesions on the buccal mucosa.2. Exanthem Phase○ Maculopapular rash begins on the face (especially around the hairline), then spreads from head to toe. The rash typically combines into 1 big mass as it spreads, and the fever often persists during the rash.3. Recovery Phase○ Rash fades in the same order it appeared.○ Patients remain at risk for complications during and after rash resolution.Complications:● Pneumonia (most common cause of death in children)● Otitis media (most common overall complication)● Encephalitis (can lead to permanent neurologic sequelae)● Subacute sclerosing panencephalitis (SSPE): A rare, fatal, degenerative CNS disease that can occur years after measles infection.High-risk groups for severe disease include:● Infants and young children● Pregnant women● Immunocompromised individualsDiagnosisClinical diagnosis is sufficient if classic symptoms are present, especially in outbreak settings.Ashna: Laboratory confirmation:● Measles-specific IgM antibodies detected by serology.● RT-PCR from nasopharyngeal, throat, or urine samples.Notify public health authorities immediately upon suspicion or diagnosis of measles to limit spread. ManagementThere is no specific antiviral treatment for measles. Management is supportive:● Hydration (by mouth and only IV in case of severe dehydration)● Antipyretics (e.g., acetaminophen) for fever● Oxygen if hypoxicVitamin A supplementation:● Recommended for all children with acute measles, particularly in areas with high vitamin A deficiency. It has shown to reduce morbidity and mortality.Hospitalization may be neces

May 9, 202527 min

Episode 189: Intermittent Fasting (Religious and Sports)

Episode 189: Intermittent Fasting (Religious and Sports)Future Doctors Carlisle and Kim give recommendations about patients who are fasting for religious reasons, such as Ramadan. They also explain the benefits and risks of fasting for athletes and also debunked some myths about fasting. Dr. Arreaza add input about the side effects of fasting and ways to address them. Written by Cameron Carlisle, MSIV (RUSM) and Kyung Kim, MSIV (AUC). Editing 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: In the last episode on fasting (#179), we explored how intermittent fasting (IF) can help manage type 2 diabetes by improving insulin sensitivity, promoting weight loss, and lowering inflammation. We discussed the benefits of methods like 16:8 time-restricted eating and the 5:2 meal plan, and even compared IF to medications like metformin. Today, we’re bringing that science into real life. We’ll talk about how people fast for religious reasons, like during Ramadan, how athletes use IF to stay in shape, and how we can use IF as a tool in family medicine to support community health and A1c control.Intermittent Fasting in Religious PracticeRamadan just ended on 3/30/25, but this is a great time to talk about the broader role of fasting in religion and health. Many faiths incorporate fasting into spiritual practice and understanding this can help us better support our patients.Islam (Ramadan): Ramadan is a month where Muslims fast from dawn to sunset, focusing on spiritual reflection and self-control. No food or drink is consumed during daylight hours. Despite this, studies have shown that with good planning, fasting during Ramadan does not significantly impair physical performance or metabolic health.Key health tips for patients observing Ramadan:Hydrate well between iftar (sunset) and suhoor (pre-dawn).Break the fast with dates and water to gently replenish energy and electrolytes.Eat balanced meals with complex carbs, protein, and healthy fatsAvoid greasy, heavy foods right after fastingLight exercise (such as a walk) after iftar is beneficialReview medications with a healthcare provider, especially for those on insulin or sulfonylureas.For example: Metformin should be taken when you break your fast and then again before dawn. If its an extended-release metformin, take it at night. Metformin does not cause significant hypoglycemia and can be continued during Ramadan. Basal insulin is advised to be given at Iftar, and the dose should be reduced by 25-35% if the patient is not well managed. And regarding the fast-acting insulin, it requires a little more reading, so you can look it up and learn about it. Judaism: In Judaism, fasting is practiced on days like Yom Kippur and Tisha B’Av, typically lasting 25 hours without food or water. These fasts are spiritual and reflective, and patients with medical conditions may seek guidance on how to participate safely.Christianity: Many Christians fast during Lent, either by abstaining from certain foods or limiting meal frequency. Some practice partial-day fasts or water-only fasts for spiritual renewal.A branch of Christianity known as The Church of Jesus Christ of Latter-day Saintsoften observe a 24-hour fast on the first Sunday of each month, known as Fast Sunday, where they abstain from food and drink and donate the cost of meals to charity. This practice is both spiritual and communal.Cameron: Fasting for religious reasons, when done safely, can align with IF protocols and be culturally sensitive for diverse patients in family medicine.IF in Athletes and PerformanceIntermittent fasting is gaining popularity in the sports world. Athletes are using IF to improve body composition, increase fat oxidation, and enhance metabolic flexibility. A recent study, known as the DRIFT trial and published in Annals of Internal Medicine, found that fasting three non-consecutive days a week led to more weight loss than daily calorie restriction. Participants lost an average of 6.37 pounds more over 12 months.Why? Better adherence. People found the 3-day fasting schedule easier to stick to than counting calories every day.Benefits of IF for athletes:Encourages fat burning (via AMPK activation and GLUT4 upregulation, listen to ep. 179).Helps maintain lean muscle while reducing fat.No major drop in performance when meals and workouts are timed properly.What are some practical tips?Schedule workouts during or just before eating windows.Eat protein-rich meals post-workout.Avoid intense training during long fasts unless adapted.Stay hydrated, especially in hot environments or endurance sports.Broader Applications and Myths Around IFHormon

Apr 18, 202529 min

Episode 188: RSV Management and Prevention

Episode 188: RSV Management and PreventionDr. Sandhu and future Dr. Mohamed summarize the management of RSV and describe how to prevent it with chemoprophylaxis and vaccines. Dr Arreaza adds some comments about RSV vaccines.Written by Abdolhakim Mohamed, MSIV, Ross University School of Medicine. Comments by Ranbir Sandhu, MD, and 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 RSV? -The Respiratory syncytial Virus (RSV) is an enveloped, negative-sense, single-stranded RNA virus of the Orthopneumovirus genus within the Pneumoviridae family. -RSV is a major cause of acute respiratory tract infections, particularly bronchiolitis and pneumonia, in infants and young children, and it also significantly affects older adults and immunocompromised individuals. -RSV infections cause an estimated 58,000–80,000 hospitalizations among children younger than 5 years and 60,000–160,000 hospitalizations among adults older than 65 years each year.-RSV is highly contagious and spreads through respiratory droplets and direct contact with contaminated surfaces. The virus typically causes seasonal epidemics, peaking in the winter months in temperate climates and during the rainy season in tropical regions. -Virtually all children are infected with RSV by the age of two, and reinfections can occur throughout life, often with milder symptoms.-Per the 2014 Clinical Practice Guideline: The Diagnosis, Management, and Prevention of Bronchiolitis, from the American Academy of Pediatrics, the most common etiology of bronchiolitis is RSV. -About 97% of children are infected with RSV in the first 2 years of life, about 40% will experience lower respiratory tract infection during the initial infection. Other viruses that cause bronchiolitis include human rhinovirus, human metapneumovirus, influenza, adenovirus, coronavirus, and parainfluenza viruses.When is RSV season?-Classically, the highest incidence of infection occurs between December and March in North America. Per CDC, there were typical prepandemic RSV season patterns, but the COVID-19 pandemic disrupted RSV seasonality during 2020–2022. -Before we dive into the seasonality patterns, for context, in order to describe RSV seasonality in the US, data was gathered and analyzed from polymerase chain reaction (PCR) test results reported to the National Respiratory and Enteric Virus Surveillance System (NREVSS) during July 2017–February 2023. -Seasonal RSV epidemics were defined as the weeks during which the percentage of PCR test results that were positive for RSV was ≥3%. Per 2017–2020 data, RSV epidemics in the United States typically follow seasonal patterns, that began in October, peaked in December or January, and ended in April. -However, during 2020–21, the typical winter RSV epidemic did not occur. The 2021–22 season began in May, peaked in July, and ended in January. -The 2022–23 season started (June) and peaked (November) later than the 2021–22 season, but earlier than prepandemic seasons. CDC notes that the timing of the 2022–23 season suggests that seasonal patterns are returning toward those observed in prepandemic years, however, warn that clinicians should be aware that off-season RSV circulation might continue.Treatment of RSVSome key points of the 2014 pediatric guidelines from the American Academy of Pediatrics.-AAP strongly do not recommend beta agonists or steroids for viral associated bronchiolitis because of no significant improved outcomes. “Clinicians should not administer albuterol (or salbutamol) to infants and children with a diagnosis of bronchiolitis (Evidence Quality: B; Recommendation Strength: Strong Recommendation).”-Epinephrine is not recommended for infants and children with a diagnosis of bronchiolitis (Evidence Quality: B; Recommendation Strength: Strong Recommendation).-Nebulized hypertonic saline should not be administered to infants with a diagnosis of bronchiolitis in the emergency department (Evidence Quality: B; Recommendation Strength: Moderate Recommendation), but hypertonic saline may be administered when they are hospitalized (Evidence Quality: B; Recommendation Strength: Weak Recommendation [based on randomized controlled trials with inconsistent findings]).-Chest physiotherapy should not be used in infants and children with a diagnosis of bronchiolitis (Evidence Quality: B; Recommendation Strength: Moderate Recommendation).-Antibiotics should not be administered in bronchiolitis unless there is a concomitant bacterial infection, or a strong suspicion of one (Evidence Quality: B; Recommendation Strength: Strong Recommendation).-Oxygen therapy may not be administered if the oxyhemoglo

Apr 11, 202515 min

Episode 187: Autism Fundamentals

Episode 187: Autism FundamentalsFuture Dr. Ayyagari explains the recommended screenings for autism, how to diagnose it and sheds some light on the management. Dr. Arreaza mentions the Savant Syndrome and the need to recognize ASD as a spectrum and not a “black or white” condition.Written by Tejasvi Ayyagari, 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.Introduction:Autism, or Autism Spectrum Disorder (ASD), is a neurodevelopmental disorder that affects how a person thinks, interacts with others, and experiences the world. It is characterized by deficits in social communication and interaction and restricted and/or repetitive behavior patterns, interests, and activities. Autism is considered a "spectrum" disorder because it encompasses a wide range of symptoms, skills, and levels of functioning, including Asperger’s, Auditory processing disorder, Rett syndrome, etc. The exact causes of autism are not fully understood, but many question genetic and environmental factors at play. What are some of the main characteristics of autism?1. Social difficulties: Individuals with autism may experience trouble understanding social cues or body language, leading to difficulty forming meaningful relationships. Children may display little interest in playing with others or engage in limited imaginative play (doll playing, pretend playing).2. Repetitive behaviors and interests: People with autism may engage in repetitive movements with their arms or hands and focus intensely on specific topics or activities. They may become distressed when routines are disrupted.3. Overstimulation: Individuals with autism may find multiple stimuli too overwhelming and gravitate towards either minimal stimulation or certain appealing stimulations best suited for their needs. 4. Intellectual variation: People with autism can have varying intellectual abilities, from severe mental disabilities to those who excel in specific disciplines, such as accounting or history (savants). Savant syndrome. It is a syndrome popularized by movies, TV shows and social media. The Good Doctor is a good example of it. Savant syndrome manifests by having a superior specific set of skills in a developmentally disabled person. Savants are like human supercomputers—while the rest of us are buffering, they can recall in 4K. We must not assume all people with autism are savants, unless we are particularly told about their exceptional talent.Another famous person with Savant syndrome was Kim Peek, portrayed by Dustin Hoffman in the 1988 movie The Rain Man. Kim Peek was later diagnosed with the FG syndrome and not autism spectrum disorder.What is the prevalence of autism?Worldwide, it is estimated that about 1 in 100 to 1 in 150 children are diagnosed with autism, though this number can vary based on the country and diagnostic practices. In the United States, according to the CDC, as of 2023, approximately 1 in 36 children are diagnosed with autism. Some studies even claim that boys are 4x more likely to be diagnosed with autism than girls.It is a very prevalent condition, and we have some recommendations about screenings. I feel like most parents have a “feeling” that something may be wrong with their kid, but I think most parents may feel that way, especially when they have their first baby.The American Academy of Pediatrics recommends that all children should be screened for autism at 18 months and 24 months of age during routine well-child visits, using standardized tools like the Modified Checklist for Autism in Toddlers (M-CHAT) or other validated autism screening tools. MCHAT is a two-step screening that requires a second visit if the first test shows moderate risk. Also, we must continue to follow up the development of kids in well child visits and be on the lookout for signs of autism, even outside of the recommended screening ages. How is autism diagnosed?Autism is typically diagnosed between the ages of 2 and 3, but it is often identified in early childhood. According to the DSM-5, there are two main clusters of symptoms for autism.- Cluster A: Involves social communication and interaction impairments in various settings.- Cluster B: Involves repetitive behavioral patterns, limited areas of interest, and atypical sensory behaviors/experiences.According to the DSM-5-TR criteria, a diagnosis of ASD requires that the following criteria are met:All three of the following Cluster A symptoms:- Social-emotional reciprocity: Difficulty engaging in mutually enjoyable conversations or interactions due to a lack of shared interests or understanding of others' though

Mar 21, 202521 min

Episode 186: Exercise Prescriptions

Episode 186: Exercise PrescriptionsDr. Sandhu and future Dr. Daoud explain the way to prescribe exercise, what are the general guidelines for exercise and how to overcome barriers to exercise. Dr. Arreaza emphasized the importance to screen our patients before exercise and using the term “physical activity” to improve receptivity by patients. Written by Wessam Daoud, MSIV, Ross University School of Medicine. Edits and comments by Ranbir Sandhu, MD, and 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.Arreaza: I’m Dr. Arreaza, and today, we will talk about a topic that is both simple and powerful: exercise. Previous episodes: 158, 100 (sexercise), 95, We all know exercise is good for us, but how do we prescribe it like we do medications? How can we tailor exercise recommendations to our patients' needs and lifestyles? To help us unpack this, I’m joined today by Dr. Ranbir Sandhu, and Medical Student, Wessam Daoud, who has a passion for preventive medicine. Welcome to the show!Ranbir: Thanks, Dr. Arreaza! We’re excited to be here and to discuss something so fundamental to health.Segment 1: Understanding Exercise PrescriptionArreaza: Let’s start with the basics. In medicine, we prescribe medications with precise instructions—dosage, frequency, duration. But how do we apply this concept to exercise?Ranbir: Great question! Before we prescribe exercise, we have to make sure that it is not contraindicated. We can use a system to stratify our patients based on risk factors, such as older age, smoking, baseline level of activity, etc. For example, a patient who had a heart attack within the last 6 weeks should not exercise yet, a person with heart failure exacerbation, asthma exacerbation, uncontrolled heart arrhythmia, etc. Wes: Exercise prescription follows a structured approach, similar to medications. We use the FITTE mnemonics to guide recommendations: Frequency – How often?Intensity – How hard should the patient work?Time – How long should each session last?Type – What kind of exercise is best?Enjoyment – Does the patient enjoy this activity?By adjusting these components, we can tailor exercise to each patient’s needs, whether it’s improving cardiovascular health, managing chronic disease, or building strength.Segment 2: How Much Exercise Do Adults Need?Arreaza: Now, when we talk about exercise, there’s a lot of conflicting advice out there. What do the official guidelines say about how much adults should exercise?Ranbir: The American College of Sports Medicine (ACSM) and CDC provide clear guidelines:Aerobic Exercise: At least 150 to 300 minutes of moderate-intensity exercise per week, OR 75 to 150 minutes of vigorous-intensity exercise (or a mix of both).Muscle Strengthening: At least two days per week of resistance training targeting major muscle groups.Balance & Flexibility: Particularly important for older adults to reduce fall risk.These guidelines are adaptable, meaning patients can break them into shorter sessions throughout the week.Arreaza: For weight regain, you may need to exercise a little bit more, about 300 minutes/week, and >2 days of resistance activity.Segment 3: Choosing the Right Type of ExerciseArreaza: With so many options—cardio, strength training, yoga—how do you guide patients in choosing the right type of exercise for them?Wes: It depends on the patient’s goals, health conditions, and personal preferences. Here’s how we might break it down:For cardiovascular health: Activities like brisk walking, jogging, cycling, or swimming.For strength and bone health: Resistance exercises, bodyweight exercises, or weightlifting.Ranbir: For flexibility and balance: Yoga, Pilates, or tai chi, especially for older adults.For chronic disease management: Customized plans—e.g., low-impact options for arthritis or supervised exercise for heart disease.The key is finding something they enjoy, because sustainability is the most important factor.Arreaza: We can use our physical therapy friends to design an appropriate plan for our patients.Segment 4: Overcoming Common Barriers to ExerciseArreaza: I hear this all the time in the clinic—patients want to exercise but struggle to stay consistent. What are the biggest barriers, and how do we help patients overcome those barriers?Wes: Absolutely. Some common barriers include:Lack of time: Patients think they need hours at the gym, but even short bouts of 10 minutes throughout the day add up.Low motivation: Encouraging goal setting and accountability, such as a workout buddy or an activity tracker, helps.Arreaza: Instagram post from Ranbir: Go to the gym even if you don’t want to go. Wes: Pain or chronic illness: We

Mar 10, 202517 min

Episode 185: Aging 101

Episode 185: Aging 101. Dr. Schlaerth explained the physiology, how to slow down and how to prevent aging. Dr. Ayyagari inquired about how to fight ageism in our clinic and in our society. Dr. Arreaza highlights the importance of treating elderly patients with dignity and empathy. A new book written by Dr. Schlaerth is introduced (“The Ways our Bodies Age.”) Written by Katherine Schlaerth, MD (Clinica Sierra Vista). Edits and comments by Hector Arreaza, MD (Clinica Sierra Vista), and Tejasvi Ayyagari, MSIV (Ross University School of Medicine.)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.InterviewArreaza: Question 1: What are some early signs that may indicate that your body is aging? (Pain? Memory? Weight loss?)Schlaerth: Maximum bone mass, muscle strength and mass and general strength and endurance generally peak in the third and early fourth decades of life. However, genetics and environment play a big role in aging for each of us. People can have problems with visual accommodation in their early forties, if not before. Many people feel that a realization of the possibility of aging begins when they must have magnification to read very small print. Women often complain of menopause as a benchmark for aging. Men don’t really have such a well demarcated event in their lives. Arreaza: Sure, men do not have a specific event, but I think an undeniable sign of aging in men is urinary frequency. I normally tell my patients that the nose, the ears, and the prostate are organs that tend to grow with age. So, if a male patient complains that they must use the bathroom more frequently, that may be a sign that their prostate is growing, after ruling out other conditions, if needed, we can reassure the patient that this can be a normal sign with aging. We will not neglect the patient because “it is normal” but we must offer interventions when needed.Schlaerth: The bottom line may be that aging is multifactorial, involves everything from the demands of one’s employment, through genetics, diet, and exercise right up to how many friends one has. It is also a stealth process, and all our body parts may even age at different rates! One individual may have great kidneys but an erratic thyroid, and another a shrinking liver but a superb array of teeth.Arreaza: (Humor) Plastic surgery and cosmetics can hide some signs of aging (not all). A wise woman said that you can hide your age, but your hands and neck will surely reveal it.Schlaerth: Many of us use external clues to measure aging. Teenage daughters accuse us of being behind the times, or new wrinkles and white streaks in our hair bring the reality of time passing to us. So, the realization of aging may be rather subjective, or it may be signaled by reduced energy, a falling off of the athletic skills we once had, or weight gain when we eat the same exact quantity and type of food we did at a younger age without gaining weight. So subjective aging mirrors incompletely the aging we are undergoing at a cellular and subcellular level.TJ: Question 2:How can we slow down aging?Schlaerth: One unpopular way would be to increase the age at which people are eligible for social security if in good health. WHY would this help? Because work adds a valuable dimension to the daily lives of seniors. It provides socialization, intellectual challenges, exercise and allows people to continue giving the results of their valuable life experience to others. Now there are issues here. Positions may have to change to accompany the changes of aging. People may choose different occupations from those held in adulthood. Part time work may compel employers to decrease salaries and to make accommodating changes in the workplace. Arreaza: I see your point. As you stay active, your aging slows down. Schlaerth: On the opposite side of the equation, social security may be saved from being turned into a funding responsibility of the federal government, raising taxes on younger workers and making them even less likely to be able to afford housing and even children. TJ: [In your experience Dr. Schlaerth, are professions, especially healthcare, moving in that direction to provide appropriate accommodations for aging workforce?] Schlaerth: There are variability. Schlaerth: To continue about slowing down aging, as an alternative, acquire a new skill or hobby that allows you to grow instead of vegetating in front of a TV or other screen, and brings you into contact with others, young and older, who share your interest.More popular ideas would include expanding opportunities to exercise and socialize within one’s own community, with local initiatives geared to the specifics of t

Mar 1, 202526 min

Episode 184: Multiple Myeloma Basics

Episode 184: Multiple Myeloma BasicsSub-Interns and future Drs. Di Tran and Jessica Avila explain the symptoms, work up and treatment of multiple myeloma. Written by Di Tran, MSIV, Ross University School of Medicine; Xiyuan Yang, MSIV, American University of the Caribbean. Comments by Jessica Avila, MSIV, American University of the Caribbean. 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.Di: Hi everyone, this is Di Tran, 4th year medical student from Ross university. It’s a pleasure to be back. To be honest, this project is a part of teamwork of two medical students, myself and another 4th year, her name is XiYuan. She came from the AUC. Unfortunately, due to personal matters she was unable to make it to the recording today which makes me feel really sad. Jessica: My name is Jessica Avila, MSIV, American University of the Caribbean.Di: The topic we will present today is Multiple Myeloma. Multiple myeloma is typically a rare disease and it’s actually a type of blood cancer that affects plasma cells in the bone marrow.Jessica: Let’s start with a case: A 66-year-old male comes to his family doctor for an annual health checkup. He is not in any acute distress but he reports that he has been feeling tired and weaker than usual for the last 3 months. He also noticed that he tends to bruise easily. He has a history of arthritis and chronic joint pain, but he thinks his back pain has gotten worse in the last couple of months. Upon checking his lab values, his family doctor found that he has a calcium level of 10.8 and a creatinine level of 1.2, which has increased from his baseline. Given all that information, what do you think his family doctor is suspecting? And what kind of tests she can order for further evaluation?Di: Those symptoms sound awfully familiar – are we talking about the CRAB? You know, the diagnostic criteria for Multiple Myeloma.Jessica: Exactly! Those are called “myeloma-defining events.” Do you remember what those are?Di: CRAB criteria comes in 4 flavors. It’s HYPERCALCEMIA with >1mg/dL, RENAL INSUFFICIENCY with serum creatinine >2mg/dL, ANEMIA with hemoglobin value BONE LESION, with one or more osteolytic lesions seen in imaging, be it CT or PET/CT scans.Jessica: You’re correct about the CRAB criteria! If our patient meets those conditions, myeloma is highly suspected. Other than the CRAB, there’s something else that has to be met before we can diagnose multiple myeloma. Patients must undergo a bone marrow biopsy and if there are > 10% plasma cells, PLUS any one or more of the CRAB features, we can make the official diagnosis of multiple myeloma. Di: Before we go deeper, let’s back up a little bit and do a little background. So, what do we know about the immunoglobulins, also known as antibodies? Back from years of studying from medical school, we know that the plasma cells are the ones that producing the antibodies that help fight infections. There are various kinds that come with various functions. Each antibody is made up of 2 heavy chains and 2 light chains. For heavy chains, we have A, D, E, G, M and for light chains we have Kappa and Lambda.Jessica: Usually, the 5 possible types of immunoglobulins for heavy chains would be written as IgG, IgA, IgD, IgE, and IgM. And the most common type in the bloodstream is nonetheless the IgG. Di: What is multiple myeloma? In myeloma, all the abnormal plasma cells make the same type of antibody, the monoclonal antibody. The cause of myeloma is unknown, but there are lots of studies and evidence that show a number of potential etiologies, including viral, genetic, and exposure to toxic chemicals, especially the Agent Orange, which is a chemical used as herbicide and defoliant. It was used as a chemical warfare by the U.S. military during the Vietnam War from 1961 to 1971.Jessica: We need to order some specific blood tests to see if there is elevated monoclonal proteins in the blood or urine. So, to begin with we’ll need to take a very thorough history and physical exam. Next, we’ll do labs, such as CBC, basic metabolic panel, calcium, serum beta-2 microglobulin, LDH, total protein, and some not so common tests: serum protein electrophoresis (SPEP), immunofixation of blood or urine (IFE), quantitative immunoglobulins (QIg), serum free light chain assay, and serum heavy/light chain ratio assay.If any of the results is abnormal, we should consider referring our patient to an oncologist.Di: Interesting! I read that Multiple Myeloma symptoms vary in different patients. In fact, about 10-20% of patients with newly diagnosed myeloma do not have any symptoms at all. Otherwise, classic symptomatic presen

Feb 14, 202512 min

Episode 183: Colorectal Cancer in Young Adults

Episode 183: Colorectal Cancer in Young AdultsFuture Dr. Avila and Dr. Arreaza present evidence-based information about the screening and diagnosis of colorectal cancer and explain the increasing incidence among young adult and the importance to screen early in high risk groups. Written by Jessica Avila, MS4, American University of the Caribbean 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.IntroductionJessica: Although traditionally considered a disease only affecting older adults, colorectal cancer (CRC) has increasingly impacted younger adults (defined as those under 50) at an alarming rate. According to the American Cancer Society, CRC is now the leading cause of cancer-related death in men under 50 and the second leading cause in women under 50 (American Cancer Society, 2024). Arreaza: Why were you motivated to talk about CRC in younger patients?Jessica: Because despite advancements in early detection and treatment, younger patients are often diagnosed at later stages, resulting in poorer outcomes. We will discuss possible causes, risk factors, common symptoms, and why early screening and prevention are important. Arreaza: This will be a good reminder for everyone to screen for colorectal cancer because 1 out of every 5 cases of colorectal cancer occur in adults between the ages of 20 and 54. The Case of Chadwick BosemanJessica: Many people know Chadwick Boseman from his role as T'Challa in Black Panther. His story highlights the worrying trend of increasing CRC in young adults. He was diagnosed with stage III colorectal cancer at age 39. This diagnosis was not widely known until he passed away at 43. His case shows how silent and aggressive young-onset CRC can be. Like many young adults with CRC, his symptoms may have been missed or thought to be less serious issues. His death drew widespread attention to the rising burden of CRC among young adults and emphasized the critical need for increased awareness and early screening efforts.Arreaza: Black Panther became a hero not only in the movie, but also in real life, because he raised awareness of the problem in young AND in Black adults. EpidemiologyJessica: While rates of CRC in older populations have decreased since the 1990s, adults under 50 have seen an increase in CRC rates of nearly 50%. (Siegel et al., 2023). Currently, one in five new CRC diagnoses occurs in individuals younger than 55 (American Cancer Society, 2024).Arreaza: What did you learn about the incidence by ethnic groups? Are there any trends? Jessica: Yes, certain ethnic groups are shown to have higher rates of CRC. Black Americans, Native Americans, and Alaskan Natives have the highest incidence and mortality rates from CRC (American Cancer Society, 2024). Black Americans have a 20% higher incidence and a 40% higher mortality rate from CRC compared to White Americans, primarily due to disparities in access to screening, healthcare resources, and early diagnosis. Hispanic and Asian American populations are also experiencing increasing CRC rates, though to a lesser extent.Arreaza: It is important to highlight that Black Americans have the highest rate of both diagnoses and deaths of all groups in the United States. Who gets colorectal cancer?Risk FactorsJessica: Anyone can get colorectal cancer, but some are at higher risk. In most cases, environmental and lifestyle factors are to blame, but early-onset CRC are linked to hereditary conditions. Arreaza: There is so much to learn about colorectal cancer risk factors. Tell us more.Jessica: The following are key risk factors:Modifiable risk factors:Diet and processed foods: A diet high in processed meats, red meat, refined sugars, and low fiber is strongly associated with an increased risk of CRC. Fiber is essential for gut health, and its deficiency has been linked to increased colorectal cancer risk (Dekker et al., 2023).Obesity and sedentary lifestyle: Obesity and physical inactivity contribute to CRC risk by promoting chronic inflammation, insulin resistance, and metabolic disturbances that promote tumor growth (Stoffel & Murphy, 2023).Gut microbiome imbalance: Disruptions in gut microbiota, especially an overgrowth of Fusobacterium nucleatum, have been noted in CRC pathogenesis, potentially causing tumor development and progression (Brennan & Garrett, 2023).Arreaza: As a recap, processed foods, obesity, sedentarism, and gut microbiome. We also have to mention smoking and high alcohol consumption as major risks factors, but the strongest risk factor is a family history of the disease.Non-modifiable risk factors:Genetic predisposition: Although o

Feb 7, 202527 min

Episode 182: HPV Vax

Episode 182: HPV VaxFuture Dr. Zuaiter and Dr. Arreaza briefly discuss HPV infection but pocus on the prevention of the infection with the vaccine. Dr. Arreaza mentions that HPV vaccine is also recommended by ASCCP to medical professionals. Written by Amanda Zuaiter, MS4, 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.Human Papilloma Virus (HPV).According to the World Health Organization, cervical cancer is the 4th most common cancer affecting women globally. Annually, there are over 600,00 new cases and more than 300,000 deaths. The leading cause of cervical cancer is HPV. HPV, or human papillomavirus, is a prevalent virus that is spread through close skin-to-skin contact, mainly by sexual intercourse. It is the most common sexually transmitted disease in the United States. The term STI and STD are used indistinctively, but some people make a difference, such as Dr. Cornelius Reitmeijer. STI refers to sexually transmitted infection, which can be asymptomatic, and STD stands for sexually transmitted disease, which are the signs and symptoms caused by the multiplication of the infectious agent and disruption of bodily functions. STI is the preferred term, as recommended by experts during the last few years. Low risk vs High risk HPV.There are over 200 strains of HPV which fall into two categories: low risk and high risk. The low-risk types, HPV 6 and 11, cause warts around the genitals, anus, mouth or throat. The high-risk types, HPV 16 and 18, are linked to cervical, vaginal, anal, and other cancers. Persistent infection with high-risk HPV types is the primary cause of cervical cancer, accounting for 70% of cervical cancer cases. While often asymptomatic, persistent HPV infections can develop into papular lesions which can cause bleeding and pain or cause sore throat and hoarseness if warts develop in the throat.Not all warts will turn into cancer, but the risk of a wart turning into cancer is higher than normal skin or mucosa that has not been infected by HPV.Even though cervical cancer is the most well-known condition linked to HPV, it’s important to note that HPV isn’t just a women’s health issue. It can also cause cancers in men, such as throat, penile and anal cancers. Men, however, are not screened for HPV if they have no signs or symptoms of infection.HPV Prevention: General measures that can be taken are maintaining a healthy immune system by exercising regularly and a balanced diet and quitting smoking.Male circumcision has been shown to reduce the risk of penile cancer in men and their sexual partners may have a lower risk of cervical cancer. Screening: Women should undergo regular pap smears with HPV screening. Pap smear screening begins at the age of 21 and is recommended every 3 years. From ages 30-65, co-testing should be done every 5 years, according to the guidelines by the American College of Obstetrics and Gynecology. Also, HPV test self-collection is now available in the US since May 2024, and it is useful especially in rural areas.The most effective ways to prevent the transmission of HPV is to practice safe sex, using condoms, and getting vaccinated. HPV vaccine. For medical providers: It was announced only to ASCP (American Society for Colposcopy and Cervical Pathology) members in the middle of the pandemic. On February 19, 2020, ASCCP recommended HPV vaccination for clinicians routinely exposed to the virus.This recommendation encompasses the complete health care team, including but not limited to, physicians, nurse practitioners, nurses, residents, and fellows, as well as office and operating room staff in the fields of obstetrics and gynecology, family practice, gynecologic oncology, and dermatology. Let’s remember that in 2018, the FDA a supplemental application for Gardasil 9 to include persons aged 27 to 45 years old. The ASCCP letter states “While there is limited data on occupational HPV exposure, ASCCP, as well as other medical societies, recommend that members actively protect themselves against the risks” among medical providers. For patients: The vaccine is given to prevent the types of HPV that are most likely to cause cancer and other health problems. It works by training the immune system to recognize and fight HPV before an infection can take hold. Gardasil-9® is the brand name that is offered in the US. The 9 means it targets 9 strains of the virus (6, 11, 16, 18, 31, 33, 45, 52, and 58). It’s important to note that the vaccine is preventative, and it is not considered a treatment. This means it’s most effective when given BEFORE any exposure to HPV, ideally duri

Jan 17, 202516 min

Episode 181: Cannabinoid Hyperemesis Syndrome

Episode 181: Cannabinoid Hyperemesis SyndromeFuture Dr. Johnson explains the pathophysiology, assessment, and management of Cannabinoid Hyperemesis syndrome. Dr. Arreaza adds some insights on the topic. Written by Tyler Johnson, MSIV, Western University of Health Sciences, College of Osteopathic Medicine of the Pacific-Northwest. Editing 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 Cannabinoid hyperemesis syndrome (CHS) is a syndrome of cyclic abdominal pain, vomiting, or nausea in older adolescents and adults who have chronic ϲаnոаbis use.The term “marijuana” is considered racist by some people. In the 1930s, American politicians popularized the term “marijuana” in the U.S. to portray the drug as a “Mexican vice” and to have a justification to persecute Mexican immigrants. Epidemiology The overall prevalence of cannabinoid hyperemesis syndrome is unknown due to a lack of definitive criteria or diagnostic tests. It occurs in a population that may not disclose substance use. One study conducted in 2015 in a United States urban emergency department not named, found one-third of patients with near-daily cannabis use met criteria for having had CНЅ in the prior six months.Why are rates of CHS increasing?Between 2005-2014 hospitalizations cyclic vomiting syndromes increased by 60 %. concurrent cannabis use in hospitalized patients increasing from 2 to 21 percent. 7 years after the commercialization of cannabis in Canada, the Canadian health services found a 13-fold increase in cyclic vomiting syndromesPotential correlations for the increase in CHS are increased legalization and commercialization of cannabis, higher tetrahydrocannabinol concentrations in cannabis products, and increased recognition of the syndrome.Legal status of Cannabis in the USCannabis is legal in 24 states: Alaska, Arizona, California, Colorado, Connecticut, Delaware, Illinois, Maine, Maryland, Massachusetts, Michigan, Minnesota, Missouri, Montana, Nevada, New Jersey, New Mexico, New York, Ohio, Oregon, Rhode Island, Vermont, Virginia, and Washington. It is also legal in Washington, D.C. Cannabis is approved for medical use in 38 states.Federal level: Cannabis is a Schedule I drug, under the Controlled Substance Act (added in 1970) in the group of Hallucinogenic or psychedelic substances. Tetra-hydro-cannabinol (THC, a “mind-altering substance in cannabis”) is on the same list. However, cannabidiol (CBD, derived from hemp or non-hemp plants) was removed from the Controlled Substances Act in 2018. CBD is FDA-approved (under the name of Epidiolex®) to treat rare seizure disorders. CBD is still on the list of controlled substances in some states. I see THC as a problem.THC increased concentration As recreational Cannabis becomes more normalized, innovators look to find new ways to differentiate their product and increasing THC has become a common way to perform this similar to alcohol content in the beer, wine, and liquor industry. An article by Yale School of Medicine titled “Marijuana: Rising THC Concentrations in Cannabis Can Pose Health Risks” states, “In 1995, the average THC content in cannabis seized by the Drug Enforcement Administration was about 4%. By 2017, it had risen to 17% and continues to increase. Beyond the plant, a staggering array of other cannabis products with an even higher THC content like dabs, oils, and edibles are readily available—some as high as 90%.”Recently, cannabis-infused water started to be sold in some grocery stores.Pathophysiology of CHSIt is not entirely understood. Some suggest multifactorial involving cannabinoid metabolism, exposure dose and tolerance modifying receptor regulation, complex pharmacodynamics at Cannabinoid receptors, and even changes in genetics and cannabinoid variation in plants. CB1 receptors are involved in gastric secretion, sensation, motility, inflammation, and lipogenesis. The activation of CB1 and CB2 receptors has been suggested as the possible cause of CHS.Risk FactorsCHS can occur after acute or acute on chronic use but many report daily 3-5x cannabis use cannabis use over one year and many over at least two years. Median age 24 years. Interesting factsMedical visits for inhaled cannabis are more likely associated with CHS while edibles are more likely for acute psychiatric reactions.Also, CHS is a paradoxical effect since cannabis and cannabinoid receptor agonists are known antiemetics (as seen in nabilone and dronabinol (synthetic analogs of THC)) and prescribed by some physicians to combat chemotherapy effects.Clinical Features of CHSCyclical pattern with abdominal pain, severe nausea, and vomiti

Dec 20, 202421 min

Episode 180: Pediatric Hip Pain

Episode 180: Pediatric Hip PainFuture Dr. Pena-Brockett explains the differential diagnosis in a 14-year-old patient who has a new onset of left hip pain. Dr. Arreaza adds comments and explains toxic synovitis. Written by Natalie Pena-Brockett, MSIV, California Health Sciences University. 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.Having a limping kid can be terrifying. Many questions may cross your mind: Is this a permanent damage? What is going on here? Where is the pain located? Do I need to send this child to the hospital? Today, hopefully, we can help you ease some of your fears. Case: This is a 14-year-old boy with no past medical history, no trauma, presents to the family medicine clinic with a complaint of left-sided hip pain. Mom notes that her son has been limping for the last week and complaining of pain in his left hip and knee when he walks. He has never experienced this pain before this week. He does not take any medications. Physical exam: He is afebrile and all of his vitals are within normal limits. On exam, you note that his BMI is at the 90th percentile (overweight), and has an antalgic gait where he is favoring the right side and has tenderness on his left groin. His left foot is turned outward while standing up straight. His left knee has negative findings on specialized tests, but he has restricted movement of the left hip. Discussion: This is a common topic that you will see on board exams or limping into your office. Although pediatric hip pain may seem like a benign musculoskeletal concern, taking the time to take a complete history and perform a thorough physical exam is critical to assess the severity of the patient’s concern.Physical Exam for Pediatric Hip Pain.Observation: Every physical exam begins the moment you first see the patient. This allows you to gauge the patient’s comfort level, the natural stature, length, and positioning of the patient’s extremities, skin changes, gait, and ability to bear weight. Palpation: In medicine, our hands are one of our greatest tools for evaluating patients, especially those with musculoskeletal concerns. This is the time to palpate the area for any tenderness or gross deformities of the pelvis, hip, knee, or leg. Special Tests: In the world of MSK, we have all sorts of tests to evaluate the range of movement of our joints and tendons. When specifically evaluating the hip, the most common are the FABER(flexion, abduction, external rotation),test to assess the sacroiliac joint, Ober’s Test to assess the iliotibial band, and Straight Leg Raise to assess for lumbar radiculopathy.Legg-Calve Perthes Disease-Legg-Calve Perthes disease is an idiopathic avascular necrosis of the femoral head. -It is most commonly observed in patients between the ages of 2-12 years and in a higher ratio of males to females 1. -It often manifests as an atraumatic limp with limited movement in abduction and internal rotation. -X-ray imaging may demonstrate a widening of the joint space and sclerosis of the femur, and MRI will confirm osteonecrosis of the femoral head. -Early diagnosis is key to minimizing the risk of developing osteoarthritis of the hip. -The goal of treatment is to maintain the shape of the femoral head and the range of motion of the hip. -The first-line treatment includes managing pain with NSAIDs, limiting weight-bearing activity, and physical therapy for range of motion.-If the disease progresses, bracing and casting can be used to retain the femoral head within the acetabulum to keep the shape and integrity of the femoral head. In more serious cases, a surgical osteotomy may be done to cut and realign the bones. Developmental Dysplasia of the Hip (DDH)-Developmental Dysplasia of the Hip (DDH) is a pediatric condition that results in unilateral or bilateral instability of the hip due to the abnormal development of the acetabulum or femur. -This is most commonly seen in newborns, especially those which develop in a breech position. -These patients often present with a shortened leg or asymmetric gluteal creases and a Trendelenburg gait when walking. -The Trendelenburg gait is an abnormal gait caused by weak hip abductor muscles. The person's trunk shifts over the affected hip during the stance phase of walking and away from it during the swing phase, making it look like the person is missing steps or limping. -On physical exam, hip joint laxity can be evaluated with the Ortolani and Barlow maneuvers to apply pressure to the proximal femur to assess dislocatability of the hip joints. These maneuvers would both be considered positive if a “clunk” is felt over the hip as this means tha

Nov 15, 202428 min

Episode 179: Impact of intermittent fasting on T2DM.

Episode 179: Impact of intermittent fasting Impact on T2DMFuture Dr. Carlisle explains the physiology of fasting and how it can help revert type 2 diabetes. Dr. Arreaza adds details on how to do intermittent fasting. Written by Cameron Carlisle, MSIV, Ross University School of Medicine. Comments and edits by Hector Arreaza, MD, FAAFP.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 type 2 Diabetes Mellitus (T2DM)?-Type 2 Diabetes Mellitus (T2DM) is a metabolic disorder characterized by insulin resistance and impaired glucose regulation. -This impaired regulation can lead to hyperglycemia, contributing to complications in a myriad of organs: heart, kidneys, eyes, nerves, etc. (target organs). According to the CDC, more than 38 million Americans have T2DM (about 1/10 people). -Multiple mechanisms are believed to contribute to insulin resistance in obese patients with T2DM, such as increased lipid deposition throughout the body and systemic inflammation.What is Intermittent Fasting (IF)? Intermittent fasting (IF) has recently gained popularity as a dietary approach for health benefits, but it has been around for thousands of years. IF is an eating pattern that alternates between eating and fasting (no calories consumed) over a specific period of time. When you are fasting, you are allowed and encouraged to keep drinking water and non-caloric drinks, like coffee, tea, and even homemade bone broth.-According to the International Food Information Council Foundation (IFIC), 10% of Americans engage in IF daily. -According to Mark Mattson, a neuroscientist and IF expert for over 25 years, a mechanism called “metabolic switching” is seen with IF. This is when your body runs out of glucose and starts burning fat (i.e., fatty oxidation). These metabolic changes can help protect your organs and reduce the risk of chronic conditions, like T2DM. Common IF methods: Time-restricted eating: Most common method, involves eating within a specific time frame (e.g., the 16:8, 18:6, 12:12 method is also common. [16:8 means you have 16 hours of fasting and 8 hours of eating.]Alternate-day fasting: Alternating between fasting days and normal eating days. [Find more info in The Complete Guide to Fasting, by Jason Fung, who is a nephrologist, he explains that alternate-day is basically eating every other day, which would give 36 hours of fasting, but if you are a beginner you can try a 24 hours fasting, in short, not eating breakfast any day of the week and having lunch 4 days a week, and dinner every night.]5:2 diet (aka periodic fasting): Maintaining a normal diet for 5 days, with 2 days (usually non-consecutive) of caloric restriction (25% of normal caloric intake; e.g., 500 calorie meal). IF is strongly believed to improve metabolic health in individuals with T2DM by reducing insulin resistance via increasing insulin sensitivity, promoting weight loss (patients with obesity and DM… AKA patients with diabesity), and enhancing lipolysis via fat oxidation.While fasting, the body goes through several phases that affect how energy is metabolized. Between 0 and 4 hours after eating, the body enters a feeding state, using glucose as its main energy source. After fasting for 12-16 hours, the body enters ketosis and starts to use fat for energy. Within 24-36 hours, autophagy begins, a process that recycles damaged cells and allows for cellular repair. This process can have great benefits for people with T2DM, such as improved insulin sensitivity and glucose regulation. Pathophysiology of Implementing IF in T2DM. -IF is thought to increase insulin sensitivity by decreasing fatty tissue in the body (i.e., visceral adipose tissue), which is correlated to insulin resistance. Insulin resistance is defined as higher than normal circulating insulin levels needed for a glucose lower response, which is thought to be the culprit for the generation of T2DM. It means you need high levels of insulin to keep glucose normal. -Obesity is an important risk factor for T2DM. Visceral adipose tissue functions as an organ via the secretion of adipokines (cytokines or cellular messengers produced by adipose tissue): leptin and adiponectin. Leptin: proinflammatory, leading to chronic inflammation. Patients with higher BMI levels and increased insulin resistance were found to have increased leptin levels.[Leptin is a good hormone at normal levels, but there is leptin resistance] Adiponectin: anti-inflammatory and antidiabetic effects. Higher adiponectin levels result in decreased hepatic gluconeogenesis, enhanced glucose absorption, and enhanced skeletal muscle and hepatic fatty acid oxidation. Levels drop as visceral fat incr

Oct 27, 202425 min

Episode 178: Social Media in Medicine

Episode 178: Social Media in MedicineDr. De Luna and Dr. Song explain the role of social media in medical education and how online journal clubs have become more useful in recent years. Dr. Arreaza offers insights into our role as educators and sources of truth.Written by Patrick De Luna, MD. Comments by David Zheng Song, MD, and Hector Arreaza, MDYou 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.Intro to episode (voiceover): Get ready to listen to a great conversation between three doctors diving into the impact of social media on medicine. It’s no secret that social media shapes our lives—not just as professionals, but also as humans and members of our society. Every second, new information floods our feeds, and with the rise of artificial intelligence, it’s becoming harder to separate fact from fiction. As doctors, we have a crucial role in clearing up confusion and supporting evidence-based practices. You’ll hear insightful tips from Dr. De Luna, Dr. Song, and Dr. Arreaza—but remember, you also have a role in spreading the truth, you must be a reliable source of online truth and correct misinformation quickly. Also, use reliable sources, recommend fact-check websites, including Snopes, and FactCheck.org, and avoid “back-and-forth” arguing about fake news online, because as you keep arguing, fake news will continue to spread.Social Media in Medicine.Patrick: Social media has helped both physicians and patients obtain and expand their knowledge of medicine. This role in medical knowledge expansion has been more prevalent since the COVID-19 pandemic, especially in the form of podcasts (like this one), medical content creators, and personalities. This growing medium has helped physicians to deliver medical knowledge in an efficient, but layman, format which can become a great outreach and educational tool. Arreaza: This podcast was created 3 days before the lockdown. It has been an educational tool for those who record and hopefully for those who listen to us.Patrick: In today’s episode, we will explore a little about how this more accessible approach to medical learning has shaped our medical education landscape. We’ll explore a recent study that shows the breakdown of how social media is used among medical professionals and the concerns that physicians have about medical education through social media. We will discuss how platforms such as X/Twitter have “Journal Club” threads and their implications. Furthermore, will discuss how online personalities have been able to bring medical education discussion to the broader population, and what we can learn from their work. David: Who is your favorite medical educator?Patrick: Dr. Mike (YouTube FM), Dr. Glaucomflecken (ophthalmologist comedian), and HealthyGamerGG (gamer), and yours?David: Curbsiders (THE internal medicine podcast)Arreaza: I like Dr. Glaucomflecken as well. He is a comedian but he is becoming a little more political. The AFP podcast is my favorite.David: We will explore and discuss how we could make quality and accurate medical education content and, hopefully, mitigate concerns about creating future educational content for physicians and patients alike. Analysis of Healthcare Professional Social Media UsePatrick: Social media has traditionally been used to share about your social life (posting pictures of your cat and family vacation), stay up to date on news and what is happening among your peers, as well as (for some select folks) a platform for content creation and a means of a career. Healthcare professionals also participate in social media in the same manner. David: Some social media users are called “influencers”. Arreaza: The term “influencer” is becoming a somewhat negative term online because many “influencers” are giving a bad reputation to that term, to the point that many prefer to be called “content creator.”Patrick: In a recent study published in Taylor and Francis’ Medical Education Online, 72.1% of the participants reported use of social media to some degree. Out of the 72%, 11.5% of the surveyed report using social media sites exclusively for professional purposes, 22.8% for strictly personal use, and 65.7% for both. David: The most used social media platforms among healthcare workers were Facebook at 70%, YouTube 58%, LinkedIn 52%, Instagram 42%, Twitter (now called X) 27%, TikTok 10%, and Reddit at 5% among those surveyed. Those are 6 different media, which ones do you currently use, Patrick?Patrick: [Add response]. 20.4% of the surveyed indicated they use clinically focused social media platforms as well. This same survey found that respondents specializing in addiction medicine, family medicine,

Oct 18, 202432 min

Episode 177: Urinary Incontinence in Older Adults

Episode 177: Urinary Incontinence in Older AdultsFuture Dr. Nguyen explains the evaluation and treatment of older adults with urinary incontinence. Dr. Arreaza adds insights into the conservative management of urinary incontinence.Written by Vy Nguyen, MSIV, Western University of Health Sciences, College of Osteopathic Medicine of the Pacific-Northwest. Editing 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 of urinary incontinence. The International Continence Society (ICS) defines it as any involuntary urine leakage. Epidemiology of urinary incontinence. Data analysis from the National Health and Nutrition Examination Survey (NHANES) from 2015 to 2018 shows that more than 60% of adult women which is equivalent to around 78,000,000 females living in the United States experience urinary incontinence with 32.4% reporting symptoms monthly. More data analysis shows the strongest association with urinary incontinence include age greater than 70, prior vaginal delivery, and BMI of 40 or greater. Despite urinary incontinence commonly affecting the senior population, this medical condition can also affect the quality of life of younger adult females and males. On top of that, urinary incontinence is often underestimated due to the low report level for various reasons and the obtained data might not accurately reflect the true prevalent rate. Types and etiology.Urinary incontinence is divided into 5 categories: stress, urge, mixed, overflow, and functional. Stress urinary incontinence has the highest prevalence of 37.5% followed by mixed urinary incontinence at 31.3%, urgency at 22%, and unspecified urinary incontinence at 9.2%. Due to time constraints, we will discuss the most prevalent type which is stress urinary incontinence.In females, stress urinary incontinence is often due to urethral sphincter hypermobility caused by weakened pelvic floor muscles. It can also be caused by dysfunction of the sphincter muscle that is exacerbated by increased intraabdominal pressure from coughing, sneezing, or physical exertion. This type of incontinence is commonly seen in pregnant women, those who experienced childbirth, and young women active in sports. In males, the most common etiology for stress urinary incontinence in males is prostate surgery such as radical prostatectomy which can damage the external urethral sphincter. Another cause is spinal cord injury or disease that can interfere with sphincter function. Evaluation. Urinary incontinence is first evaluated by a thorough history taking that includes inquiries about the type, severity, burden, and duration of incontinence. The initial evaluation includes a voiding diary that can provide clarity and help distinguish between the different types of incontinence or identify the dominating type in the case of mixed incontinence. Examples of voiding diary can be found on the websites of International Urogynecological Association (IUGA). Medical conditions such as COPD and asthma can induce cough; heart failure can cause volume overload; neurological disorders and musculoskeletal conditions can interfere with bladder emptying and urinary retention and thus should also be investigated. It is also helpful to ask about medication and substance use as the adverse effects can directly or indirectly contribute to urinary incontinence. For our female-identifying patients, a gynecological and obstetrical history such as birth history (vaginal versus c-section), current pregnancy as well as low estrogen (menopause) can contribute to reversible urinary incontinence. Management. There are various treatment modalities for stress urinary incontinence ranging from conservative to more invasive surgical management. Conservative treatment: -Initial treatment includes pelvic floor strengthening exercises and bladder training with scheduled void. -Pelvic floor muscle training (PFMT) is very effective, and it is proven to help achieve cure and improve the quality of life in women with ALL types of urinary incontinence. -For stress urinary incontinence, the median cure rate is around 58.8% for women after 12 months and 78.8% for men at 6 months of supervised pelvic floor muscle training (PFMT). -Certain behavioral modifications such as fluid intake management (-According to an AFP article, Cochrane for Clinicians, patients who have obesity may benefit from weight loss, improving the cure rate and improvement of symptoms in any type of urinary incontinence. SOR: B.-Conservative management should be implemented for 6 weeks before considering other options. -Supplemental modalities can also be introduced in addition to

Sep 13, 202417 min

Episode 176: Self-sampling for HPV screening

Episode 176: Self-sampling for HPV screeningFuture Dr. Markarian explains the importance of HPV screening for the prevention of cervical cancer. Dr. Arreaza adds some insight about cervical cancer.Written by Chantal Markarian, MSIV, American University of the Caribbean. Editing 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.Insights into Cervical Cancer.Chantal: Cervical cancer stands as the most prevalent form of cancer in women globally costing the lives of approximately 350,000 women annually. About 4,000 women die of cervical cancer a year in the US. Cervical cancer is initially asymptomatic, allowing it to advance to a more severe stage if not detected early. The positive news is that cervical cancer is highly preventable through screening for precancerous lesions or the presence of HPV —the primary culprit behind most cases.The role of HPV: Human Papilloma Virus, according to the World Health Organization, caused an estimated 620,000 cancer cases in women and 70,000 cancer cases in men.Cervical cancer is more prevalent in certain regions. In regions with established screening initiatives, the incidence rate and mortality rate of cancer are lower than in resource-limited areas. This highlights that resource-constrained countries continue to bear a burden of this disease. In nations like the United States, access to the HPV vaccine along with routine screenings, like Pap smears and HPV tests has significantly decreased the prevalence of cervical cancer.Screening recommendations from the US Preventive Services Task Force (USPSTF) and the American Cancer Society (ACS).The U.S Preventive Services Task Force advises that women aged 21 to 29 undergo a Pap test every three years while those aged 30 to 65 should opt for co-testing (Pap and HPV tests) every five years. These examinations are usually conducted in outpatient facilities, where a medical professional collects a sample of cervical cells that are later examined under a microscope.A normal result states that the sample was adequate for evaluation, in other words, that endocervical/transformation zone components are present, and that the patient is “Negative for intraepithelial lesion or malignancy.” ACS recommends cervical cancer screening begin at age 25 for women and people with a cervix. Those aged 25 to 65 should have a primary HPV test every 5 years. (A primary HPV test means the HPV test is done without cytology; follow-up screening can be done with a Papanicolaou (Pap) test if needed.) If primary HPV testing is not available, screening may be done with either a co-test every 5 years, which combines an HPV test with a Papanicolaou (Pap) test, or a Pap test alone every 3 years. How is Cervical Cancer Classified?Two systems categorize lesions: the Cervical Intraepithelial Neoplasia (CIN) scale and the Bethesda system.The CIN scale categorizes lesions based on the degree of involvement of the cervical lining ranging from mild (CIN I) to moderate (CIN II) to severe dysplasia (CIN III).The Bethesda system emphasizes cytological findings organizing results into categories such as atypical squamous cells, low-grade lesions (LSIL), and high-grade lesions (HSIL).ASCUS (Atypical Squamous Cells of Undetermined Significance) is the most common abnormality seen in pap smears. It may or may not indicate a problem, you have to make a decision based on the patient. Cervical cancer is largely linked to high-risk HPV (hrHPV), mostly HPV 16 and 18, and scientists are investigating tests that identify hrHPV DNA or RNA. These tests may provide a more accurate evaluation of cancer risk compared to traditional cytology. Examples include DNA amplification tests like Cobas test and the Xpert HPV test.Obstacles to Screening.Despite the efficacy of cervical cancer screening, many women face many obstacles to testing. In regions with limited resources, fear, embarrassment, lack of awareness, and restricted healthcare access pose challenges to screening.In Nigeria, a study revealed that women often avoid Pap smears due to a lack of awareness. Similarly, healthcare providers in Ecuador highlighted issues like the absence of screening programs and inadequate health promotion efforts. Women in Peru face obstacles such as long waiting times preferences for female healthcare providers and limited access to health facilities. In 2022, 31% of minority women in the US did not undergo Pap smears in the past three years; many of these women were uninsured, unemployed, or low-income. These challenges contribute to higher rates of cervical cancer among women who do not follow recommended screening guidelines.We must ment

Sep 6, 202418 min

Episode 175: Alcohol Use Disorder Basics

Episode 175: Alcohol Use Disorder Basics Future Dr. Sangha explains the clinical presentation, diagnosis, and fundamentals of the treatment of alcohol use disorder (AUD). Dr. Arreaza offers insights about the human aspect of the treatment of AUD. Written by Darshpreet Sangha, MS4, Ross University School of Medicine. Editing 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.What is Alcohol Use Disorder?AUD is characterized as the inability to stop or control alcohol use despite adverse physical, social and occupational consequences. According to DSM-5, it is a pattern of alcohol use that, over 12 months, results in at least two of the following symptoms, indicating clinically substantial impairment or distress: Alcohol is frequently used in higher quantities or for longer periods than planned.There is a persistent desire or unsuccessful attempt to reduce or manage alcohol use.Activities that are required to get alcohol, consume alcohol, or recuperate from its effects take up a lot of time.A strong need or desire to consume alcohol—a craving.A pattern of drinking alcohol that prevents one from carrying out important responsibilities at work, school, or home.Sustained alcohol consumption despite ongoing or recurring interpersonal or social issues brought on by or made worse by alcohol's effects.Alcohol usage results in the reduction or cessation of important social, professional, or leisure activities.Frequent consumption of alcohol under risky physical circumstances.Continuing to drink even when one is aware of a chronic or recurrent health or psychological issue that may have been brought on by or made worse by alcoholTolerance: requiring significantly higher alcohol intake to produce the same intended effect. Withdrawal: Characterized by the typical withdrawal symptoms or a noticing relief after taking alcohol or a closely related substance, such as benzodiazepine.How can we determine the severity of AUD? Mild: 2–3 symptomsModerate: 4–5 symptomsSevere: >/= 6 symptomsWho is at risk for AUD?Note: Ancestry offers a DNA analysis to find out about your heritage. You can also send that DNA to a third party to learn about your risks for diseases and conditions (for example, Prometheus.) Anyone can find out about their risk for alcoholism by doing a DNA test. The risk factors for AUD are: Male genderAges 18-29Native American and White ethnicitiesHaving Significant disabilityHaving other substance use disorderMood disorder (MDD, Bipolar)Personality disorder (borderline, antisocial personality)What is heavy drinking?According to the National Institute of Alcohol Abuse and Alcoholism (NIAAA), heavy alcohol use is characterized as: Males who drink > 4 drinks daily or > 14 drinks per week Females who drink > 3 drinks on any given day or > 7 drinks per weekPathophysiology of AUD.The pathogenesis of AUD is not well understood, but factors that may play a role are genetics, environmental influences, personality traits, and cognitive functioning. Also, genetic factors may decrease the risk of AUD, i.e., the flushing reaction, seen in individuals who are homozygous for the gene that encodes for aldehyde dehydrogenase, which breaks down acetaldehyde. Who should be screened?A person with AUD may not be easy to diagnose in a simple office visit, but some clues may point you in that direction. First of all, patients with AUD may present to you during their sober state, that´s why ALL adults (including pregnant patients) must be screened for AUD in primary care )Grade B recommendation). The frequency has not been determined but as a general rule, at least in Clinica Sierra Vista, we screen once a year. The USPSTF has concluded that there is insufficient evidence to recommend screening adolescents between 12-17 years old. What are the clinical manifestations of AUD?Some symptoms may be subtle, including sleep disturbance, GERD, HTN, but some may be obvious, such as signs of advanced liver disease (ascites, jaundice, bleeding disorders, etc.)If you draw routine labs, you may find abnormal LFTs (AST:ALT ratio >2:1), macrocytic anemia (MCV >100 fL), and elevated Gamma-glutamyl transferase (GGT). All these findings are highly suggestive of AUD. Patients with AUD may present in either an intoxication or withdrawal state. Signs and symptoms of acute intoxication may include “slurred speech, nystagmus, disinhibited behavior, incoordination, unsteady gait, hypotension, tachycardia, memory impairment, stupor, or coma.” Signs and symptoms of withdrawal range from tremulousness to hallucinations, seizures, and death. They are seen between 4 and 72 hours after the last drink, peak

Aug 30, 202418 min

Episode 174: GERD in Adults

Episode 174: GERD in AdultsCommon and atypical symptoms are presented. Pathophysiology, diagnosis, and management are discussed. H. pylori's role is discussed during this episode. Written by Jacquelyn Garcia MS4 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.Definitions: Gastroesophageal reflux (GER): occasional backflow of stomach acid into the esophagus. It's a common physiological process that happens to many people, especially after meals. Occurs less than twice a week. Associated with mild and temporary symptoms such as heartburn or regurgitation. Gastroesophageal reflux disease (GERD): a chronic and more severe form of GER. It occurs when acid reflux happens frequently, typically more than twice a week, and/or causes esophageal injury/complications. -Non-erosive reflux disease (NERD)= GER without evidence of esophageal injury on endoscopy. -Erosive reflux disease (ERD)= GER with evidence of esophageal injury on endoscopy.AFP Journal, January 2024: “Nonerosive GERD does not increase the likelihood of esophageal cancer. However, erosive GERD is associated with a doubled, but still low, risk of developing cancer, with the likelihood increasing over time.”Pathophysiology:The main pathophysiology behind GERD is lower esophageal sphincter (LES) dysfunction which can occur due to the following:-LES Pressure: The LES is a muscular ring at the junction of the esophagus and stomach. It normally maintains a high-pressure zone to prevent reflux. In GERD, the intragastric pressure is higher than the pressure created by the LES. The tone of the LES can be reduced by caffeine, nitroglycerin, and scleroderma. -Transient LES Relaxations (TLESRs): These are normal relaxations of the LES that occur independently of swallowing. In GERD, these relaxations are more frequent or prolonged, allowing acid to reflux into the esophagus.-Anatomic abnormalities: A hiatal hernia occurs when a portion of the stomach protrudes through the diaphragm into the chest cavity. This disrupts the normal anatomy of the gastroesophageal junction, reducing the pressure barrier and promoting reflux.Epidemiology: It affects 10-20% of adults in Western cultures and less than 5% in Asia. Prevalence in the US ranges from 18.1% to 27.8% with a slightly higher rate in men. Risk factors: -Obesity, pregnancy, scleroderma, hiatal hernia; smoking, caffeine, alcohol, stress, fatty/fried/spicy foods. Spicy foods can be a challenge in some cultures (e.g. Mexican and Indian.) Sometimes, patients may ask for “something” to stop GERD but all they may need is dietary modification. -Medications: -aspirin, ibuprofen, clindamycin, tetracycline, bisphosphonates (irritate the esophagus and cause heartburn pain similar to GERD) -anticholinergics, TCA’s, CCB’s, ACEi, statins, benzodiazepines, theophylline, opioids, progesterone (increase acid reflux and worsen GERD)Clinical features: Typical symptoms: -heartburn (burning retrosternal pain) -regurgitation (acidic stomach contents)Atypical symptoms: -chest pain (can mimic angina pectoris, squeezing/burning substernal, radiates to back/neck/jaw/arm) -water brash (hypersalivation)-globus sensation (lump in throat)-nausea -belching-bloating Alarm features in GERD: -dysphagia-odynophagia (pain with swallowing)-new onset of dyspepsia in ≥60yo -weight loss-GI bleeding-vomiting-anemia Diagnosis: -There is no gold standard test -Patient with typical symptoms: diagnosis can be based on clinical symptoms alone -Patient with atypical symptoms: these symptoms can be seen in GERD but are not sufficient for diagnosis of GERD in the absence of typical symptoms. Need to rule out other disorders before associating the symptoms with GERD. (ex: chest pain r/o other causes such as MI with ECG) -Patient with alarm features: refer to GI for upper GI endoscopy. Complications: -Esophagitis: Erosive reflux disease (ERD) = GER with evidence of esophageal distal injury on endoscopy; in untreated GERD 30% have esophagitis. -Iron deficiency anemia: due to mucosal ulcerations -> chronic bleeding.-Esophageal stricture: narrowing near GE junction, solid food dysphagia.-Barrett Esophagus: intestinal metaplasia of esophagus due to chronic GERD (stratified squamous epithelium replaced by columnar epithelium)-Risk factors: GERD for 5-10 years, >50yo, males, obesity, Caucasian, Tobacco use, family history -Predisposes to esophageal adenocarcinoma Role of H. pylori.Sometimes we tend to think that H. pylori is the cause of GERD. “H. pylori infection appears to protect the esophagus from gastroesophageal reflux disease, Barrett's esophagus, dysplasia in Barrett's

Jul 19, 202419 min