What are statins?

Zohal: Statins are medications that lower cholesterol by inhibiting the enzyme HMG-CoA reductase, which prevents cholesterol synthesis in the liver. By doing so, statins decrease low-density lipoprotein cholesterol (LDL-C). 

Why should we lower LDL?

Zohal: There are four main lipoproteins that transport fats in blood, including chylomicrons, VLDL, LDL, and HDL. This is where we get our “bad cholesterol” vs. “good cholesterol”. Of these, LDL is most associated with an increased risk in cardiovascular disease, while a higher HDL is associated with lower risk. Thus, reducing LDL subsequently reduces the risk of cardiovascular disease. 

Arreaza: The lowest LDL I’ve seen was 25, and the highest HDL was 60. HDL doesn’t really have a strict upper limit, but most people fall between 40 and 60. Extremely high HDL—above 100—may not always be protective and can sometimes signal underlying issues.

Zohal: My HDL is 70! Statins are used for both primary prevention, meaning preventing cardiovascular disease before it occurs, and secondary prevention, meaning preventing disease progression in patients who already have cardiovascular disease.

History of statins.

Zohal: In the early 1900’s, researchers were studying the association between cholesterol and atherosclerosis, and at that time, they primarily used animal subjects. These studies were initially not taken seriously, because most believed cardiovascular disease in humans were simply due to aging and was not preventable. 

It wasn’t until the middle of the century when researchers began observing that increased levels of LDL and decreased HDL was correlated with an increased rate of heart attacks. This finding prompted interest in determining the pathway of cholesterol synthesis in the human body. 

Statins were first discovered in the 1970s when researchers identified compounds that inhibit a critical step in cholesterol synthesis. The first statin approved for clinical use was Lovastatin in 1987.

Since then, multiple statins have been developed, including Atorvastatin, Rosuvastatin, Simvastatin, and Pravastatin. Further clinical trials in the 1990s and 2000s showed that statins significantly reduce myocardial infarction, stroke, and cardiovascular mortality.

Why do Statins Matter in Primary Prevention

Zohal: Cardiovascular disease is the most common cause of death worldwide. As previously mentioned, elevated LDL cholesterol contributes to the development of atherosclerotic plaques within arteries, which can lead to heart attack and stroke. By lowering LDL cholesterol and stabilizing plaque formation, statins implemented in a timely manner significantly reduce the risk of atherosclerotic cardiovascular disease.

Arreaza: One of the things I love most about primary care is prevention. You’re working upstream, often quietly, humbly, helping people avoid disease before it starts. And the truth is—you rarely see the full impact of your actions. You don’t get a notification that says, “this patient didn’t have a heart attack because of you.” But every time you help someone control their blood pressure, quit smoking, improve their diet, or stay consistent with their medications, you’re shifting their tracks. You’re reducing risk in ways that may never be fully visible. That’s the paradox and the beauty of it: in primary care, your highest victories are often events that never happen. 

Who Should Receive Statins for Primary Prevention?

Zohal: Recommendations slightly differ depending on who you ask. We look to the U.S. Preventive Services Task Force, the American College of Cardiology, and the American Heart Association for their recommendations regarding statins for primary prevention.

USPSTF on statins.

The U.S. Preventive Services Task Force (or USPSTF for short) is an organization that works to improve the health of people nationwide by making evidence-based recommendations on effective ways to prevent disease & prolong life. They recommend statins for the primary prevention of cardiovascular disease in:

• Adults 40–75 years old
• With one or more cardiovascular risk factors such as dyslipidemia, diabetes, hypertension, or smoking
• AND a 10-year cardiovascular risk of 10% or greater

Their recommendations are graded A, B, C, D, and I, depending on the strength of evidence and this is a Grade B recommendation.

Arreaza: So, you have to meet all the criteria to receive a statin, according to USPSTF: 40-75, one CV risk factor and a high 10-y ASCVD score, by the way, the ASCVD risk calculator was introduced in 2013 by AHA/ACC. It is available online for free and many EHRs have integrated this tool into their software. For example, if you use EPIC, you can type .ascvd and get a score automatically. What about patients with a cardiovascular risk less than 10%?

Zohal: For patients with a 7.5–10% risk, some may offer statin therapy on a case-by-case basis as this is a Grade C recommendation. But I’ll get more into this later.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

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References:

1. Grundy SM, et.al, Guideline on the Management of Blood Cholesterol: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2019 Jun 18;139(25):e1082-e1143. doi: 10.1161/CIR.0000000000000625. Epub 2018 Nov 10. Erratum in: Circulation. 2019 Jun 18;139(25):e1182-e1186. doi: 10.1161/CIR.0000000000000698. Erratum in: Circulation. 2023 Aug 15;148(7):e5. doi: 10.1161/CIR.0000000000001172. PMID: 30586774; PMCID: PMC7403606. https://pubmed.ncbi.nlm.nih.gov/30586774/
2. U.S. Preventive Services Task Force. (2022, August 23). Statin use for the primary prevention of cardiovascular disease in adults: Preventive medication.
   https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/statin-use-in-adults-preventive-medicatio
3. American College of Cardiology ASCVD Risk Estimator: https://tools.acc.org/ascvd-risk-estimator-plus/#!/calculate/estimate/
4. Guideline Central. (2026, March). ACC/AHA dyslipidemia guideline spotlight (March 2026).
   https://www.guidelinecentral.com/insights/mar-2026-accaha-dyslipidemia-guideline-spotlight/
5. Endo A. A historical perspective on the discovery of statins. Proc Jpn Acad Ser B Phys Biol Sci. 2010;86(5):484-93. doi: 10.2183/pjab.86.484. PMID: 20467214; PMCID: PMC3108295. https://pubmed.ncbi.nlm.nih.gov/20467214/
6. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

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 markers are not only diagnostic tools, but they also help guide staging and follow-up care. That’s an important board question. Why don’t we perform a biopsy in a testicular mass? 

Ebenezer: Testicular masses suspicious of cancer are not biopsied because biopsy can disrupt lymphatic drainage and potentially spread tumor cells. Instead, the standard treatment is radical inguinal orchiectomy, which both removes the tumor and establishes the diagnosis.

Dr. Arreaza: Brandon, can you briefly explain the two main categories of testicular cancer?

Brandon: Let’s start with the germ cell tumors. They are broadly divided into seminomas and non-seminomatous germ cell tumors (NSGCT). Seminomas tend to grow more slowly and are highly sensitive to radiation therapy.

Ebenezer: Non-seminomatous tumors include embryonal carcinoma, yolk sac tumor, choriocarcinoma, and teratoma. These tumors tend to be more aggressive but are still highly responsive to treatment.

Dr. Arreaza: How are patients staged once the diagnosis is made?

Ebenezer: Staging typically includes a CT scan of the chest, abdomen, and pelvis to evaluate for metastasis, especially to the retroperitoneal lymph nodes, which are the most common site of spread.

Dr. Arreaza: And how is testicular cancer managed?

Brandon: The initial step is almost always radical inguinal orchiectomy. Depending on staging and tumor type, treatment may include active surveillance, chemotherapy, radiation therapy, or retroperitoneal lymph node dissection.

Ebenezer: One reason outcomes are so favorable is that germ cell tumors respond extremely well to cisplatin-based chemotherapy.

Dr. Arreaza: Let’s talk about prognosis.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week!

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References:

1. Honda K, Kawai T, Taguchi S, Shiratori T, Miyakawa J, Nakamura Y, Kaneko T, Suzuki K, Suda S, Kamei J, Kakutani S, Niimi A, Yamada Y, Urakami S, Fukuhara H, Nakagawa T, Kume H. Impact and Risk Factors of Diagnostic Delay in Patients With Testicular Cancer: A Multicenter Retrospective Study. Int J Urol. 2025 Nov;32(11):1593-1601. doi: 10.1111/iju.70187. Epub 2025 Jul 28. PMID: 40726135; PMCID: PMC12586796. https://pubmed.ncbi.nlm.nih.gov/40726135/
2. Singla N, Bagrodia A, Baraban E, Fankhauser CD, Ged YMA. Testicular Germ Cell Tumors: A Review. JAMA. 2025;333(9):793–803. doi:10.1001/jama.2024.27122 https://jamanetwork.com/journals/jama/article-abstract/2829847?utm_source=openevidence&utm_medium=referral
3. Chavarriaga J, Nappi L, Papachristofilou A, Conduit C, Hamilton RJ. Testicular cancer. Lancet. 2025 Jul 5;406(10498):76-90. doi: 10.1016/S0140-6736(25)00455-6. Epub 2025 May 29. PMID: 40451233. https://pubmed.ncbi.nlm.nih.gov/40451233/
4. Tateo V, Thompson ZJ, Gilbert SM, Cortessis VK, Daneshmand S, Masterson TA, Feldman DR, Pierorazio PM, Prakash G, Heidenreich A, Albers P, Necchi A, Spiess PE. Epidemiology and Risk Factors for Testicular Cancer: A Systematic Review. Eur Urol. 2025 Apr;87(4):427-441. doi: 10.1016/j.eururo.2024.10.023. Epub 2024 Nov 13. PMID: 39542769. https://pubmed.ncbi.nlm.nih.gov/39542769/
5. Langn RC, Puente MEE. Scrotal Masses. Am Fam Physician. 2022 Aug;106(2):184-189. PMID: 35977130. https://pubmed.ncbi.nlm.nih.gov/35977130/
6. Xu P, Wang J, Abudurexiti M, Jin S, Wu J, Shen Y, Ye D. Prognosis of Patients With Testicular Carcinoma Is Dependent on Metastatic Site. Front Oncol. 2020 Jan 10;9:1495. doi: 10.3389/fonc.2019.01495. PMID: 31998648; PMCID: PMC6966605. https://pubmed.ncbi.nlm.nih.gov/31998648/

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.

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References:

1. 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.
2. 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.
3. Häuser W, Ablin J, Fitzcharles MA, et al. Fibromyalgia. Am Fam Physician. 2023;107(2):158‑166.
4. 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.
5. Kleykamp BA, Ferguson MC, McNicol E, et al.The prevalence of psychiatric and chronic pain comorbidities in fibromyalgia: An ACTION systematic review. Semin Arthritis Rheum. 2021;51(1):166‑174. PMID: 33383293. doi:10.1016/j.semarthrit.2020.10.006.
6. Magen E, Tolkin L, Aamar S, et al.Endocrine comorbidities in fibromyalgia. Clin Endocrinol (Oxf). 2025;[Epub ahead of print]. doi:10.xxxx/clinend.2025.xxxxx.
7. Mohabbat AB, Wilkinson JM. Central sensitization: When it is not “all in your head.” Am Fam Physician. 2023;107(1):92‑96.
8. Moscati A, Faucon AB, ArnaizYépez‑Yépez C, et al.Life is pain: Fibromyalgia as a nexus of multiple liability distributions. Am J Med Genet B Neuropsychiatr Genet. 2023;192(2):134‑148. doi:10.1002/ajmg.b.32911.
9. Rivera FA, Munipalli B, Allman ME, et al.A retrospective analysis of the prevalence and impact of associated comorbidities on fibromyalgia outcomes in a tertiary care center. Front Med (Lausanne). 2023;10:1184734. doi:10.3389/fmed.2023.1184734.
10. Sleurs D, Tebeka S, Scognamiglio C, Dubertret C, Le Strat Y. Comorbidities of selfreported fibromyalgia in United States adults: A ‑reported fibromyalgia in United States adults: A crosssectional‑sectional study from the NESARC‑III. Eur J Pain. 2020;24(9):1687‑1698. doi:10.1002/ejp.1619.
11. Winslow BT, Vandal C, Dang L. Fibromyalgia: Diagnosis and management. Am Fam Physician. 2023;107(2):158‑166. PMID: 36791450. Wolfe F, Clauw DJ, Fitzcharles MA, et al. Revisions to the American College of Rheumatology fibromyalgia diagnostic criteria. Arthritis Care Res (Hoboken). 2023;75(12):2029‑2039. PMID: 41097025. doi:10.1002/acr.24963.
12. Wolfe F, Clauw DJ, Fitzcharles MA, et al.Revisions to the American College of Rheumatology fibromyalgia diagnostic criteria. Arthritis Care Res (Hoboken). 2023;75(12):2029‑2039. PMID: 41097025. doi:10.1002/acr.24963.
13. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

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, normalize. On the other end of the spectrum, continued meth use may lead to progressive fibrosis, ventricular dilation, and potentially irreversible damage, leading to death.
Complications of meth-associated HFrEF
Abishak: These patients are at increased risk for ventricular arrhythmias, sudden cardiac death, left ventricular thrombus formation, and progressive pulmonary hypertension. If the ejection fraction remains below 35 percent after at least three months of optimized therapy, implantable cardioverter-defibrillator (known as ICD) placement should be considered for primary prevention.
Addiction Treatment as Core Therapy
Dr. Arreaza: It sounds like GDMT cannot be done without talking about meth use disorder treatment.
Akbar: Absolutely. Treating the myocardium without addressing the substance use disorder is ineffective. Primary care providers can be trained to manage addictions, but if resources are available, you can place a referral to addiction medicine, psychiatric support, behavioral therapy, and social support services. This is an essential part of the treatment. Sustained abstinence is the single most powerful predictor of recovery.
Prognosis
Abishak: Prognosis is highly dependent on abstinence. Patients who stop using methamphetamine often experience meaningful improvement in EF and even return to normal. 

Dr. Arreaza: Yes, the key factor is complete abstinence, plus standard heart failure treatment. If the damage is mostly functional and inflammatory, recovery is possible. If there is extensive fibrosis (scar)
recovery is less likely. Observational studies have shown that patients with meth-associated cardiomyopathy who stop using meth have significant improvement in EF over 3–12 months, fewer hospitalizations, and lower mortality.

Akbar: Absolutely. Not all meth-associated cardiomyopathy behaves the same way. The extent of fibrosis determines recovery potential. Cardiac MRI with late gadolinium enhancement can help us estimate scar burden. Patients with minimal fibrosis often have better improvement with abstinence and medical therapy.

Dr. Arreaza: So, MRI can actually help us determine the prognosis.

Abishak: Yes, very much so. If MRI shows extensive fibrosis, the likelihood of full EF recovery is lower. That information helps us counsel patients more accurately.

Akbar: Another key issue is right ventricular involvement. Methamphetamine can affect both ventricles. When the right ventricle fails, patients may develop severe peripheral edema, ascites, and hepatic congestion. Right ventricular dysfunction also worsens prognosis significantly.

Dr. Arreaza: And pulmonary hypertension can also worsen the whole picture. 

Akbar: That’s correct. Meth is associated with pulmonary arterial hypertension independently of left-sided heart failure. In some patients, you may see a combined picture of both pulmonary vascular disease and right ventricular dysfunction. That can make management more complicated because pulmonary pressures may remain elevated even after EF improves.

Dr. Arreaza: Tells us about the role of BNP in monitoring these patients. 

Abishak: Serial BNP levels can help track response to therapy. Additionally, troponin may be elevated at times in meth users due to myocardial injury. Monitoring renal function is critical because many heart failure medications affect kidney function and potassium levels.

Akbar:Other lifestyle modifications include sodium restriction, regular follow-ups, vaccination, and avoidance of other cardiotoxic substances such as alcohol or cocaine. Sleep disorders, especially OSA, should be evaluated because untreated OSA worsens heart failure outcomes.

Dr. Arreaza: WhatIs there any role for wearable devices or remote monitoring?

Abishak: Yes, increasingly so. Remote weight monitoring, blood pressure tracking, and symptom reporting can reduce hospitalization. In select patients, implantable hemodynamic monitors may help detect rising filling pressures before symptoms occur.

Dr. Arreaza: It was a great discussion. Thank you, Abishak and Akbar for bringing all that valuable information to us. Let’s wrap it up. 

Dr. Arreaza:
Welcome back to the podcast. I’m Dr. Arreaza, and today we’re talking about a topic that’s very relevant here in the Central Valley but often not well known in the rest of the country, it is called ValleyFever, or coccidioidomycosis. For more info about the Valley Fever diagnosis and initial treatment, please go to our previous podcast on the subject! Episode 143, recorded by wonderful Dr. Lovedip Kooner.  To help us walk through this, I’m joined by Jordan, a medical student. Jordan, welcome back and Dr. Schlaerth, please introduce yourself. 

Jordan:
Thanks, Dr. Arreaza. This is such an important topic, especially in endemic areas like where we live, the Central Valley of California, and Arizona. The public may think of Valley Fever as a mild pneumonia that just goes away eventually. But that’s not always the case. Some patients develop serious, life-altering complications, and a small but important number develop disseminated disease.

Dr. Arreaza:
Exactly. So today, we’re going to break this down systematically: pulmonary complications, dissemination to other organs, CNS disease, musculoskeletal involvement, systemic symptoms, and then we’ll touch on treatment principles and why follow-up matters so much.

Dr. Schlaerth: Valley Fever can be missed in areas where it is not as common as in the Valley. 1989, earthquake in LA.Pneumonias that is not responding to treatment can be pulmonary cocci.

Dr. Arreaza:
Before we dive into specific complications, let’s zoom out. What percentage of patients get a complicated disease?

Jordan:
So, most infections are self-limited, but about 5–10% of patients develop chronic or progressive pulmonary disease, and 1% develop extrapulmonary disseminated disease. That sounds small, but given how common Valley Fever is in endemic areas, that’s still a lot of people.

Dr. Arreaza:
And the complications can be devastating, and they are not always in primary infection.

Dr. Schlaerth: Dissemination can be silent. We don’t know exactly why dissemination happens; some ethnicities are more susceptible or other groups.

Dr. Arreaza:
Let’s start where Valley Fever usually begins: the lungs. What are the major pulmonary complications clinicians should know about?

Jordan:
The most common long-term complications are chronic pulmonary sequelae. These include: cavitary disease, pulmonary nodules, bronchiectasis, pulmonary fibrosis, and pleural complications like effusions, empyema, or pneumothorax.

Dr. Arreaza:
Cavitary disease comes up a lot. What does that look like clinically?

Jordan:
Cavities form in about 5–15% of cases. Many are asymptomatic, but symptomatic cavities can cause fever, fatigue, cough, sputum production, dyspnea, and hemoptysis. The tricky part is that symptoms often wax and wane, and even with treatment, current antifungals don’t eradicate the organism from chronic cavities.

Dr. Arreaza:
That’s very unfortunate, and sometimes those cavities remain and patients might not know that they have them, and those cavitary lesions may rupture.

Jordan:
Yes, rupture can lead to pyopneumothorax, which is a surgical emergency requiring prompt intervention.

Dr. Kooner: Hello everyone, this is Dr. Kooner, and today I want to talk about one of my favorite topics: coccidioidal cavitary disease—because nothing says “fun lung pathology” like a hole in the lung that refuses to leave.

Coccidioidal cavitary disease is a chronic pulmonary manifestation of infection. Many times, it’s found incidentally on imaging. Sometimes patients are being evaluated for respiratory symptoms, sometimes for systemic complaints, and sometimes for something completely unrelated—like when a chest X-ray was ordered for a pre-op clearance and suddenly… surprise cavity.

Pulmonary cavities develop in about 5-10% of patients with Valley Fever. Most of the time, they appear as thin-walled residual lesions. They can be solitary or multiple, and they can range from a few centimeters to much larger. And while textbooks love to show the “classic look,” in real life they can be a little more… creative.

These cavities can persist for years. Some patients feel completely fine and never know they have one. Others develop chronic symptoms or complications like rupture into the pleural space, secondary infection, or bleeding, which is when everyone suddenly becomes very interested in that cavity.

Here’s an important teaching point: about 20% of patients with cavitary disease also have disseminated infection, most commonly involving bone. This challenges the old-school teaching that cavitary lung disease and dissemination rarely happen together. 

One major risk factor for cavitary disease—and for more severe or complicated infection overall—is diabetes mellitus.

So how do patients usually present?

Symptoms often overlap with classic Valley Fever symptoms. The most common presenting symptoms for cavitary disease that usually trigger evaluation are cough, hemoptysis, fever, and shortness of breath.

Diagnosis and monitoring rely heavily on chest imaging. Plain chest X-rays are usually enough for stable disease. CT scans are typically saved for when you’re worried about complications. Serologic testing is also key, especially complement fixation titers. In general, higher titers correlate with more severe disease and higher relapse risk.

Management depends on symptoms and host factors.
If the patient is asymptomatic and immunocompetent, they often don’t need antifungal therapy. These patients can usually be followed with periodic clinical and imaging monitoring watch closely and don’t panic.

Symptomatic patients are typically treated with oral triazoles, most commonly fluconazole or itraconazole. Treatment is long—usually at least 6 to 12 months, and often longer—because symptoms love to come back once therapy stops. These medications are usually suppressive rather than curative, although newer data suggests triazoles may help with cavity closure in some patients.

Relapses happen in about 25 to 33% of immunocompetent patients, and even more often in immunocompromised patients or transplant recipients. Many of these patients end up needing long-term or even indefinite therapy. Not ideal—but still better than uncontrolled disease.

Surgery still has a role, but it’s more selective now. It’s usually reserved for complications like life-threatening hemoptysis or rupture into the pleural space. Early ruptures might be managed with chest tube drainage. More complicated or delayed cases may need decortication or lung resection.

So, the big picture: symptomatic coccidioidal cavitary disease can be a chronic management challenge. It requires individualized treatment decisions, prolonged therapy for many patients, and long-term follow-up with imaging and serologic monitoring to catch relapses early and prevent complications.

And if there’s one takeaway, it’s this: if you find a stable cavity in someone known to have Valley Fever, sometimes the best move is careful monitoring—not chasing it with endless tests that make everyone nervous, including the patient.

Thanks for listening—and remember, sometimes the lung keeps souvenirs from infections… and sometimes those souvenirs stick around for years. Now, let’s continue with the discussion about pulmonary nodules. This is Dr. Kooner, signing off.

H. Nicole Magaña, medical student, reviews the history of PrEP and outlines the currently FDA-approved medications used for HIV prevention. Dr. Arreaza provides additional perspective on long-acting injectable options, including how quickly they begin to protect patients after initiation.  

Written by Nicole Magana, MSIV, American University of the Caribbean. Comments and edits by Hector Arreaza, MD.

You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.

Pre-exposure prophylaxis for HIV.

Previous episodes related to HIV: 
-Episode 67, HIV history (September 2021)
-Episode 68, HIV transmissibility (October 2021)
-Episode 70 (October 2021), HIV prevention (including HIV Prep with oral medications)
-Episode 98 (June 2022), we introduced Apretude, the first injectable for HIV PrEP. Apretude was approved in December 2021. 

What is Pre-Exposure prophylaxis (PrEP)?

Pre-exposure prophylaxis, or PrEP, is the use of antiretroviral medications taken by individuals who are HIV-negative to prevent HIV acquisition. There are 30,000 new HIV infections annually in the US. 

How effective is it?

When taken as prescribed, PrEP is highly effective at reducing the risk of HIV transmission through sexual exposure and injection drug use. Patients who are adherent to PrEP can lower their risk of contracting HIV by 99%.

The effectiveness of oral PrEP is highly adherence dependent. In trials with 70% adherence, the relative risk of HIV acquisition was 0.27, compared to 0.51 with 40-70% adherence and no significant benefit with adherence ≤40%.

How does PrEP work?

PrEP works by maintaining therapeutic drug levels in the bloodstream and in target tissues. If HIV exposure occurs, viral replication is inhibited, preventing the establishment of infection.

Brief History of PrEP.

The concept of PrEP originated from early animal studies demonstrating that antiretroviral medications could prevent retroviral transmission when administered before exposure.

In 2010, the iPrEx trial showed that daily oral tenofovir disoproxil fumarate (known as Truvada) with emtricitabine significantly reduced HIV acquisition among men who have sex with men and transgender women. This was the first large clinical trial to demonstrate the effectiveness of PrEP.

In 2012, the FDA approved oral Truvada, which is TDF/FTC (tenofovir disoproxil and emtricitabine) for HIV prevention. Since then, additional studies have expanded indications and introduced new formulations, including long-acting injectable options.

Who Should Be Offered PrEP?

PrEP should be considered for any HIV-negative individual at increased risk of HIV acquisition, including Men who have sex with men, transgender individuals, heterosexual men and women with an HIV-positive partner, individuals with recent bacterial sexually transmitted infections, people who inject drugs, individuals engaging in condomless sex with partners of unknown HIV status.

Remember that PrEP should be offered in a nonjudgmental, patient-centered manner, make it a safe space to talk openly about prevention of HIV. 

Available HIV PrEP Options.

Daily Oral PrEP: There are 2 formulations of Tenofovir. There is Tenofovir disoproxil fumarate (TDF)/ Truvada and Tenofovir alafenamide (TAF)/ Descovy. Each is available in a tablet combined with Emtricitabine a nucleoside reverse transcriptase inhibitor.

Truvada: It is approved for all populations at risk through sexual exposure or injection drug use. Something to look out for before starting this medication is for pre-existing CKD. Do not give to patients who have an estimated glomerular filtration rate of less than 60 mL/min. (6)

Descovy: This option is approved for men who have sex with men and transgender women but is not approved for individuals at risk through receptive vaginal sex. It has less impact on renal function and bone mineral density compared to Truvada. It can be used in moderately reduced kidney function (GFR between 30-60 mL/min).

Truvada and Descovy are taken orally once a day. 

After patients start taking these medications, when are they considered to be protected? 

Nicole: With daily oral PrEP, guidelines differ with WHO and International Aids Society-USA stating it takes about 7 days, while CDC states 21 days to allow for adequate concentration in tissues (1). Adherence is critical for efficacy.

Injectable HIV PrEP.

In 2021, the FDA approved the first Injectable PrEP option Long-acting cabotegravir (CAB-LA)- known on the market as Apretude. Cabotegravir is an integrase strand transfer inhibitor administered as an intramuscular injection.Dosing consists of an initial injection, a second injection one month later, and then maintenance injections every two months (1).

Another option is Lenacapavir (Yeztugo). The Yeztugo as a pre-exposure prophylaxis (PrEP) for HIV in Oct 2024. Yeztugo is the first and only FDA-approved HIV prevention treatment that requires just two injections per year, offering a long-acting option for people who weigh at least 35kg. It is given as 2 injections every 6 months. First dose is given with 2 tablets on Day 1 and Day 2, then every 6 months 2 injections on the same day.

Clinical trials, including HPTN 083 and HPTN 084, demonstrated that injectable cabotegravir is superior to daily oral PrEP in preventing HIV infection. This advantage is largely due to improved adherence rather than differences in intrinsic drug potency.

There have been no head-to-head comparisons between Yeztugo and Apretude, but they are both very effective. Apretude starts protecting 7 days after the first dose, and Yeztugo starts protecting 2 hours after Day 2 (if patient takes the oral loading dose) or 3-4 weeks if no oral load is taken.

Injectable PrEP is particularly beneficial for patients who struggle with daily pill adherence, have trouble swallowing pills, prefer a discreet option, have difficulty storing their medication or have renal or bone disease that limits the use of tenofovir-based regimens like Truvada and Descovy (6). In one unpublished report by Medline, patients who received Apretude had an increase in bone mineral density compared to those who received Truvada (1).

Tests prior to starting PrEP.

Before initiating PrEP, patients must be confirmed to be HIV-negative. Baseline evaluation includes HIV testing with a fourth-generation antigen/antibody assay, HIV RNA testing if acute infection is suspected, renal function testing for oral PrEP, Hepatitis B screening, sexually transmitted infection screening, and pregnancy testing when appropriate. PrEP should not be started in individuals with known or suspected acute HIV infection.

Monitoring for patients on HIV PrEP.

Monitoring typically includes HIV testing every 2 to 3 months, STI screening every 3 to 6 months, renal function monitoring for those on oral PrEP (tenofovir- based), ongoing adherence and risk-reduction counseling. And for injectable PrEP, adherence to the injection schedule is essential, as delayed dosing may increase the risk of resistance if HIV infection occurs.

HIV PrEP is not a prevention for other STIs. Screening for STIs and counseling about prevention is essential.

Breakthrough HIV infections on PrEP are rare and most often associated with poor adherence or delayed diagnosis.

Truvada is more studied in all populations and is considered safe during pregnancy and breastfeeding. There is less data regarding the injectable option in patients who are pregnant, may become pregnant, or whose primary risk factor is injection drug use (1). Injectable PrEP provides an important alternative for patients with chronic kidney disease and bone disease (1).

Key Takeaway

Pre-exposure prophylaxis is a safe, effective, and evidence-based strategy for HIV prevention. With both daily oral and long-acting injectable options available, PrEP can be individualized to meet patient needs. Normalizing PrEP discussions in clinical practice is essential to reducing new HIV infections and advancing public health goals. 

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

References:

1. Antiretroviral Drugs for Treatment and Prevention of HIV in Adults: 2024 Recommendations of the International Antiviral Society–USA Panel. The Journal of the American Medical Association. 2025. Gandhi RT, Landovitz RJ, Sax PE, et al.
2. Long-Acting Lenacapavir Acts as an Effective Preexposure Prophylaxis in a Rectal SHIV Challenge Macaque Model. The Journal of Clinical Investigation. 2023. Bekerman E, Yant SR, VanderVeen L, et al.
3. Pharmacokinetics and Safety of Once-Yearly Lenacapavir: A Phase 1, Open-Label Study. Lancet. 2025. Jogiraju V, Pawar P, Yager J, et al.

Hyo Mun and Jordan Redden (medical students) explain how to manage HFpEF with medications and touch some basics about nonpharmacologic treatments. Dr. Arreaza asks insightful questions to guide the discussion. 

Written by Hyo Mun, MSIV, American University of the Caribbean; and Jordan Redden, MSIV, Ross University School of Medicine. Comments by Hector Arreaza, MD.

You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.

Treatment of HFpEF

Arreaza: Mike, if you had to name the one therapy everyone with HFpEF should be on, what is it?

Mike: That's easy! SGLT-2 inhibitors. This is the one slam-dunk we have in HFpEF. Empagliflozin (Jardiance) or dapagliflozin (Farxiga) should be started in essentially every patient with HFpEF, and it doesn't matter if they have diabetes or not.

Jordan: And that’s worth repeating, because people still think of these as “diabetes drugs.” They’re not anymore. In HFpEF, SGLT-2 inhibitors reduce heart-failure hospitalizations, improve symptoms, improve quality of life, and even reduce cardiovascular death.

Dr. Arreaza: They’re also simple. Empagliflozin 10 mg daily or dapagliflozin 10 mg daily. No titration, no drama. The effectiveness of these meds was established around 2019 with DAPA-HF and later with DELIVER. These were trials thatdemonstrated that dapagliflozin reduces worsening heart failure and cardiovascular events across the full spectrum of heart failure, from reduced to preserved ejection fraction, independent of diabetes status.

Mike: And the number needed to treat is about 28 to prevent one heart-failure hospitalization. That’s excellent for a disease where we historically had almost nothing that worked.

Jordan: They’re also safe in chronic kidney disease down to an eGFR of about 25, which makes them even more useful in this population.

Dr. Arreaza: Alright. We got SGLT-2 inhibitor, what’s next?

Mike: Volume management. Loop diuretics are still the backbone of symptom control in HFpEF. If the patient is volume overloaded, you diurese, and you diurese aggressively.

Jordan: The goal is euvolemia. Dry weight, no edema, no orthopnea, no waking up gasping for air. A lot of these patients end up needing chronic oral loop diuretics to stay there.

Dr. Arreaza: Something to remember: HFpEF patients don’t tolerate congestion well, and being “a little wet” is not benign. Let’s move into RAAS inhibition. Where do ARBs and ACE inhibitors fit in?

Mike: Between ARBs and ACE inhibitors, ARBs are the winners in HFpEF. They actually reduce heart failure hospitalizations—drugs like candesartan, losartan, valsartan. ACE inhibitors? Not so much. They showed minimal benefit in older HFpEF patients, which is why we go with ARBs instead.

Jordan: But a lot of clinicians get nervous about ACE inhibitors and ARBs because of kidney function, so it’s worth talking through how these drugs actually work in the kidney.

Dr. Arreaza: Yes, misunderstanding may lead to unnecessary drug discontinuation.

Jordan: Under normal conditions, the afferent arteriole brings blood into the glomerulus, and the efferent arteriole is constricted by angiotensin II. That constriction keeps pressure high in the glomerulus and maintains filtration.

Mike: Here's what happens with an ACE inhibitor: you block angiotensin II, the efferent arteriole relaxes, glomerular pressure drops, and GFR dips slightly. Creatinine bumps up a little, and that scares people, but that's actually the whole point—that's how you get kidney protection long-term.

Jordan: High intraglomerular pressure causes hyperfiltration injury and scarring over time. Lowering that pressure protects the kidney long-term. The short-term GFR drop is the price you pay for long-term benefits.

Dr. Arreaza: So let’s talk about CKD, because this is where people panic.

Mike: Right. ACE inhibitors and ARBs are not contraindicated in chronic kidney disease. In fact, they’re recommended even in advanced stages. They reduce progression to kidney failure by about a third.

Jordan: The key is how you use them. Start low. Check creatinine and potassium one to two weeks after starting, then periodically. A creatinine rise up to 30% from baseline is acceptable. That’s not kidney injury, that’s physiology.

Dr. Arreaza: And what about potassium creeping up?

Mike: You adjust the dose or add a potassium binder. You don’t just automatically stop the drug.

Dr. Arreaza: Now there is one absolute contraindication everyone needs to know about! (board exam test)

Jordan: Bilateral renal artery stenosis. This is the big one. In these patients, the kidneys are completely dependent on angiotensin II–mediated efferent constriction to maintain GFR. Take that away, and GFR collapses.

Mike: Creatinine can jump dramatically within days. If you see a creatinine rise of 20% or more shortly after starting an ACE inhibitor, you should be thinking about bilateral renal artery stenosis and stopping the drug immediately.

Dr. Arreaza: After revascularization, though, many patients can tolerate ACE inhibitors again, so this isn’t always permanent. What about cardiorenal syndrome? That’s where things get uncomfortable.

Mike: It is uncomfortable, but cardiorenal syndrome isn't a contraindication. These patients have severe heart failure and kidney disease, and their mortality is actually higher than patients with heart failure alone.

Jordan: ACE inhibitors still reduce mortality and slow kidney disease progression in this group. Studies show that stopping ACE inhibitors during acute heart-failure admissions increases in-hospital mortality three- to four-fold.

Dr. Arreaza: So we are cautious, but we don’t avoid it.

Mike: Exactly. Start low, titrate slowly, monitor labs closely, accept up to a 30% creatinine rise. You only stop if kidney function keeps worsening, or potassium gets dangerously high.

Dr. Arreaza: Alright. Let’s move on. What about mineralocorticoid receptor antagonists… MRA?

Jordan: Spironolactone or eplerenone might reduce hospitalizations in HFpEF, but the data is mixed. This is more of a “select patients” situation.

Mike: And you have to watch potassium and kidney function carefully, especially if they’re already on an ACE inhibitor or ARB.

Dr. Arreaza: What about sacubitril-valsartan, also known as Entresto®?

Mike: Entresto may help patients with mildly reduced EF roughly in the 45 to 57% range. It’s not first-line for HFpEF, but in select patients, it's reasonable.

Dr. Arreaza: Now let’s clarify one of the biggest sources of confusion: beta blockers.

Jordan: Beta blockers are not a treatment for HFpEF itself. They’re only indicated if the patient has another reason to be on them, like coronary disease or atrial fibrillation.

Mike: And timing really matters here. You absolutely do not start beta blockers during acute decompensated heart failure. Their negative inotropic effects can make things worse when patients are volume overloaded.

Jordan: But, and this is critical, you also don’t stop them if the patient is already taking one. Abrupt withdrawal causes a sympathetic surge and dramatically increases mortality.

Dr. Arreaza: If a patient is admitted on a beta blocker, what do we do?

Mike: Continue it at the same dose or reduce it slightly if they’re really unstable. Once they’re euvolemic and stable, you can carefully titrate up.

Jordan: And watch for chronotropic incompetence. HFpEF patients often rely on heart-rate response to exercise, and beta blockers can worsen exercise intolerance.

Dr. Arreaza: Beyond medications, HFpEF is really about treating comorbidities. Aerobic activity can be an initial strategy to improve exercise intolerance and has evidence of improving aerobic function and quality of life. Sodium restriction: improves symptoms, does not decrease risk of death or hospitalizations.

Mike: Hypertension control is huge. For diabetes, the SGLT-2 inhibitors will perform double duty. For obesity, weight loss improves symptoms, and GLP-1 agonists like semaglutide are absolute gamechangers.

Jordan: Don’t forget sleep apnea, atrial fibrillation, and lifestyle. Exercise improves the quality of life, even if it doesn’t change hard outcomes. Lifestyle is the main treatment. 

Dr. Arreaza: And when should you refer to cardiology?

Mike: You should refer when the diagnosis isn't clear; symptoms are not responding to treatment, difficult volume management, end-organ dysfunction, or if you are concerned about advanced heart failure.

Dr. Arreaza: So, it has been a great discussion. What is the takeaway?

Mike: HFpEF treatment isn't about one magic drug -- it's about volume control, SGLT2 inhibitors, smart use of RAAS blockade, and aggressive management of comorbidities.

Jordan: And it's understanding the physiology, so you don’t withhold life-saving therapies out of fear.

Dr. Arreaza: Well said. If you found this helpful, share it with a friend or colleague and rate us wherever you listen. This is Dr. Arreaza, signing off.

Jordan/Mike: Thanks! 

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. Barzin A, Barnhouse KK, Kane SF. Heart Failure With Preserved Ejection Fraction. Am Fam Physician. 2025;112(4):435-440.
2. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure. Circulation. 2022;145(18):e895-e1032.
3. Kittleson MM, Panjrath GS, Amancherla K, et al. 2023 ACC expert consensus decision pathway on management of heart failure with preserved ejection fraction. J Am Coll Cardiol. 2023;81(18):1835-1878.
4. Anker SD, Butler J, Filippatos G, et al. Empagliflozin in heart failure with a preserved ejection fraction. N Engl J Med. 2021;385(16):1451-1461.
5. Solomon SD, McMurray JJV, Claggett B, et al. Dapagliflozin in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2022;387(12):1089-1098.
6. Pitt B, Pfeffer MA, Assmann SF, et al. Spironolactone for heart failure with preserved ejection fraction. N Engl J Med. 2014;370(15):1383-1392.
7. Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction. Lancet. 2003;362(9386):777-781.
8. Solomon SD, McMurray JJV, Anand IS, et al. Angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med. 2019;381(17):1609-1620.
9. Kosiborod MN, Abildstrøm SZ, Borlaug BA, et al. Semaglutide in patients with heart failure with preserved ejection fraction and obesity. N Engl J Med. 2023;389(12):1069-1084.
10. Xie Y, Xu E, Bowe B, Al-Aly Z. Long-term cardiovascular outcomes of COVID-19. Nat Med. 2022;28(3):583-590.
11. Puntmann VO, Carerj ML, Wieters I, et al. Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from COVID-19. JAMA Cardiol. 2020;5(11):1265-1273.
12. Basso C, Leone O, Rizzo S, et al. Pathological features of COVID-19-associated myocardial injury. Eur Heart J. 2020;41(39):3827-3835.
13. Nalbandian A, Sehgal K, Gupta A, et al. Post-acute COVID-19 syndrome. Nat Med. 2021;27(4):601-615.
14. Badve SV, Roberts MA, Hawley CM, et al. Effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in adults with estimated GFR less than 60 mL/min per 1.73 m². Ann Intern Med. 2024;177(8):953-963.
15. Navis G, Faber HJ, de Zeeuw D, de Jong PE. ACE inhibitors and the kidney: a risk-benefit assessment. Drug Saf. 1996;15(3):200-211.
16. Textor SC, Novick AC, Tarazi RC, et al. Critical perfusion pressure for renal function in patients with bilateral atherosclerotic renal vascular disease. Ann Intern Med. 1985;102(3):308-314.
17. Hackam DG, Spence JD, Garg AX, Textor SC. Role of renin-angiotensin system blockade in atherosclerotic renal artery stenosis and renovascular hypertension. Hypertension. 2007;50(6):998-1003.
18. Ronco C, Haapio M, House AA, et al. Cardiorenal syndrome. J Am Coll Cardiol. 2008;52(19):1527-1539.
19. Prins KW, Neill JM, Tyler JO, et al. Effects of beta-blocker withdrawal in acute decompensated heart failure. JACC Heart Fail. 2015;3(8):647-653.
20. Jondeau G, Neuder Y, Eicher JC, et al. B-CONVINCED: Beta-blocker CONtinuation Vs. INterruption in patients with Congestive heart failure hospitalizED for a decompensation episode. Eur Heart J. 2009;30(18):2186-2192.
21. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Hyo Mun and Jordan Redden (medical students) explain the pathophysiology of heart failure with preserved ejection fraction (HFpEF) and how it differentiates from HFrEF. Dr. Arreaza asks insightful questions and summarizes some key elements of HFpEF. 

Written by Hyo Mun, MS4, American University of the Caribbean; and Jordan Redden, MS4, Ross University School of Medicine. Comments and edits by Hector Arreaza, MD.

You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.

What is EF? Just imagine, the heart is a pump, blood gets into the heart through the veins, the ventricles fill up and then squeeze the blood out. So, the percent of blood that is pumped out is the EF. Let’s start at the beginning. 

What is HFpEF?

Mike: HFpEF stands for heart failure with preserved ejection fraction. Basically, these patients squeeze normally—their ejection fraction is 50% or higher—but here's the thing: the heart can't relax and fill the way it should. The muscle gets stiff, almost like a thick leather boot that just won't stretch. And because the ventricle can't fill properly, pressure starts backing up into the lungs and the rest of the body. That's when patients start experiencing shortness of breath, leg swelling, fatigue—all those classic symptoms.

Dr. Arreaza: And this is where people get fooled by the ejection fraction.

Mike: Exactly. The ejectionfraction tells you total left ventricular emptying, not just forward flow.

Jordan: The classic example is severe mitral regurgitation. You can eject 60% of your blood volume and still be in cardiogenic shock because most of that blood is leaking backward into the left atrium instead of going into the aorta. So, you get pulmonary edema, hypotension, fatigue, all with a “normal” EF. Which is honestly terrifying if you’re over-relying on echo reports without thinking clinically.

Dr. Arreaza: And in HFpEF, functional mitral regurgitation often shows up later in the disease. It’s not usually the primary cause; it’s more of a marker of advanced disease. Moderate to severe MR in HFpEF independently predicts worse outcomes, including a higher risk of mortality or heart failure hospitalization. So, let’s contrast this with HFrEF. How are these two different?

Mike: HFrEF—heart failure with reduced ejection fraction—is a pumping problem. The heart muscle is weak and can't contracteffectively. Ejection fraction drops below 40%, and this is your classic systolic dysfunction.

Jordan: HFpEF, on the other hand, is diastolic dysfunction. The heart muscle is thick, fibrotic, and noncompliant. It squeezes fine, but it just doesn’t relax, even though the EF looks reassuring on paper.

Mike: I like to explain it this way: HFrEF is a weak heart that can't squeeze. HFpEF is a stiff heart that can't relax. Totally different problems.

Dr. Arreaza: And then there’s the gray zone: heart failure with mildly reduced EF, or HFmrEF. That’s an EF between 41 and 49% with evidence of elevated filling pressures. It really shares the features of both worlds. So, what actually causes HFpEF versus HFrEF?

Jordan: HFpEF is basically what happens when all the problems of modern living catch up with you. You've got chronic hypertension, obesity, diabetes, metabolic syndrome, aging, systemic inflammation—all of these things slowly remodel the heart over years. The muscle gets thick and stiff, and eventually the ventricle just loses its ability to relax. So, HFpEF is really a disease of metabolic dysfunction and chronic stress in the heart. 

Mike: HFrEF is more about direct injury. Think about myocardial infarctions, ischemic cardiomyopathy, viral myocarditis, alcohol toxicity, chemotherapy like doxorubicin, genetic cardiomyopathies, or chronic uncontrolled tachycardia. These insults actually damage or kill heart muscle cells, leading to a dilated, weak ventricle that can’t pump effectively.

Dr. Arreaza: So the short version: HFpEF is caused by chronic metabolic and hypertensive stress, while HFrEF is caused mainly by myocardial damage. A question we get a lot: does HFpEF eventually turn into HFrEF? What do you guys think?

Mike: In most cases, no. HFpEF patients usually stay HFpEF throughout their disease course. They don’t just “burn out” and turn into HFrEF.

Jordan: They’re generally separate disease entities with different pathophysiology. A patient with HFpEF can develop HFrEF if they have a big myocardial infarction or ongoing ischemia that damages the muscle, but that’s not the natural progression.

Mike: Interestingly though, the opposite can happen. Some HFrEF patients actually improve their ejection fraction with good medical therapy—that's called HF with improved EF—and it's a great sign that treatment is working.

Dr. Arreaza: Another question. How do HFpEF and HFrEF compare to restrictive cardiomyopathy and constrictive pericarditis?

Jordan: Clinically, they can all look very similar: dyspnea, edema, fatigue, but the underlying mechanisms are completely different.

Mike: In HFpEF, the myocardium itself is stiff from hypertrophy and fibrosis. The problem is intrinsic to the heart muscle, and EF stays preserved. Echoshows diastolic dysfunction with elevated filling pressures.

Jordan: In HFrEF, the myocardium is weak. The ventricle is often dilated and contracts poorly, with a reduced EF.

Mike: Restrictive cardiomyopathy is different. Here, the myocardium gets infiltrated by abnormal stuff—amyloid, iron, sarcoid—and that makes it extremely stiff. It can look like HFpEF on the surface, but it's usually more severe. On Echo You'll see biatrial enlargement, small ventricles, and preserved EF. And importantly, it's a pathologic diagnosis, so you need advanced imaging or biopsy to confirm it.

Jordan: 

Constrictive pericarditis is another mimic, but here the myocardium is usually normal. The problem is that the pericardium is thickened, calcified, and rigid. This will physically prevent the heart from being filled. Imaging shows pericardial thickening, septal bounce, and respiratory variation in flow, and cath shows equalization of diastolic pressures, which is the hallmark of constrictive pericarditis.

Dr. Arreaza: So the takeaway is: HFpEF is a clinical syndrome driven by common metabolic and hypertensive causes, while restrictive and constrictive diseases are specific pathologic entities. If “HFpEF” is unusually severe or not responding to treatment, you need to think beyond HFpEF. Which type of heart failure is more common right now?

Mike: Good question, the answer is: HFpEF. It now accounts for up to 60% of all heart failure cases, and it’s still rising.

Dr. Arreaza: Why is that?

Jordan: Because people are living longer, gaining weight, and developing more metabolic syndrome. HFpEF thrives in older, or people with obesity, hypertension, or diabetes: basically, the modern American population. At the same time, better treatment of acute MIs means fewer people are developing HFrEF from massive heart attacks.

Mike: HFpEF is the heart failure epidemic of the 21st century. It’s honestly the cardiology equivalent of type 2 diabetes.

Dr. Arreaza: Let’s talk aboutCOVID-19. (2025 and still talking about it) Does it actually increase heart failure risk?

Mike: Yes, absolutely. COVID increases both acute and long-term heart failure risk.

Jordan: During acute infection, COVID can cause myocarditis, trigger massive inflammation, and precipitate acute decompensated heart failure, especially in patients with pre-existing disease. It also causes microthrombi, which can injure the myocardium.

Mike: And after infection, even mild cases are linked to a significantly higher risk of developing new heart failure within the following year. Both HFpEF and HFrEF rates go up.

Dr. Arreaza: I remember seeing this in 2021, we had a patient with acute COVID and HFrEF, her EF was about 10%, I lost contact with the patient and at the end I don’t know what happened to her. What’s the pathophysiology of COVID and heart failure?

Mike: COVID causes direct viral injury through ACE2 receptors, triggers massive inflammation that damages the endothelium and heart muscle, leads to microvascular clotting and fibrosis—all mechanisms that promote HFpEF.

Jordan: Add autonomic dysfunction, persistent low-grade inflammation, and worsening metabolic syndrome, and you’ve got a perfect storm for heart failure.

Dr. Arreaza: Bottom line: COVID is a cardiovascular disease as much as a respiratory one. If someone had COVID and now has unexplained dyspnea or fatigue, think about heart failure. Get an echo, get a BNP, start treatment. Last big question: why did we have so many therapies for HFrEF but essentially none for HFpEF for years?

Mike: HFrEF is mechanistically straightforward. You've got a weak heart with excessive neurohormonal activation going on — so you block RAAS, block the sympathetic system, drop the afterload. The drugs make sense.

Jordan: HFpEF is messy. It’s not one disease. It’s stiffness, fibrosis, inflammation, microvascular dysfunction, metabolic disease, atrial fibrillation, all overlapping. One drug can’t fix all of that.

Mike: And some drugs that worked beautifully in HFrEF actually made HFpEF worse. Take Beta blockers, for example.  They slow heart rate, which is a problem because HFpEF patients rely on heart rate to maintain their cardiac output.

Jordan: The breakthrough came with SGLT-2 inhibitors: diabetes drugs that unexpectedly addressed multiple HFpEF mechanisms at once: volume, metabolism, inflammation, and myocardial energetics.

Dr. Arreaza: The miracle drug for HFpEF! Alright, let’s wrap up.

Mike: Bottom line: HFpEF is common, complex, and dangerous: even if the EF looks “normal.”

Jordan: And if you’re relying on ejection fraction alone, HFpEF will humble you every time.

Dr. Arreaza: If you liked this episode, share it with a friend or a colleague and rate us wherever you listen. This is Dr. Arreaza, signing off.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. Barzin A, Barnhouse KK, Kane SF. Heart Failure With Preserved Ejection Fraction. Am Fam Physician. 2025;112(4):435-440.
2. Heidenreich PA, Bozkurt B, Aguilar D, et al. 2022 AHA/ACC/HFSA guideline for the management of heart failure. Circulation. 2022;145(18):e895-e1032.
3. Kittleson MM, Panjrath GS, Amancherla K, et al. 2023 ACC expert consensus decision pathway on management of heart failure with preserved ejection fraction. J Am Coll Cardiol. 2023;81(18):1835-1878.
4. Anker SD, Butler J, Filippatos G, et al. Empagliflozin in heart failure with a preserved ejection fraction. N Engl J Med. 2021;385(16):1451-1461.
5. Solomon SD, McMurray JJV, Claggett B, et al. Dapagliflozin in heart failure with mildly reduced or preserved ejection fraction. N Engl J Med. 2022;387(12):1089-1098.
6. Pitt B, Pfeffer MA, Assmann SF, et al. Spironolactone for heart failure with preserved ejection fraction. N Engl J Med. 2014;370(15):1383-1392.
7. Yusuf S, Pfeffer MA, Swedberg K, et al. Effects of candesartan in patients with chronic heart failure and preserved left-ventricular ejection fraction. Lancet. 2003;362(9386):777-781.
8. Solomon SD, McMurray JJV, Anand IS, et al. Angiotensin-neprilysin inhibition in heart failure with preserved ejection fraction. N Engl J Med. 2019;381(17):1609-1620.
9. Kosiborod MN, Abildstrøm SZ, Borlaug BA, et al. Semaglutide in patients with heart failure with preserved ejection fraction and obesity. N Engl J Med. 2023;389(12):1069-1084.
10. Xie Y, Xu E, Bowe B, Al-Aly Z. Long-term cardiovascular outcomes of COVID-19. Nat Med. 2022;28(3):583-590.
11. Puntmann VO, Carerj ML, Wieters I, et al. Outcomes of cardiovascular magnetic resonance imaging in patients recently recovered from COVID-19. JAMA Cardiol. 2020;5(11):1265-1273.
12. Basso C, Leone O, Rizzo S, et al. Pathological features of COVID-19-associated myocardial injury. Eur Heart J. 2020;41(39):3827-3835.
13. Nalbandian A, Sehgal K, Gupta A, et al. Post-acute COVID-19 syndrome. Nat Med. 2021;27(4):601-615.
14. Badve SV, Roberts MA, Hawley CM, et al. Effects of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers in adults with estimated GFR less than 60 mL/min per 1.73 m². Ann Intern Med. 2024;177(8):953-963.
15. Navis G, Faber HJ, de Zeeuw D, de Jong PE. ACE inhibitors and the kidney: a risk-benefit assessment. Drug Saf. 1996;15(3):200-211.
16. Textor SC, Novick AC, Tarazi RC, et al. Critical perfusion pressure for renal function in patients with bilateral atherosclerotic renal vascular disease. Ann Intern Med. 1985;102(3):308-314.
17. Hackam DG, Spence JD, Garg AX, Textor SC. Role of renin-angiotensin system blockade in atherosclerotic renal artery stenosis and renovascular hypertension. Hypertension. 2007;50(6):998-1003.
18. Ronco C, Haapio M, House AA, et al. Cardiorenal syndrome. J Am Coll Cardiol. 2008;52(19):1527-1539.
19. Prins KW, Neill JM, Tyler JO, et al. Effects of beta-blocker withdrawal in acute decompensated heart failure. JACC Heart Fail. 2015;3(8):647-653.
20. Jondeau G, Neuder Y, Eicher JC, et al. B-CONVINCED: Beta-blocker CONtinuation Vs. INterruption in patients with Congestive heart failure hospitalizED for a decompensation episode. Eur Heart J. 2009;30(18):2186-2192.
21. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Written by Jacob Dunn, MS4, American University of the Caribbean. Edits and comments by Hector Arreaza, MD.

You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.

Definition:
Heat stroke represents the most severe form of heat-related illness, characterized by a core body temperature exceeding 40°C (104°F) accompanied by central nervous system (CNS) dysfunction. 

Arreaza: Key element is the body temperature and altered mental status. 

Jacob: This life-threatening condition arises from the body's failure to dissipate heat effectively, often in the context of excessive environmental heat load or strenuous physical activity. 

Arreaza: You mentioned, it is a spectrum. What is the difference between heat exhaustion and heat stroke? 

Jacob: Unlike milder heat illnesses such as heat exhaustion, heat stroke involves multisystem organ dysfunction driven by direct thermal injury, systemic inflammation, and cytokine release. You can think of it as the body's thermostat breaking under extreme stress — leading to rapid, cascading failures if not addressed immediately. 

Arreaza: Tell us what you found out about the pathophysiology of heat stroke?

Jacob: Pathophysiology: 

Under normal conditions, the body keeps its core temperature tightly controlled through sweating, vasodilation of skin blood vessels, and behavioral responses like seeking shade or drinking water. But in extreme heat or prolonged exertion, those mechanisms get overwhelmed.

Once core temperature rises above about 40°C (104°F), the hypothalamus—the brain’s thermostat—can’t keep up. The body shifts from controlled thermoregulation to uncontrolled, passive heating. Heat stroke isn’t just someone getting too hot—it’s a full-blown failure of the body’s heat-regulating system. 

Arreaza: So, it’s interesting. the cell functions get affected at this point, several dangerous processes start happening at the same time.

Jacob: Yes: 

1. Cellular Heat Injury
   High temperatures disrupt proteins, enzymes, and cell membranes. Mitochondria start to fail, ATP production drops, and cells become leaky. This leads to direct tissue injury in vital organs like the brain, liver, kidneys, and heart.

Arreaza: Yikes. Cytokines play a big role in the pathophysiology of heat stroke too. 

Jacob: 

1. Systemic Inflammatory Response
   Heat damages the gut barrier, allowing endotoxins to enter the bloodstream. This triggers a massive cytokine release—similar to sepsis. The result is widespread inflammation, endothelial injury, and microvascular collapse.

Arreaza: What other systems are affected?

1. Coagulation Abnormalities
   Endothelial damage activates the clotting cascade. Patients may develop a DIC-like picture: microthrombi forming in some areas while clotting factors get consumed in others. This contributes to organ dysfunction and bleeding.
2. Circulatory Collapse
   As the body shunts blood to the skin for cooling, perfusion to vital organs drops. Combine that with dehydration from sweating and fluid loss, and you get hypotension, decreased cardiac output, and worsening ischemia.

Arreaza: And one of the key features is neurologic dysfunction.

Jacob: 

1. Neurologic Dysfunction
   The brain is extremely sensitive to heat. Encephalopathy, confusion, seizures, and coma occur because neurons malfunction at high temperatures. This is why altered mental status is the hallmark of true heat stroke.

Arreaza: Cell injury, inflammation, coagulopathy, circulatory collapse and neurologic dysfunction. 

Jacob: Ultimately, heat stroke is a multisystem catastrophic event—a combination of thermal injury, inflammatory storm, coagulopathy, and circulatory collapse. Without rapid cooling and aggressive supportive care, these processes spiral into irreversible organ failure.

Background and Types:
Arreaza: Heat stroke is part of a spectrum of heat-related disorders—it is a true medical emergency. Mortality rate reaches 30%, even with optimal treatment. This mortality correlates directly with the duration of core hyperthermia. I’m reminded of the first time I heard about heat stroke in a baby who was left inside a car in the summer 2005. 

Jacob: There are two primary types: 

-nonexertional (classic) heat stroke, which develops insidiously over days and predominantly affects vulnerable populations like children, the elderly, and those with chronic illnesses during heat waves; 

-exertional heat stroke, which strikes rapidly in young, otherwise healthy individuals, often during intense exercise in hot, humid conditions. 

Arreaza: In our community, farm workers are especially at risk of heat stroke, but any person living in the Central Valley is basically at risk.

Jacob: Risk factors amplify vulnerability across both types, including dehydration, cardiovascular disease, medications that impair sweating (e.g., anticholinergics), and acclimatization deficits. Notably, anhidrosis (lack of sweating) is common but not required for diagnosis. Hot, dry skin can signal the shift from heat exhaustion to stroke. 

Arreaza: What other conditions look like heat stroke?

Differential Diagnosis:
Jacob: Presenting with altered mental status and hyperthermia, heat stroke demands a broad differential to avoid missing mimics. 

-Environmental: heat exhaustion, syncope, or cramps. 

-Infectious etiologies like sepsis or meningitis must be ruled out. 

-Endocrine emergencies such as thyroid storm, pheochromocytoma, or diabetic ketoacidosis (DKA) can overlap. 

-Neurologic insults include cerebrovascular accident (CVA), hypothalamic lesions (bleeding or infarct), or status epilepticus. 

-Toxicologic culprits are plentiful—sympathomimetic or anticholinergic toxidromes, salicylate poisoning, serotonin syndrome, malignant hyperthermia, neuroleptic malignant syndrome (NMS), or even alcohol/benzodiazepine withdrawal. 

When it comes to differentials, it is always best to cast a wide net and think about what we could be missing if this is not heat stroke. 

Arreaza: Let’s say we have a patient with hyperthermia and we have to assess him in the ER. What should we do to diagnose it?

Jacob: Workup:
Diagnosis is primarily clinical, hinging on documented hyperthermia (>40°C) plus CNS changes (e.g., confusion, delirium, seizures, coma) in a hot environment. 

Arreaza: No single lab confirms it, but targeted testing allows us to detect complications and rule out alternative diagnosis. 

Jacob: 

-Start with ECG to assess for dysrhythmias or ischemic changes (sinus tachycardia is classic; ST depressions or T-wave inversions may hint at myocardial strain). 

-Labs include complete blood count (CBC), comprehensive metabolic panel (electrolytes, renal function, liver enzymes), glucose, arterial blood gas, lactate (elevated in shock), coagulation studies (for disseminated intravascular coagulation, or DIC), creatine kinase (CK) and myoglobin (for rhabdomyolysis), and urinalysis. Toxicology screen if history suggests. 

Arreaza: I can imagine doing all this while trying to cool down the patient. What about imaging?

-Imaging: chest X-ray for pulmonary issues, non-contrast head CT if neurologic concerns suggest edema or bleed (consider lumbar puncture if infection suspected). 

It is important to note that continuous core temperature monitoring—via rectal, esophageal, or bladder probe—is essential, not just peripheral skin checks. 

Arreaza: Treatment

Management:
Time is tissue here—initiate cooling en route, if possible, as delays skyrocket morbidity. ABCs first: secure airway (intubate if needed, favoring rocuronium over succinylcholine to avoid hyperkalemia risk), support breathing, and stabilize circulation. 

-Remove the patient from the heat source, strip clothing, and launch aggressive cooling to target 38-39°C (102-102°F) before halting to prevent rebound hypothermia. 

-For exertional cases, ice-water immersion reigns supreme—it's the fastest method, with immersion in cold water resulting in near-100% survival if started within 30 minutes. 

-Nonexertional benefits from evaporative cooling: mist with tepid water (15-25°C) plus fans for convective airflow. 

-Adjuncts include ice packs to neck, axillae, and groin; 

-room-temperature IV fluids (avoid cold initially to prevent shivering); 

-refractory cases, invasive options like peritoneal lavage, endovascular cooling catheters, or even ECMO. 

-Fluid resuscitation with lactated Ringer's or normal saline (250-500 mL boluses) protects kidneys and counters rhabdomyolysis—aim for urine output of 2-3 mL/kg/hour. 

Arreaza: What about medications?

Jacob: Benzodiazepines (e.g., lorazepam) control agitation, seizures, or shivering; propofol or fentanyl if intubated. Avoid antipyretics like acetaminophen. For intubation, etomidate or ketamine as induction agents. Hypotension often resolves with cooling and fluids; if not, use dopamine or dobutamine over norepinephrine to avoid vasoconstriction. 

Jacob: What IV fluid is recommended/best for patients with heat stroke?

Both lactated Ringer’s solution and normal saline are recommended as initial IV fluids for rehydration, but balanced crystalloids such as LR are increasingly favored due to their lower risk of hyperchloremic metabolic acidosis and AKI. However, direct evidence comparing the two specifically in the setting of heat stroke is limited. 

Arreaza: Are cold IV fluids better/preferred over room temperature fluids?

Cold IV fluids are recommended as an adjunctive therapy to help lower core temperature in heat stroke, but they should not delay or replace primary cooling methods such as cold-water immersion. Cold IV fluids can decrease core temperature more rapidly than room temperature fluids. For example, 30mL/kg bolus of chilled isotonic fluids at 4 degrees Celsius over 30 minutes can decrease core temperature by about 1 degree Celsius, compared to 0.5 degree Celsius with room temperature fluids. 

Arreaza: Getting cold IV sounds uncomfortable but necessary for those patients. Our favorite topic.

Screening and Prevention:
-Heat stroke prevention focuses on public health and individual awareness rather than routine testing. 

-High-risk groups—elderly, children, athletes, laborers, or those on impairing meds—should acclimatize gradually (7-14 days), hydrate preemptively (electrolyte solutions over plain water), and monitor temperature in exertional settings. 

-Communities during heat waves need cooling centers and alerts. 

-For clinicians, educate patients with CVD or obesity about early signs like dizziness or nausea. 

-No formal "screening" exists, but vigilance in EDs during summer surges saves lives. 

-Arreaza: I think awareness is a key element in prevention, so education of the public through traditional media like TV, and even social media can contribute to the prevention of this catastrophic condition.

Jacob: Ya so heat stroke is something that should be on every physician’s radar in the central valley especially in the summer time given the hot temperatures. Rapid recognition is key. 

Arreaza: Thanks, Jacob for this topic, and until next time, this is Dr. Arreaza, signing off.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

References:

1. Gaudio FG, Grissom CK. Cooling Methods in Heat Stroke. J Emerg Med. 2016 Apr;50(4):607-16. doi: 10.1016/j.jemermed.2015.09.014. Epub 2015 Oct 31. PMID: 26525947. https://pubmed.ncbi.nlm.nih.gov/26525947/.
2. Platt, M. A., & LoVecchio, F. (n.d.). Nonexertional classic heat stroke in adults. In UpToDate. Retrieved September 7, 2025, from https://www.uptodate.com/contents/nonexertional-classic-heat-stroke-in-adults. (Key addition: Emphasizes insidious onset in at-risk populations and the role of urban heat islands in exacerbating classic cases.) 
3. Heat Stroke. WikEM. Retrieved December 3, 2025, from https://wikem.org/wiki/Heat_stroke. (Key additions: Details on cooling rates for immersion therapy, confirmation that anhidrosis is not diagnostic, and fluid titration to urine output for rhabdomyolysis prevention.)
4. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

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.

Written by Ebenezer Dadzie

You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.

Episode 201: Cough – Revised Version (Host + 1 Resident; Resident speaks Nigerian Pidgin, Host speaks regular English)

[Play intro music, start loud, then lower volume under speech, fade out later]

HOST 1:
[Introduction]

Today we're tackling one of the most common complaints in clinic: the cough. Joining me is one of our amazing residents. Doctor, please introduce yourself.

RESIDENT:
Na Dr. Resident from Rio Bravo. I dey here to gist about cough wey dey disturb plenty patients for area.

Segment 1 – Cough Basics

HOST 2:
Let’s start simple. When a coughing patient walks into the exam room, what is the first step?

RESIDENT:
First tin na history. You gats ask whether na dry cough or cough wey dey bring sputum, whether e just start or don tey. Whether person get exposure, dust, new medicine—history dey open many doors pass Google.

HOST 1:
Exactly. And as we know, acute coughs are usually viral, but chronic coughs lasting more than eight weeks can point to asthma, GERD, ACE inhibitor side effects, or more.

Segment 2 – Valley Fever

HOST 2:
And since we’re here in Kern County, we have to mention Valley Fever. We see thousands of cases every year, many of them presenting with cough.

RESIDENT:
True. Valley Fever fit look like pneumonia, bronchitis, or even TB. Patient go come with cough, tiredness, sometimes rash. If person dey work for outside or dey around dusty area, you suppose reason am.

Segment 3 – Workup and Treatment

HOST 1:
So let’s talk evaluation. When you have a cough here in California’s Central Valley, what is your approach?

RESIDENT:
Start from basic: chest X-ray, CBC, ask good history. If e no improve, add Valley Fever blood test. If cough get phlegm, you fit send sputum. If weight dey drop or sweats dey night, you reason TB or cancer. Treatment depend on severity. Mild one fit resolve, but if no be small, na antifungals—like fluconazole—and you go monitor liver enzymes well.

Segment 4 – Humor Break

HOST 2:
Alright—quick humor break. Got any memorable cough stories?

RESIDENT:
One man tell me say “doctor, my neighbor ghost na cause my cough.” We check-am finish, na allergy. Ghost no dey push fungus, sha!

[Both laugh]

Segment 5 – Takeaways

HOST 1:
Before we wrap up, give listeners top key points on cough.

RESIDENT:
One—ask better history. Cough dey tell story.
Two—if person dey Bakersfield, reason Valley Fever, e fit sneak.
Three—no dey give antibiotics anyhow. Virus and fungus no go respond like bacteria.

Trivia Time

HOST 2:
Trivia question: In adults who don’t smoke and aren’t on ACE inhibitors, what is the most common cause of chronic cough?

A) Asthma
B) GERD
C) Chronic bronchitis
D) Postnasal drip (Upper airway cough syndrome)

RESIDENT:
I go choose D—postnasal drip. Na e dey cause that tickle wey no dey go.

HOST 1:
And that’s correct—postnasal drip is the number one cause of chronic cough. Nicely done! You win bragging rights and a cough drop.

HOST 2:
Thank you for joining us today on Rio Bravo QWeek. To all our listeners—stay curious, keep learning, and if someone sounds like a barking seal in the waiting room, you know it might be more than a cold.

HOST & RESIDENT (together):
¡Hasta luego!

[Music fades in, rises, then fades out after 10 seconds]

References:

1. 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)
2. 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)
3. 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)
4. 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)
5. Prasad, K. T., & LoSavio, P. S. (2023). Approach to the adult with chronic cough. In UpToDate (L. M. Leung, Ed.). Retrieved June 20, 2025, from https://www.uptodate.com
   (Evidence-based resource for differential diagnosis and workup of cough in primary care)
6. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Written by Michael Ozoemena, MD.

You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.

Hypertension

Segment 1: What Is Hypertension?

HOST:
Let’s start with the basics. Blood pressure is the force of blood pushing against the walls of your arteries. Think of it like water running through a garden hose—if the pressure stays too high for too long, that hose starts to wear out.

Hypertension, or high blood pressure, means this pressure is consistently elevated. It is measured using two numbers:

• Systolic: the pressure when the heart beats
• Diastolic: the pressure when the heart relaxes

Normally 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 attack
• Stroke
• Kidney disease

Think of high blood pressure as a constant stress test on your blood vessels. The longer it goes uncontrolled, the higher the chance of complications.

Segment 3: What Causes High Blood Pressure?

HOST:
Hypertension usually doesn’t have a single cause. It often results from a combination of genetic factors, lifestyle, and underlying medical conditions.

Modifiable Factors

• High-salt diet and low potassium intake
• Physical inactivity
• Tobacco use
• Excessive alcohol intake
• Overweight or obesity
• Chronic stress
• Poor sleep or sleep apnea

Non-Modifiable Factors

• Family history of hypertension
• Black race (higher prevalence and severity)
• Age over 65

Hypertension may also be secondary to other conditions, such as kidney disease, thyroid disorders, adrenal conditions, or medications like NSAIDs or steroids.

Segment 4: How Is It Diagnosed?

HOST:
Diagnosis requires multiple elevated blood pressure readings taken on different occasions. This includes office readings, home blood pressure monitoring, or ambulatory blood pressure monitoring.

If you haven’t had your blood pressure checked recently, this is your reminder. It’s simple—and it could save your life.

Segment 5: Treatment and Management

HOST:
Lifestyle changes are often the first line of treatment:

• Reduce salt intake
• Eat more fruits, vegetables, and whole grains
• Aim for 150 minutes of moderate exercise per week
• Manage stress
• Maintain a healthy weight
• Get enough sleep
• Limit alcohol
• Quit smoking

If these steps aren’t enough, medications may be necessary. These include:

Diuretics, ACE inhibitors, ARBs, Calcium channel blockers, Beta-blockers

Your healthcare provider will choose the best medication based on your health profile.

Segment 6: What You Can Do Today

HOST:
Here are three simple, actionable steps you can take right now:

1. Check your blood pressure—at a clinic, pharmacy, or at home.
2. Pay attention to your salt intake—much of it is hidden in processed foods.
3. Move more—even a 20-minute daily walk can help reduce blood pressure over time.

Small steps can lead to big, lasting improvements.

Summary

Hypertension may be silent but understanding it gives you power. Early action can add healthy years to your life. Take charge of your blood pressure today.

Diabetes

1. Wetin Diabetes Be and Wetin E Go Do to Person Body?

Q: Wetin diabetes mean?
A: Diabetes na sickness wey make sugar (glucose) for person blood too high. E happen because the body no fit produce insulin well, or the insulin wey e get no dey work as e suppose.

Q: Wetin go happen if diabetes no dey treated well?
A: If diabetes no dey treated well, e fit damage the blood vessels, nerves, kidneys, eyes, and even the heart.

2. Wetin Cause Diabetes and Why Black People Suffer Pass?

Q: Wetin cause diabetes?
A: E no be one thing wey cause diabetes. E dey happen because of mix of gene, lifestyle, environment, and society factors.

Q: Why Black/African Americans get diabetes more?
A: Black people for America get diabetes more because of long-standing inequality, stress, low access to healthcare, and the kind environment wey many of them dey live in. These things dey make Black people more at risk.

3. Diabetes Rates for America and Black People?

Q: How many people get diabetes for America?
A: For America today, over 38 million people get diabetes, and the number dey rise every year.

Q: Why Black people dey suffer diabetes more than White people?
A: About 12% of Black adults get diabetes, compared to just 7% for White adults. Black people also dey get the sickness earlier and e dey more severe.

4. Signs and Symptoms of Diabetes?

Q: Wetin be the early signs of diabetes?
A: The early signs no too strong, but when e show, e fit include:

• Too much urine (polyuria)
• Thirst (polydipsia)
• Hunger, tiredness, and blurred vision
• Wounds no dey heal fast
• Tingling for hand or leg
• Sometimes weight loss

5. How Doctor Go Diagnose Diabetes?

Q: How doctor fit confirm say person get diabetes?
A: Doctor go do some lab tests to confirm:

• Fasting Plasma Glucose (FPG): 126 mg/dL (7.0 mmol/L) or higher
• HbA1c: 6.5% or higher
• 2-hour Oral Glucose Tolerance Test (OGTT): 200 mg/dL (11.1 mmol/L) or higher after person drink glucose.
• Random Blood Glucose: 200 mg/dL (11.1 mmol/L) or higher plus classic symptoms like too much urination, thirst, or weight loss.

Q: Wetin happen if HbA1c test no match the person?
A: If HbA1c result no match person symptoms, doctor fit repeat test or try other tests like FPG or OGTT.

6. Wetin Screening and Early Diagnosis Fit Do?

Q: Why screening for diabetes dey important?
A: Screening dey important because early detection fit prevent serious complications from diabetes.

Q: How often person go do diabetes test?
A: Adults wey get overweight or obesity, between 35–70 years, suppose do diabetes screening every three years. But because Black adults get higher risk, doctors dey start screening earlier and more often.

7. How Person Fit Manage Diabetes?

Q: Wetin be the best way to manage diabetes?
A: The two main ways to manage diabetes be:

• Lifestyle changes: Eat better food (vegetables, fruits, whole grain, beans, fish, chicken) and exercise regularly.
• Medicine: If person sugar still high, doctor fit give drugs like metformin, SGLT-2 inhibitors, or GLP-1 receptor agonists.

Q: Wetin be SGLT-2 inhibitors and GLP-1 drugs?
A: SGLT-2 inhibitors dey help with kidney and heart problems, while GLP-1 drugs dey help with weight loss and prevent stroke.

Q: Wetin be first-line treatment for diabetes?
A: First-line treatment for diabetes be metformin, unless person no fit tolerate am.

Q: How much exercise a person suppose do?
A: Person suppose do at least 150 minutes of moderate exercise per week. This fit include things like brisk walking, swimming, or cycling. E also good to add muscle-strength training two or three times weekly to help control sugar.

Q: When insulin therapy go be needed?
A: Insulin therapy go be needed if person A1c is higher than 10%, or if person dey hospitalized and their glucose dey above the 140-180 range. This go help bring the blood sugar down quickly.

8. Wetin Be the Complications of Diabetes?

Q: Wetin fit happen if diabetes no dey well-managed?
A: Complications fit include kidney disease, blindness, nerve damage, leg ulcers, heart attack, stroke, and emotional issues like depression.

Q: Why Black adults get more complications?
A: Black people get higher risk of these complications because of inequality, stress, and poor access to healthcare.

9. Wetin Dey Affect Access to Diabetes Treatment?

Q: Wetin make Black people struggle to get treatment for diabetes?
A: Many Black people no dey get new effective treatments like GLP-1 and SGLT-2 inhibitors because of price, insurance issues, and lack of access. COVID-19 also worsen things.

Q: Wetin government and doctors fit do?
A: Policymakers dey work on improving access to drugs, better community programs, and screening for social issues wey fit affect diabetes care.

10. Conclusion

Q: Wetin be the solution to reduce diabetes impact?
A: The solution go need medical treatment, early screening, lifestyle support, and policy changes. With proper treatment and community support, e possible to reduce the impact of diabetes, especially for Black communities.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References: 

1. Whelton PK, Carey RM. Overview of hypertension in adults. UpToDate. 2024.
2. Carey RM, Moran AE. Evaluation of hypertension. UpToDate. 2024.
3. Mann SJ, Forman JP. Lifestyle modification in the management of hypertension. UpToDate. 2024.
4. Giles TD, Weber MA. Initial pharmacologic therapy of hypertension. UpToDate. 2024.
5. American Heart Association. Understanding Blood Pressure Readings. Accessed 2025.
6. American Heart Association. AHA Dietary and Lifestyle Recommendations. Accessed 2025.
7. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Mohammed Wase (medical student) and Dr. Singh describe what it is like to provide health care on the streets. They share their personal experiences working in a street medicine team. They describe the practice of harm reduction and emphasize the importance of respecting autonomy and being adaptable in street medicine. 

Written by Mohamed Wase, MSIV, American University of the Caribbean. Editing by Hector Arreaza, MD. Hosted by Harnek Singh, MD.

You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.

Introduction 

Dr. Singh: Welcome to another episode of our podcast, my name is Dr. Harnek Singh, faculty in the Rio Bravo Family Medicine Residency Program. Today we have prepared a great episode about street medicine, a field that has grown a lot during the last decade and continues to grow now. We are joined by a guest who is passionate about this topic. Wase, please introduce yourself.

Wase: Hello everyone, my name is Mohammed, many know me as Wasé, I am a 4th year medical student from the American University of the Caribbean. Today we’re diving into a topic that sits at the intersection of medicine, compassion, and public health — Street Medicine and Harm Reduction. We’re going to step outside with this episode, literally, away from the clinic and hospital, to explore more about what care looks like in the streets. 

Historic background: How did street medicine start?

Wase: The roots of Street Medicine in the United States go back to Dr. Jim Withers in Pittsburgh in the 1990s, who literally began by dressing as a homeless person and providing care on the streets to build trust. His efforts have shaped street medicine to what it is today. It combines primary care, mental health, and social support. 

Dr. Singh: For family physicians, this model aligns perfectly with our holistic approach. We don’t just treat diseases; we treat people in context — their environment, their challenges, their stories. What is the main population seen by a street medicine team?

Wase: This patient population includes those struggling with homelessness, housing insecurity, food insecurity, substance use disorders; with patients being preoccupied on where they will sleep that night or when their next meal comes, they do not have the luxury of prioritizing their health. Street Medicine is a powerful outreach program to bring care to them in order to provide equitable care within our community. 

Dr. Singh: How is street medicine different than caring for patients in the clinic?

Wase: Working on the street means we have to think differently about what healthcare looks like — and that’s whereharm reductioncomes in.

What is Harm Reduction?

Wase: Harm reduction is a public health philosophy that focuses on reducing the negative consequences of high-risk behaviors, rather than demanding complete abstinence.

Dr. Singh: Preventive care is the backbone of family medicine. For example, we keep up with the USPSTF guidelines and make sure our patients are up to date with their screenings. But what does that look like in the street medicine setting? 

Wase: In practice, that might mean:

-needle exchange program: Offering clean syringes to prevent HIV transmission and removing used needles

-distributing naloxone to prevent overdose deaths

-offering fentanyl test-strips to prevent use of substances that are unknowingly laced with fentanyl

Dr. Singh: Also:

-providing condoms to prevent sexually transmitted infections

-providing wound care to prevent further spread of infection

Wase: Yes, the idea is: people are going to engage in risky behaviors whether or not we approve of it, so let’s meet them with compassion, tools, and trust instead of judgment. Harm reduction also applies beyond substance use; think about safer sex education, or even diabetic foot care among people who can’t refrigerate insulin or change shoes daily. It’s all about meeting people where they areandkeeping them alive and engaged in care. 

Planning in Street Medicine: 

Wase: It takes careful disposition planning and aftercare for this population. Instead of the traditional outpatient setting where we can place referrals and expect our patients to follow through with them. On street medicine, for follow up visits it requires arranging transportation, finding a pharmacy close in proximity, educating and counseling on medication adherence and how to make it, and making sure they have some sort of shelter to get by. 

Dr. Singh: Let’s describe a typical street med encounter.

Wase: A typical Street Medicine encounter might look like this: a small team — usually a physician, nurse, social worker, and sometimes a peer advocate — goes out with backpacks of supplies. They might start with wound care, blood pressure checks, or even medication refills. But what’s just as important is the relationship-building. Sometimes, the first visit isn’t about medicine at all — it’s about showing up consistently.

Over time, that trust opens the door for conversations about addiction treatment, mental health, and preventive care. For example, in some California Street Medicine programs, teams are treating chronic conditions like hypertension, diabetes, and hepatitis C, right where patients live with the same evidence-based care we’d give in a clinic. One of my favorite quotes from Street Medicine teams is: “We’re not bringing people to healthcare; we’re bringing healthcare to people.”

Challenges in Street Medicine:

Wase: The populations that you will encounter include many people who will often downplay their own health concerns and prior diagnoses. Unfortunately, this is usually from countless months or years of feeling neglected by our healthcare system. Some may even express distrust in our healthcare system and healthcare providers. Patient will, at times, be apprehensive to receive care or trust you enough to tell their story. 

Dr. Singh: Interviewing patients is a critical aspect of providing equitable care on the streets. It is always important to offer support and medical care, even if the patient denies it, always reassure that your street medicine clinic will be around every week and ready for them when they would like to seek care. 

Wase: Respecting patient autonomy is an utmost concern as well. Another element of interviewing to consider is to invite new ideas and information; instead of lecturing patients about taking medications on time or telling them they need to stop doing drugs—simply asking a patient “would you like to know more about how we can help you stop using opioids?” respects their choice but can also spark new ideas for them to consider. 

Singh: Adaptability is another key component to exceling patient care in street medicine. Like, performing physical exams on park benches or in the back of a minivan. Always doing good with our care but also respecting their autonomy is crucial in building a trust that these patients once lost with our system. 

Wase: Each patient has their own timeline, but we as providers should always assure them that our door is always open for them when they are ready to seek care. 

Conclusion.

Wase: So, to wrap up — Street Medicine and harm reduction remind us that healthcare isn’t just about hospitals and clinics. It’s about relationships, trust, and dignity.

Every patient deserves care, no matter where they sleep at night.

If you’re a resident or student listening, I encourage you to seek out these experiences — volunteer with Street Medicine teams, learn from harm reduction workers, and let it shape how you practice medicine. Thank you for listening to this episode of the Rio Bravo qWeek podcast. I’m Mohammed — and I hope this conversation inspires you to meet patients where they are and walk with them on their journey to health.

Dr. Singh: If you liked this episode, share it with a friend or a colleague. This is Dr. Singh, signing off.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. Doohan, N.C. “Street Medicine: Creating a ‘Classroom Without Walls’ for People Experiencing Homelessness.” PMC – National Library of Medicine, 2019.
2. Hawk, M., et al. “Harm Reduction Principles for Healthcare Settings.” Harm Reduction Journal, vol. 14, no. 1, 2017.
3. Withers, J.S. “Bringing Health Professions Education to Patients on the Streets.” Journal of Ethics, AMA, vol. 23, no. 11, Nov. 2021.
4. “Our Story.” Street Medicine Institute, 2025, www.streetmedicine.org/our-story.
5. “Principles of Harm Reduction.” National Harm Reduction Coalition, 2024, https://harmreduction.org/about-us/principles-of-harm-reduction/.
6. Salisbury-Afshar, Elizabeth, Bryan Gale, and Sarah Mossburg. “Harm Reduction Strategies to Improve Safety for People Who Use Substances.” PSNet, Agency for Healthcare Research & Quality, 30 Oct. 2024.
7. Douglass, A.R. “Exploring the Harm Reduction Paradigm: The Role of Boards in Drug Policy and Practice.” PMC – National Library of Medicine, 2024.
8. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Kara Willbanks (medical student) explains the definition, pathophysiology, and treatment of eczema. Dr. Arreaza adds some input about bleach baths and topical steroids. 

Written by Kara Willbanks, MSIV, American University of the Caribbean. Comments and edits by Hector Arreaza, MD.

You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.

October is the Eczema Awareness Month!

What Is Atopic Dermatitis? 

Atopic dermatitis, a form of eczema, is a chronic, relapsing inflammatory skin disorder that often begins in childhood but can affect people of all ages. 

Other eczematous dermatoses include seborrheic dermatitis, contact dermatitis, juvenile plantar dermatosis, and stasis dermatitis. 

Atopic dermatitis is one of the most common skin conditions in the developed world, typically affecting up to 20% of children and 5-10% of adults. Patients usually present with severe pruritus (itchiness) and dry, inflamed patches of skin. Common sites include the face and extensor surfaces in infants, and flexural areas — like the elbows and knees — in older children and adults. 

Atopic dermatitis is often associated with other allergic conditions like asthma and allergic rhinitis — what we call the “atopic triad.” These conditions should also be considered when diagnosing someone with atopic dermatitis. 

Pathophysiology

Atopic dermatitis is believed to occur due to a combination of genetic, immune, and environmental factors. A major component is a defective skin barrier, often linked to mutations in the filaggrin gene. This allows irritants, allergens, and microbes to penetrate the skin more easily, triggering inflammation.

Differential Diagnosis

Atopic dermatitis can sometimes mimic other skin conditions, so it’s important to keep a differential in mind: 

-Contact dermatitis – triggered by allergens or irritants; often limited to the area of exposure but also tends to be very itchy. 

-Seborrheic dermatitis – greasy scales, typically on the scalp, eyebrows, and nasolabial folds 

-Psoriasis – well-demarcated plaques with silvery scales; sometimes found in similar areas of the body as eczema. 

-Tinea (fungal infections) – ring-shaped lesions with active, scaly borders -Important to note that treatment of tinea with topical steroids can make the rash much worse. 

-Scabies – intense itching, especially at night, with burrows between fingers. 

Ruling out these conditions helps guide the right treatment and prevent chronic mismanagement. As a recap our main differential diagnosis: contact dermatitis, seborrheic dermatitis, psoriasis, tinea, and scabies.

The treatment cornerstone: Moisturizers 

The most important daily treatment for atopic dermatitis is regular moisturizing. Moisturizers repair the skin barrier, reduce water loss, and protect against irritants. They should be applied at least twice daily, ideally right after bathing while the skin is still damp (within 3 minutes is most ideal). Use greasy ointments or thick creams rather than lotions — think products with ceramides or glycerin (hydrates and protects skin). 

It is best to choose ointments or creams without additives, perfumes or fragrances. Greasier ointments are the preferred vessel; however, patient compliance may be less as they may be unpleasant to some.

Bleach Baths 

For patients with frequent skin infections or severe eczema, dilute bleach baths can be a game-changer. How to do it? Use ¼ to ½ cup of household bleach in a full standard bathtub of water (about 40 gallons) and soak for 10 minutes, twice a week. This helps reduce bacterial colonization — particularly Staphylococcus aureus — which commonly worsens eczema. 

After the bath, pat the skin dry and immediately apply a moisturizer (within 3 minutes). 

Bleach baths are endorsed by the American Academy of Pediatrics and the American Academy of Dermatology as an adjunctive treatment for atopic dermatitis, especially in patients with moderate to severe disease and frequent bacterial infections, but the evidence for their efficacy is mixed, and further well-designed studies are needed.

Medical Treatments

-Topical corticosteroids: When moisturizers alone aren’t enough, we move to anti-inflammatory therapy. Topical corticosteroids are the first-line treatment for flares. Some studies suggest that a short burst of a high-potency topical corticosteroid to rapidly control active disease, followed by a quick taper in potency, is most effective, whereas others use the lowest-potency agent thought to be needed and adjust upward only if this fails. Common steroids used are hydrocortisone (low potency), triamcinolone (medium potency), or betamethasone (high potency). 

-High-potency steroids should never be applied to sensitive skin like the face. With short-term use of lower-potency steroids, there is a low likelihood of skin atrophy but use for more than 6 months is linked with greater levels of skin thinning 

-Wet wrap therapy: Wet wrap therapy improves absorption of topic steroid. Apply a topical steroid, then layer a wet dressing and then a dry dressing over the top of that. This can be beneficial in providing  both relief of symptoms and prevention of itching. In pediatric patients it is called “daddy’s socks therapy” because large socks may be used to cover the arms of kids.

-Topical calcineurin inhibitors — like tacrolimus — are great alternatives for sensitive areas or for maintenance once inflammation is under control. They may burn upon application which can scare patients away from their use.

-PO antihistamines can help with itching, especially at night, but they don’t treat inflammation itself.

-Systemic therapies, like dupilumab (Dupixent®), an IL-4 receptor antagonist, are reserved for moderate to severe cases unresponsive to topical therapy. This is a great time to refer to your local dermatologist for management! Many of the newer treatments are highly effective but can require more frequent monitoring.

Recent Research 

One recent study is the 2024 Cochrane network meta-analysis comparing effectiveness of topical anti-inflammatory treatments for eczema that was recently published in the AFP Journal in July of 2025.

Here are the highlights:

-Over 291 RCTs with ~45,846 participants were included. 

-The analysis ranked potent topical corticosteroids, JAK inhibitors (for example ruxolitinib (Opzelura® 1.5 %), and tacrolimus 0.1 % among the most effective for reducing signs and symptoms of eczema. 

-In contrast, PDE-4 inhibitors [like crisaborole (Eucrisa®) 2 %] were among the least effective in this comparison. 

-Regarding side effects: tacrolimus and crisaborole were more likely to cause burning or stinging at the application site; corticosteroids were less likely in the short term to cause local irritation.

-Long-term outcomes regarding effectiveness or safety of treatments for eczema were not addressed by the review because they are rarely reported.”

-Another insight from this study is considering cost when initiating treatment. Most topical steroids are significantly more cost effective than JAK inhibitors or calcineurin inhibitors so it may be best to start with a cheaper solution in an uninsured patient considering their relative effectiveness. 

Additional Tips & Lifestyle 

-Keep baths and showers short and in lukewarm water.

-Avoid harsh soaps and detergents — use gentle, fragrance-free cleansers.

-Wear soft cotton clothing instead of wool or synthetics.

-Identify and avoid triggers — common ones include stress, sweating, allergens, and certain foods (especially in kids).

-Ice packs can help reduce itching and relieve any burning sensation.

-Keep fingernails short, especially in children, help cause less trauma to the skin from repeated itching. 

Living with eczema 

Many celebrities like Kerry Washington, Jessica Simpson, Kelly Rowland, Brad Pitt and Kristen Bell have spoken out about their lives with eczema. They have shared personal stories about how they were diagnosed, what treatment works for them, and the general impact it has had on their lives and mental health. I feel like it can be so important for celebrities to speak out about their lives with certain conditions because it helps to normalize the condition, raise awareness of the struggles, and encourages more open dialogue.

It is important to remember that for patients living with eczema, the persistent itch-scratch cycle can be very distressing, causing patients to struggle with their sleep and day-to-day activities. Anxiety and depression are common in patients with eczema so as physicians it is vital to monitor for signs of distress. Support groups can be incredibly helpful for patients [National Eczema Association]

If you are interested in providing additional information to your patients or getting this for yourself, you can find more resources on altogethereczema.org or nationaleczema.org. 

Key Takeaways 

Atopic dermatitis is chronic but manageable. Moisturizers are the foundation of treatment. Topical steroids and calcineurin inhibitors control inflammation. Bleach baths help reduce bacterial load and flare severity. Always rule out other skin conditions to ensure appropriate management. Atopic dermatitis can be managed by the primary care physician but in certain cases (cases refractory to standard topical treatment, recurrent infections, etc.), a referral to dermatology can be especially helpful.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

References:

1. Coping with eczema. Allergy & Asthma Network. (2025, May 20). https://allergyasthmanetwork.org/what-is-eczema/coping-with-eczema/.
2. Eichenfield LF, Tom WL, Chamlin SL, et al. Guidelines of care for the management of atopic dermatitis: section 1. Diagnosis and assessment of atopic dermatitis. J Am Acad Dermatol. 2014 Feb;70(2):338-51. doi: 10.1016/j.jaad.2013.10.010. Epub 2013 Nov 27. PMID: 24290431; PMCID: PMC4410183. https://pubmed.ncbi.nlm.nih.gov/24290431/.
3. Yancey, J. R., & Green, S. (2025, July 15). Effectiveness of topical anti-inflammatory drugs for eczema. American Family Physician. https://www.aafp.org/pubs/afp/issues/2025/0700/cochrane-eczema.html.
4. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

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 older
• Adults 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:

1. PCV21 once
2. PCV20 once
3. PCV15 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 with influenza or mRNA COVID-19 vaccines.

Some patients are hesitant to receive vaccines, Are there side effects and contraindications to the vaccine?

Local reactions are most common: pain/tenderness; swelling/induration (~20%); redness (~15%). Some people “baby” the arm for a couple of days. These typically resolve in 3–4 days; NSAIDs and warm compresses help.

• Systemic symptoms: fatigue, headache, myalgias/arthralgias, chills; fever ≥38°C is uncommon (<5%). Usually mild and self-limited.
• Contraindications: history of severe allergy (e.g., anaphylaxis) to a pneumococcal vaccine or components.

Bottom line: If a patient is 50+, or younger with specific risks, they likely need one conjugate dose—PCV21 or PCV20—and they’re done. Use PCV15 followed by PPSV23 when needed, and remember the serotype 4 caveat.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. Musher DM, Rodriguez-Barradas MC. [Pneumococcal Vaccination in adults. UpToDate Inc. Literature review current through September 2025. Topic last updated January 13, 2025. https://www.uptodate.com/contents/pneumococcal-vaccination-in-adults
2. Centers for Disease Control and Prevention. (2025, May 29). Pneumococcal conjugate vaccine (interim) VIS: What you need to know. U.S. Department of Health and Human Services. Retrieved [access date], from https://www.cdc.gov/vaccines/hcp/current-vis/pneumococcal-conjugate.html?CDC_AAref_Val=https://www.cdc.gov/vaccines/hcp/vis/vis-statements/pcv.html
3. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

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.

Intro

Welcome 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 started in Switzerland around 2016. It is also known as the “Bernese method” (named after the city of Bern, Switzerland). 

With this method, instead of stopping opioids cold turkey, patients start with tiny doses of buprenorphine—fractions of a milligram. These doses gradually increase over several days while the patient continues their regular opioid use. While they begin this titer, they can continue use of the full agonist they were previously using–methadone, fentanyl, or heroin, while the buprenorphine begins to take effect. 

Once the buprenorphine builds up to a therapeutic level, the full agonist is stopped. This method uses buprenorphine’s unique pharmacology to stabilize the brain’s opioid system without triggering those really nasty withdrawal symptoms.

Early studies and case reports suggest this is safe, tolerable, and effective method to do. Microinduction is changing the game, and it has been spreading quickly in North America. 

Instead of forcing patients to stop opioids completely, the dose is slowly increased over the next three to seven days, while the patient keeps using their usual opioids.By the end of that week, the buprenorphine has built up to a therapeutic level and the full agonist is stopped. The difference is really dramatic. Instead of a painful crash into withdrawal, patients describe the process as a gentle step down, or a ramp instead of a cliff. 

It’s a flexible method. It can be done in a hospital, a clinic, or even outpatient with good follow-up. Once a patient and doctor develop a strong relationship built on the principles of patient autonomy and patient-centered care, microinduction can be closely monitored on a monthly basis including televisits. Microinduction has been shown to help more patients stay in treatment. 

The Role of Harm Reduction 

Instead of demanding perfection, harm reduction focuses on best practices providers can implement to reduce risk and keep patients safe. Harm reduction can vary from providing naloxone to reverse overdoses, giving out clean syringes, or offering safer injection education. 

It also means allowing patients to stay in treatment even if they keep using other substances, and tailoring care for groups like adolescents, parents, or people recently released from incarceration. Harm reduction says that instead of demanding perfection, let’s focus on progress. Instead of all-or-nothing, let’s devote resources to keeping people alive and safe. 

As mentioned,an option is providing naloxone kits so overdoses can be reversed in the moment. Also, giving out clean syringes so the risk of HIV or hepatitis infection is reduced while injecting heroin. Another way to reduce harm is teaching safer injection practices so people can protect themselves until they’re ready for that next step in their treatment. 

It also means keeping the doors open, even when patients slip. If someone is still using other substances, they still deserve care. And it means tailoring support for groups who oftentimes get left behind. For people like adolescents, parents balancing childcare, or people coming out of incarceration who are at the highest risk of overdose. 

Harm reduction recognizes that recovery isn’t a straight line. It’s about meeting people where they are and walking with them forward. 

Conclusion:

Microinduction is itself a harm reduction strategy. It lowers barriers by removing the need for painful withdrawal.When paired with a harm reduction culture in clinics, patients are more likely to enter care, stay engaged, and build trust with doctors for continued care. 

Managing opioid use disorder is one of the greatest health challenges of our time. But solutions like buprenorphine microinduction and harm reduction strategies are reshaping treatment—making it safer, more humane, and more accessible. If we embrace these approaches, we can turn barriers into bridges and help more people find recovery. 

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you. Send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. Bluthenthal, R. N., Simpson, K., Ceasar, R. C., Zhao, J., Wenger, L., & Kral, A. H. (2020). Opioid withdrawal symptoms, frequency, and pain characteristics as correlates of health risk among people who inject drugs. Drug and Alcohol Dependence, volume 211, 1 June 2020, 107932. https://doi.org/10.1016/j.drugalcdep.2020.107932.
2. De Aquino, J. P., Parida, S., & Sofuoglu, M. (2021). The pharmacology of buprenorphine microinduction for opioid use disorder. Clinical Drug Investigation, 41 (5), 425–436. https://doi.org/10.1007/s40261-021-01032-7. 
3. Taylor, J. L., Johnson, S., Cruz, R., Gray, J. R., Schiff, D., & Bagley, S. M. (2021). Integrating harm reduction into outpatient opioid use disorder treatment settings. Journal of General Internal Medicine, 36 (12), 3810–3819. https://doi.org/10.1007/s11606-021-06904-4.
4. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Written 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 is
• Show how it affects the human body
• Explain how you and your patients can limit exposure
• Empower both clinicians and the public with real, practical information

Arreaza: 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 bottles
• Canned food linings
• Baby bottles (pre-2012)
• Takeout containers
• Cash register receipts
• Dental sealants

Arreaza: 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 Body

Cam: 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)
• Neurodevelopment
• Thyroid signaling
• Pancreatic β-cell function
• Metabolism and fat storage

Even 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 Says

Here’s where it gets serious. Let’s go system-by-system:

1. Reproductive Health

• Females: Linked to PCOS, infertility, and early puberty (Peretz et al., 2014).
• Males: Reduced sperm count and motility; altered testosterone levels.

2. Pregnancy and Birth Outcomes

• Increased 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 Development

• Associated with ADHD, anxiety, and impaired executive function in children exposed in utero (Mustieles et al., 2015).

4. Metabolism and Diabetes

• BPA exposure is linked to insulin resistance, obesity, and type 2 diabetes, even at low doses (Lang et al., 2008).

5. Cancer

• Animal and human data link BPA to increased risk of breast and prostate cancer via estrogenic mechanisms.

6. Mortality

• A 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 Exposure

Let’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 wet or lotioned.
• Canned soups: One study showed that eating canned soup daily for five days led to a 1000% increased urinary BPA levels (Carwile et al., 2011).
• Plastic water bottles left in the car on hot days or plastic food trays for microwaving = chemical leaching.
• Baby bottles and pacifiers (pre-2012): primary concern for newborns.

Arreaza: So, Cameron, you were exposed to BPA as a baby.

Cam: Here’s the jaw-dropper: We ingest up to 5 grams of plastic per week, roughly the weight of a credit card (WWF, 2019; University of Newcastle). This includes microplastics like BPA, which enter through food, water, and air.

Arreaza: So, it translates into 40 lbs of plastic in a lifetime, by age 70. What can we do as family physicians?

Family Medicine and Preventive Care

As family physicians, we are at the frontlines of prevention. Our role includes:

• Anticipatory guidance: during prenatal visits, well-child visits, and chronic disease management
• Screening opportunities: ask about storage habits, microwave use, and receipt handling
• Environmental health counseling: AAFP recommends addressing endocrine disrupting chemicals (EDCs) when relevant to a patient’s concerns.

It’s not just about treating diabetes or obesity. It’s about recognizing that environmental exposure may be a root cause.

Arreaza: Prevention is my favorite topic!

Cam: One helpful clinical practice:

Arreaza: What else can we do to reduce BPA exposure?

Practical Steps to Reduce BPA

Here’s what patients and doctors alike can do today:

• Switch to BPA-free products, but be careful, as replacements like BPS or BPF may also be harmful (Rochester & Bolden, 2015).
• Avoid microwaving or dishwashing plastic containers.
• Use digital receipts.
• Filter tap water using carbon filters, which can reduce microparticle ingestion.
• Choose fresh produce over canned goods when possible.

Also, wash your hands after handling receipts, especially before eating or touching your face.

Arreaza: What is our government doing to protect us?

Public Health and Policy Updates

Regulations are slowly catching up:

• The FDA banned BPA in baby bottles and sippy cups in 2012.
• The European Union has stricter limits, and France banned BPA in all food packaging in 2015.
• California’s Proposition 65 requires BPA warning labels.

Arreaza: Proposition 65, passed by direct voter initiative in 1986, “WARNING: This product contains chemicals known to the State of California to cause cancer and birth defects or other reproductive harm.”

Arreaza: The FDA is planning to phase out petroleum-based food dyes (certified color additives) from the American food supply – marking a significant milestone in the efforts to protect the public. 

Cam: Many products still contain BPA analogs (BPS, BPF), which are not yet well-regulated.

This is where clinician advocacy matters, where we can guide public opinion and support legislative change.

Arreaza: So, millions of pounds of toxic substances are produced by many industries in the US. As physicians, we have to stay informed and update our patients.

Cameron: How can we wrap up this episode?

Conclusion and Takeaways

• BPA is a hormone disruptor hiding in plain sight.
• People are exposed to BPA every day, but small lifestyle changes can dramatically reduce it.
• Family medicine has a role in education, prevention, and advocacy.

Let’s all be part of the solution for our health and future generations. Stanley (tumblers) are not sponsoring this episode, and we did not receive any money from them. 

Arreaza: That’s it for today’s episode of Rio Bravo qWeek. If you enjoyed this episode, share it with a colleague or medical student who may need to know about BPA. I’m Dr. Arreaza, signing off.

Cameron: Hopefully, in the future I will talk to you about more endocrine disrupting chemicals. Thanks for listening.

_____________________

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. Carwile, J. L., & Michels, K. B. (2009). Urinary bisphenol A and obesity: NHANES 2003–2006. Environmental Research, 111(6), 825–830.
2. Carwile, J. L., et al. (2011). Canned soup consumption and urinary bisphenol A: A randomized crossover trial. JAMA, 306(20), 2218–2220.
3. Centers for Disease Control and Prevention (CDC). (2004). Fourth National Report on Human Exposure to Environmental Chemicals.
4. Gao, X., et al. (2020). Urinary bisphenol A and mortality risk. JAMA Network Open, 3(8), e2011620.
5. Lang, I. A., et al. (2008). Association of urinary bisphenol A with medical disorders and laboratory abnormalities in adults. JAMA, 300(11), 1303–1310.
6. Manikkam, M., et al. (2013). Epigenetic transgenerational inheritance of disease. PLOS ONE, 8(1), e55387.
7. Mustieles, V., et al. (2015). Bisphenol A and neurodevelopmental outcomes in children. Environmental Health Perspectives, 123(7), 689–695.
8. Peretz, J., et al. (2014). Bisphenol A and reproductive health. Environmental Health Perspectives, 122(8), 775–786.
9. Rochester, J. R., & Bolden, A. L. (2015). Bisphenol S and F: A systematic review. Environmental Health Perspectives, 123(7), 643–650.
10. Snijder, C. A., et al. (2013). Fetal growth and prenatal exposure to bisphenol A. Environmental Health Perspectives, 121(3), 393–398.
11. World Wildlife Fund (WWF). (2019). No Plastic in Nature: Assessing Plastic Ingestion from Nature to People.
12. University of Newcastle (Australia). (2019). Human Consumption of Microplastics.
13. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

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, OR
• Increase in serum creatinine to ≥1.5 times baseline within the prior 7 days, OR
• Urine volume <0.5 mL/kg/h for 6 hours

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 AKI

Dr. 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 <1% suggesting a prerenal AKI because the kidneys are holding onto sodium to preserve volume.

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 AKI

Dr. 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 obstructions), but the kidney’s filter is damaged.

TJ: Major categories:

• Acute tubular necrosis (ATN): Most common intrinsic cause. Usually from ischemia or toxins (like aminoglycosides, IV contrast, ethylene glycol).
• Acute interstitial nephritis (AIN): Often an allergic reaction to drugs.  Here’s a quick little mnemonic with the 6Ps to help remember the most common causes. 

Pee — diuretics like furosemide or thiazides.
Pain-free — NSAIDs.
Penicillin — and other beta-lactam antibiotics.
Proton pump inhibitors — like omeprazole.
rifamPin — and other rifamycin antibiotics.
Cimetidine — yes, the old-school H₂ blocker still shows up on exams.

• Glomerulonephritis: Autoimmune, post-infectious, or vasculitis. You’ll see proteinuria, hematuria, and RBC casts.

Dr. Arreaza: A common cause of AKI is diabetes. Diabetes causes prerenal AKI (dehydration caused by uncontrolled diabetes) and intrinsic from renal parenchymal damage and tubular necrosis. So clinically, what would we expect?

TJ: With Intrinsic AKI, as a result of tubular damage, there is impaired urea reabsorption.  Subsequently, BUN and creatinine both rise more proportionally (BUN: Cr ratio closer to 10 –15:1). 

• With ATN, muddy brown casts can be appreciated in UA
• With AIN, look for fever, rash, and especially eosinophilia, as well as a UA displaying eosinophils or WBC casts.
• With Glomerulonephritis, look for RBC casts and proteinuria on UA, and you may even see edema on physical exam with hypertension.

Dr. Arreaza: Treating intrinsic AKI will depend on etiology. Hydration would not fix the problem in most cases. Let’s mention some treatment options for intrinsic AKI.

TJ: Intrinsic AKI is a bit like fixing a flooded house — you don’t just start bailing water; you find the source of the leak, stop it, and protect what’s left. Whether it’s ATN, AIN, or GN, the playbook is: remove the injury, give the kidney a rest, and treat the underlying cause.

Dr. Arreaza: Sure. We start with supportive care, especially treating hyper or hypotension, maintaining normovolemia, correcting electrolyte imbalances, and using antibiotics in case of infection. 

-We must identify and remove reversible causes, such as discontinuing nephrotoxic agents such as NSAIDs, aminoglycosides, and iodine contrast. -Also, other reversible factors must be corrected such as hypovolemia (IV fluids), hypotension (vasopressors) to prevent further kidney damage.

TJ: -Hemodialysis or renal replacement therapy (RRT) is reserved for severe cases of refractory hyperkalemia, metabolic acidosis, volume overload unresponsive to diuretics, and uremic symptoms (encephalopathy, pericarditis, pleuritis).

Dr. Arreaza: Immunosuppression is required for specific types of glomerulonephritis. For instance, rapidly progressive crescentic glomerulonephritis warrants high-dose glucocorticoids and cyclophosphamide. In ANCA-associated vasculitis, glucocorticoids plus cyclophosphamide or rituximab, and sometimes plasma exchange, are standard.

SECTION 4 – Postrenal AKI

Dr. Arreaza: We spent enough time in intrinsic AKI.  Why don’t we move on to our last topic of AKI, postrenal.

TJ: So, withpostrenal AKI, imagine that urine leaving the kidney encounters a roadblock.  Urine can’t get out, so pressure builds up, damaging the kidney.

Common causes:

• For men, benign prostatic hyperplasia (BPH) is a significant factor (as the prostate grows bigger, it can compress the urethra, leading to urine backflow, which can not only cause AKI, but can also lead to possible UTIs in the process).
• Kidney stones, tumors, strictures, and neurogenic bladder

When doing my urology and nephrology rotations at Kern Medical, I encountered many kidney stones and urethral strictures, and unfortunately, a fair number of patients suffering from RCC that caused not only the AKI but also extreme discomfort.

Dr. Arreaza: It seems like we need some imaging to diagnose postrenal AKI.

TJ: Yes.If you’re concerned about obstruction, a renal U/S can quickly help diagnose an underlying obstruction, or a CT scan for more details.

Lab patterns?

• In the early phase (before tubular injury):
• BUN: Cr ratio >20:1 — looks like prerenal.
• FeNa <1%.
• Urine osmolality >500 mOsm/kg.
• In the later phase (after prolonged obstruction → tubular injury):
• BUN: Cr ratio ~10–15:1 — now looks intrinsic.
• FeNa >2%.
• Urine osmolality ~300 mOsm/kg.

Dr. Arreaza: BUN:Cr ratio and FeNa are not reliable to diagnose postrenal AKI, so we must rely more in imaging and clinical presentation. Let´s talk about the management of postrenal AKI.

TJ: Absolutely!  The main way to treat a post-renal AKI is to relieve the obstruction causing it in the first place, whether it be through surgery, TURP, lithotripsy, etc.

Dr. Arreaza: I think the favorite treatment done by urology to relieve obstruction is a ureteral stent, which, remember, needs to be removed later. Typically, 1-2 weeks is sufficient to treat kidney stones. The risk of encrustation and infection increases significantly after 4–6 weeks, and stents should ideally be exchanged within 3 months to minimize complications. 

SECTION 5 – Closing

Dr. Arreaza: I know you’ve spent a decent amount of time explaining the details of the AKI types with us, TJ, but could you give us a summary?

TJ: Viewers, if there’s anything to take away from this, remember:

• Prerenal: Poor perfusion, fix the flow.
• Intrinsic: Structural damage inside the kidney — think ATN, AIN, GN.
• Postrenal: Obstruction — relieve the blockage.

When you see AKI, think: Before the kidney, in the kidney, or after the kidney? That simple framework can help you move fast and help your patient recover kidney function.

Dr. Arreaza, any advice you want to give to the viewers?

Dr. Arreaza: Yes,weare in the middle of summer, and we treat a large amount of farm workers, construction workers and people who spend time outdoors, in general, remind your patients to drink water. Water is life, especially for the kidneys, there is no substitute. That’s it for today’s episode of Rio Bravo qWeek. If you enjoyed this review, share it with a colleague or medical student who could use a quick AKI refresher. And remember — the kidneys may be small, but they’re mighty… and they hold grudges when you ignore them. I’m Dr. Arreaza, signing off.

TJ: Thank you for tuning in, everyone. Have a nice day!

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO Clinical Practice Guideline for Acute Kidney Injury. Kidney International Supplements. 2012;2:1–13. https://kdigo.org/guidelines/acute-kidney-injury/.
2. Kaur A, Sharma GS, Kumbala DR. Acute kidney injury in diabetic patients: A narrative review. Medicine (Baltimore). 2023 May 26;102(21):e33888. doi: 10.1097/MD.0000000000033888. PMID: 37233407; PMCID: PMC10219694. https://pmc.ncbi.nlm.nih.gov/articles/PMC10219694/
3. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

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 <1.1 g/dL will suggest causes such as tuberculosis, malignancy, pancreatitis, nephrotic syndrome, or inflammatory conditions. 

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 (<2.5) you proceed with an abdominal US with doppler. The ultrasound will tell you whether the liver is cirrhotic and if the hepatic vessels are patent. Once cirrhosis is identified in the patient, the workup for chronic liver disease management can be started. Another cause of low protein is Budd-Chiari syndrome. In this case anticoagulation is used. 

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 alcohol induced cirrhosis causing the ascites. The patient should also follow a low-sodium diet (less than 2 grams/day) to help prevent the fluid overload that worsens the ascites. Also, something very important is that the patient must avoid use of NSAIDs, b-blockers, and ACE/ARBs. Patients need to be educated on the importance of avoiding NSAIDS especially because these medications can be found over the counter and are readily accessible but very harmful to cirrhotic patients.

Fluid (water) restriction is generally not recommended for patients with liver cirrhosis and ascites unless they have moderate to severe hyponatremia (serum sodium ≤125–126 mEq/L). When indicated, fluid restriction is typically set at 1,000 mL per day for moderate hyponatremia. The fluid management in ascites is focused on sodium restriction.

Refractory ascites. 

Sometimes there are people who have already received diuretics and have tried lifestyle changes, but the ascites continues to recur. In these cases, serial therapeutic paracentesis or trans jugular intra-hepatic portosystemic shunts (TIPS) can be done. 

One special case is when the ascites is caused by a malignancy. In this case fluid will continue to accumulate even with repeat paracentesis. PleurX is another available treatment. PleurX is a thin, flexible silicone catheter and a one-way valve that is inserted into the peritoneal cavity to allow for drainage of the fluid. Usually, the patients are sent home with this catheter and have caregivers who help them drain fluid using vacuum bottles. This is useful in reducing hospitalization in patients. However, it is not recommended in patients with infection, chylous effusions, mediastinal shifts, or hemorrhage risks. If the patient is a good candidate, they can be put on a list for liver transplant. 

Spontaneous bacterial peritonitis. 

A patient with SBP usually presents with systemic inflammatory response syndrome (SIRS) and large volume ascites on abdominal US. SBP is confirmed via paracentesis with >250 PMNS/mL. Fluid should be sent to the lab for culture and then antibiotics should be started. IV 3rd generation cephalosporins are typically used. Fluoroquinolones are also used to prevent the recurrence of SBP.

If you desire to learn more about SBP, listen to our episode 123. By the way, propranolol is a frequently used medication to prevent GI bleeding from esophageal varices in cirrhosis and also to decrease the development of ascites. It should be used in patients who have compensated cirrhosis and must be avoided in patients with refractory ascites, hypotension, renal dysfunction or active infection. 

So, to wrap things up we should remember that once we identify ascites with our physical exam of the patient, we should make sure to obtain a paracentesis as these results will be the main guide for our treatment. The treatment can then range from medical treatment such as spironolactone and/or loop diuretics to TIPS procedures, PleurX or even liver transplant. Always be on the lookout for SBP in patients with ascites and always remember to obtain a culture on the ascitic fluid prior to starting antibiotics. 

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. Ascites, Cleveland Clinic, https://my.clevelandclinic.org/health/diseases/14792-ascites.
2. Huang LL, Xia HH, Zhu SL. Ascitic Fluid Analysis in the Differential Diagnosis of Ascites: Focus on Cirrhotic Ascites. J Clin Transl Hepatol. 2014 Mar;2(1):58-64. doi: 10.14218/JCTH.2013.00010. Epub 2014 Mar 15. PMID: 26357618; PMCID: PMC4521252. https://pmc.ncbi.nlm.nih.gov/articles/PMC4521252/.
3. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Essential Screenings for Young Adults

Dr. 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 Exam

Dr. 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 concerns

It’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 Screening

Dr. 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 entities

Dr. 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 Screenings

Dr. 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 depression?

Dr. Lopez: Screening for depression is now a standard part of primary care. The most commonly used tool is the PHQ-9 questionnaire, which asks about:

· Mood changes (sadness, hopelessness)

· Loss of interest in activities

· Sleep disturbances

· Changes in appetite

· Difficulty concentrating

A score on this test can help determine whether someone is at risk of depression and needs further evaluation or support.

Dr. Arreaza: And why should we screen for depression?

Dr. Lopez: Because early treatment makes a huge difference. Depression can affect school, work, relationships, and even physical health. But with therapy, lifestyle changes, and sometimes medication, people can and do recover.

I always tell young adults: Mental health is just as important as physical health. Seeking help is a sign of strength, not weakness.

Dr. Arreaza: This is a USPSTF recommendation GRADE B. We are encouraged to screen adults, including pregnant and postpartum women, as well as older adults.

HPV Screening & Vaccination

Dr. Lopez: Dr. Arreaza, finally, let’s talk about HPV—one of the most preventable causes of cancer. The human papillomavirus (HPV) is the most common STI worldwide, and it’s responsible for almost all cases of cervical cancer, as well as throat, anal, and penile cancers. The good news? The HPV vaccine is over 90% effective at preventing these cancers. 

Dr. Arreaza: In fact, from 2015 to 2018, U.S. women ages 14 to 19 experienced an 88% decrease in HPV-related disease. That’s a direct result of the vaccine's effectiveness.

Dr. Lopez: It’s recommended for:

· All boys and girls, starting at the age of 9. ACIP gave new recommendations for use of a 2-dose schedule for girls and boys who initiate the vaccination series at ages 9-14 years. Three doses remain recommended for persons who start HPV vaccination at ages 15-26 years and for immunocompromised persons.

· Catch-up vaccination is recommended for people up to age 26 (and in some cases, up to 45 with provider recommendation)

Dr. Arreaza: And what about screening for HPV? How do we screen?

Dr. Lopez: Great question, Dr. Arreaza. Pap smears start at age 21, for all women regardless of sexual activity, and are repeated every 3-5 years depending on HPV testing. Many people think Pap smears check for STIs, but they actually look for abnormal cervical cells that could lead to cancer. HPV vaccination plus routine screening means cervical cancer is one of the most preventable cancers today!

Closing Thoughts & Call to Action

Dr. Arreaza: That wraps up today’s discussion on essential health screenings for young adults! Dr. Lopez, any final take-home messages?

Guest: My biggest message is don’t wait until something is wrong to see a doctor. Preventative care is simple, quick, and can save lives.

If you’re between the ages of 13-26, here’s what you should do:

-Get an annual wellness exam

-Get tested for STIs if sexually active

-Check in on your mental health and talk to someone if you need support

-Get the HPV vaccine if you haven’t already and follow up on screening

Taking these small steps today leads to better health for years to come!

Host: That’s fantastic! Dr. Lopez. I hope all our primary care providers can take these easy steps to keep our young community healthy. If you found this episode helpful, share it with a friend, and don’t forget to subscribe to our podcast for more practical health discussions.

Dr. Lopez: Until next time—thanks for chiming in, medical community. Take care and take charge of your health!

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. Screening Recommendations and Considerations Referenced in Treatment Guidelines and Original Sources. U.S. Centers for Disease Control and Prevention, CDC.gov, https://www.cdc.gov/std/treatment-guidelines/screening-recommendations.htm, accessed on June 26, 2025.
2. Recommendation: Anxiety Disorders in Adults: Screening, United States Preventive Services Taskforce, June 20, 2023, https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/anxiety-adults-screening, accessed on June 26, 2025.
3. Recommendation: Depression and Suicide Risk in Adults: Screening, United States Preventive Services Taskforce, June 20, 2023, https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/screening-depression-suicide-risk-adults, accessed on June 26, 2025.
4. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

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, 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: 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 months

This 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 rest

And 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 malaise.

Important: Chronic Lyme disease is a controversial term without a consistent clinical definition and is often used to describe patients with persistent, nonspecific symptoms not supported by objective evidence of Lyme infection. Leading medical organizations reject the term and instead recognize "post-treatment Lyme disease syndrome" (PTLDS) for persistent symptoms following confirmed, treated Lyme disease, emphasizing that prolonged antibiotic therapy is not effective. Research shows no benefit—and potential harm—from extended antibiotic use, and patients with unexplained chronic symptoms should be thoroughly evaluated for other possible diagnoses.

Michael: 

Cardiopulmonary Causes

    •   Congestive Heart Failure (CHF): Fatigue from poor perfusion and low cardiac output. Often comes with dyspnea on exertion, edema, and orthopnea.

    •   Chronic Obstructive Pulmonary Disease (COPD): Look for a smoking history, chronic cough, and fatigue from hypoxia or the work of breathing.

    •   Obstructive Sleep Apnea (OSA): Daytime fatigue despite adequate hours of sleep. Patients may snore, gasp, or report morning headaches. High suspicion in obese or hypertensive patients.

Jordan:

Autoimmune / Inflammatory Causes

    •   Systemic Lupus Erythematosus (SLE): Fatigue is often an early symptom. May also see rash, arthritis, photosensitivity, or renal involvement.

    •   Rheumatoid Arthritis (RA): Fatigue from systemic inflammation. Morning stiffness, joint pain, and elevated inflammatory markers point to RA.

    •   Fibromyalgia: A chronic pain syndrome with widespread tenderness, fatigue, nonrestorative sleep, and sometimes cognitive complaints ("fibro fog").

Cancer / Malignancy

    •   Leukemia, lymphoma, or solid tumors: Fatigue can be the first symptom, often accompanied by weight loss, night sweats, or unexplained fevers. Consider when no other cause is evident.

Michael:

Medications:

Common culprits include:

    ◦   Beta-blockers: Can slow heart rate too much.

    ◦   Antihistamines: Sedating H1 blockers like diphenhydramine.

    ◦   Sedatives or sleep aids: Can cause grogginess and daytime sedation.

    •   Substance Withdrawal: Fatigue can be seen in withdrawal from alcohol, opioids, or stimulants. Caffeine withdrawal, though mild, can also contribute.

Dr. Arreaza:

Whenever we evaluate fatigue, we need to keep an eye out for red flags. These should raise suspicion for something more serious:

    •   Unintentional weight loss

    •   Night sweats

    •   Persistent fever

    •   Neurologic symptoms

    •   Lymphadenopathy

    •   Jaundice

    •   Palpitations or chest pain

This patient doesn’t have these—but that doesn’t mean we stop here.

Dr. Arreaza:

Those are a lot of causes, we can evaluate fatigue following 7 steps:

1. Characterize the fatigue.
2. Look for organic illness.
3. Evaluate medications and substances.
4. Perform psychiatric screening.
5. Ask questions about quantity and quality of sleep.
6. Physical examination.
7. Undertake investigations.

So, students, do we send the whole lab panel?

Michael:

Not necessarily. Labs should be guided by history and physical. But here’s a good initial panel:

    •   CBC: To check for anemia or infection

    • TSH: Screen for hypothyroidism

    • CMP: Look at electrolytes, kidney, and liver function

    • Ferritin and iron studies

    • B12, folate

    • ESR/CRP for inflammation (not specific)

    • HbA1c if diabetes is on the radar

Jordan:

And if needed, consider:

    • HIV, EBV, hepatitis panel

    • ANA, RF

    • Cortisol or ACTH stimulation test

Imaging? Now that’s rare—unless there are specific signs. Like chest X-ray for possible cancer or TB, or sleep study if you suspect OSA.

Dr. Arreaza:

Unaddressed fatigue isn’t just inconvenient. It can impact on quality of life, affect job performance, lead to mood disorders, delay diagnosis of serious illness, increase risk of accidents—especially driving. So, don’t ignore your patients with fatigue!

Jordan:

And some people—like women, caregivers, or shift workers—are especially at risk.

Michael:

The cornerstone of treatment is addressing the underlying cause.

Jordan:

If it’s iron-deficiency anemia—treat it. If it’s depression—get mental health involved. But there’s also: 

Lifestyle Support: Better sleep hygiene, light physical activity, mindfulness or CBT for stress, balanced nutrition—especially iron and protein, limit caffeine and alcohol

Dr. Arreaza:

Sometimes medications help—but rarely. 

And for chronic fatigue syndrome, the current best strategies are graded exercise therapy and CBT, along with managing specific symptoms. 

Beta-alanine has potential to modestly improve muscular endurance and reduce fatigue in 

older adults, but more high-quality research is needed.

SSRI: fluoxetine and sertraline. 

Iron supplements: Even without anemia, but low ferritin [Anecdote about low ferritin patient]

Jordan:

This case reminds us to take fatigue seriously. In her case, it may be multifactorial—work stress, caregiving burden, and possibly iron-deficiency anemia. So, how would we wrap up this conversation, Michael?

Michael:

We don’t need to order everything under the sun. A focused history and exam, targeted labs, and being alert to red flags can guide us.

Jordan:

And don’t forget the basics—sleep, stress, and nutrition. These are just as powerful as any prescription.

Dr. Arreaza:

We hope today’s episode on fatigue has given you a clear framework and some practical tips. If you enjoyed this episode, share it and subscribe for more evidence-based medicine!

Jordan:

Take care—and get some rest~

___________________________

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. DynaMed. (2023). Fatigue in adults. EBSCO Information Services. https://www.dynamed.com (Access requires subscription)
2. Jason, L. A., Sunnquist, M., Brown, A., Newton, J. L., Strand, E. B., & Vernon, S. D. (2015). Chronic fatigue syndrome versus systemic exertion intolerance disease. Fatigue: Biomedicine, Health & Behavior, 3(3), 127–141. https://doi.org/10.1080/21641846.2015.1051291
3. Kroenke, K., & Mangelsdorff, A. D. (1989). Common symptoms in ambulatory care: Incidence, evaluation, therapy, and outcome. The American Journal of Medicine, 86(3), 262–266. https://doi.org/10.1016/0002-9343(89)90293-3
4. National Institute for Health and Care Excellence. (2021). Myalgic encephalomyelitis (or encephalopathy)/chronic fatigue syndrome: Diagnosis and management (NICE Guideline No. NG206). https://www.nice.org.uk/guidance/ng206
5. UpToDate. (n.d.). Approach to the adult patient with fatigue. Wolters Kluwer. https://www.uptodate.com (Access requires subscription)
6. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Written 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: Intro
Today 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 implantable CGM on the market. It involves a minor in-office procedure to insert the sensor under the skin of the upper arm, which lasts up to 180 days (and a newer version, Eversense 365, lasts up to one year). A removable transmitter worn on top of the skin sends data every 5 minutes to a mobile app and vibrates for alerts. It requires 1–2 calibrations per day using a traditional fingerstick meter. It integrates with Eversense DMS software for physician monitoring. The total cost for Eversense depends on the insertion procedure and insurance, but cash pay for the full 6-month system is estimated at $2,400–$3,000, or about $400–$500/month including follow-up visits.

Will:

Additional lower-cost CGMs such as the Medtrum A6 TouchCare are available internationally and in select U.S. pilot programs. These devices offer 14-day wear, smartphone syncing, and daily calibration, but are not yet FDA-approved for wide use and lack full EMR integration.

Chris:

In terms of performance and value, Dexcom G7 offers the most advanced real-time feedback and integration, making it ideal for those on insulin pumps or needing tight control. 

Will:

FreeStyle Libre offers the best affordability and convenience, especially for non-insulin users or those who prefer not to deal with constant alerts. Eversense offers a niche but compelling option for people who want to avoid frequent sensor changes. Chris, [Are there any downsides or risks that patients should be aware of before trying out CGM?]

Chris:

CGMs are generally safe and well-tolerated, but they do have limitations. Dexcom G7 has a known failure mode where sensors sometimes fail prematurely, often before the full 10-day duration. Some users have reported “signal loss” errors or random disconnections, especially when switching between phone models or operating systems. There are occasional reports of inaccurate highs or lows due to compression during sleep or dehydration. Though the G7 is factory-calibrated, abrupt changes in hydration or blood flow can affect its readings.

Will:

FreeStyle Libre systems, particularly Libre 2, require the user to scan the sensor to retrieve data unless alerts are enabled. These devices may be affected by vitamin C (ascorbic acid), which can falsely elevate glucose readings, and they do not currently allow for automated insulin delivery integration. Some Libre 2 users have noted adhesive-related rashes or spontaneous detachment. Libre 3, while more advanced, still may lose Bluetooth connection intermittently, particularly if the phone is out of range or the app is not running in the background.

Chris:

Senseonics Eversense carries procedural risks due to its implantable nature. Minor scarring or infection at the insertion site has been reported. The transmitter must be worn during waking hours to provide alerts, and users report anxiety over losing the transmitter since data logging is interrupted without it. Calibration is still required, which adds to daily tasks. Additionally, the sensor does not communicate with insulin pumps or closed-loop systems.

Will:

All CGMs can cause mild skin irritation from adhesive, particularly in users with sensitive skin. Alert fatigue is another consideration, as frequent low- or high-glucose warnings may cause stress or lead users to silence notifications entirely. Finally, relying solely on CGM without periodic fingerstick confirmation in symptomatic scenarios can be a risk, especially during rapid glucose changes.

Chris:

Conclusion
[***] Continuous glucose monitors have reshaped the way we manage diabetes, offering unprecedented insight into glucose trends, diet responses, and insulin timing. While CGMs are not flawless, the technology continues to evolve. 

Will: 

If your patient is on insulin or struggling with glucose variability, consider whether CGM is right for your patient. For those not using insulin, consider newer OTC options like FreeStyle Libre or Dexcom Stelo, which offer accessible entry points without the need for prescriptions. As AI integration, longer sensor life, and non-invasive monitoring enter the market, CGM will only become more useful.

Dr Arreaza: Personal experience with CGMs. 

I do not have diabetes, but I have a strong family history of diabetes (including father, 2 grandmas, and about 15 uncles, aunts, and cousins.)

I wanted to try it so I could teach my patients about CGM. My first experience was with Freestyle Libre 2: 

Pros: Painless placement, easy to use, scanning with phone was easier than fingersticks.

Cons: Required some assembling to be placed, mild discomfort at night, and nighttime alarms.

Dexcom G7:

Pros: No need for scanning, feels more stable in your arm

Cons: High readings (had to calibrate for a more accurate reading)

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

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.

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 hate movement! According to AFO Journal, “In a primary care setting, the probability of a migraine is 92% in patients who report at least four of the five POUND symptoms. The probability decreases to 64% in patients with three of the symptoms, and 17% in patients with 2 or fewer symptoms.”

Jordan:
Now, cluster headaches have previously been referred to as “suicide headaches” because the pain is so intense. They’re usually one-sided, come in cycles or “clusters,” and are associated with autonomic features like tearing, nasal congestion, even ptosis or miosis, which could mimic Horner’s syndrome.

Michael:
Tension-type headaches, on the other hand, feel more like a tight band around the head. They're bilateral, pressing rather than pulsating, and usually not accompanied by nausea or sensory sensitivity.

Jordan:
And then we always keep red flags in mind. That’s where the SNOOP mnemonic helps: Systemic symptoms, Neurologic signs, Onset sudden, older age, and Pattern change. These mnemonics have been updated, and several items have been added. It has two Ns, 2 Os, and 10 Ps. For example, one of the Ns that is added is neoplasia history, and some of the Ps are Pregnancy/Postpartum, Papilledema, and Pain killer overuse. You can find the updated version in the American Family Physician journal, April 2025. 

Dr. Arreaza:
Exactly. Any of those should raise alarm bells. “Thunderclap headaches” especially! Those need immediate evaluation. I learned it in med school as “a lightning flashing in a blue sky” (Hispanics drama is real, folks [joke]).

Michael:
If we’re worried about secondary causes, that’s when labs and imaging come in. We might check CBC for infection, ESR for temporal arteritis, or even a toxicology screen if substances are a concern.

Jordan:
And imaging! Non-contrast CT is great for acute or sudden-onset headaches. But for chronic or worsening symptoms, we lean toward MRI. If vascular causes are on the table, we might add MRV or CTA. And don’t forget lumbar puncture if we’re thinking about meningitis or subarachnoid hemorrhage.

Dr. Arreaza:
Very good. The key is to tailor the workup to clinical suspicion. Not every headache needs a CT, but some definitely do. It’s not just about getting tests, it’s about getting the right tests based on the story. Let’s talk about management. How do we approach treatment?

Michael:
For acute migraine attacks, NSAIDs are a good first-line. Triptans are also effective, especially if given early. And adding an anti-emetic like metoclopramide can help with both nausea and improve absorption of oral meds.

Jordan:
And for tension-type, it’s usually NSAIDs, sometimes acetaminophen. But non-pharmacologic measures are key too, things like stress reduction, sleep hygiene, posture correction, etc.

Michael:
Cluster headaches are a different beast. The go-to is high-flow oxygen, 15 L via non-rebreather mask, and subcutaneous sumatriptan, because oral meds are too slow.

Jordan:
An even bigger challenge is treatment when headaches become chronic, especially with medication overuse. And there’s often comorbidity with depression or anxiety, which complicates management.

Michael:
Fortunately, most people with headaches don’t have chronic headaches. Some risk factors for chronic headaches include family history, female sex, poor sleep, stress, and hormonal shifts. Triggers like caffeine, dehydration, and irregular meals are also common.

Dr. Arreaza:
Those elements are important to ask about during the visit, not just the headache itself, but what might be feeding into it.

Jordan:
For patients with frequent headaches, preventive therapy is a game-changer. Think things like beta-blockers, topiramate, amitriptyline, or CGRP inhibitors. Gepants and ditans are newer medications, supported by evidence as second-line agents. Unlike triptans and ergot alkaloids, gepants and ditans do not have vascular contraindications. Their use may be limited by cost.

Michael:
And we can’t forget lifestyle modifications. Encouraging regular sleep, hydration, and stress reduction often makes an enormous difference.

Dr. Arreaza:
To wrap it up: headaches are complex, but with a structured approach, we can distinguish benign from dangerous. Michael, any final takeaway?

Michael:
Yes! Start with a good history and physical, then build your differential. Most headaches are manageable, but don’t ignore red flags.

Jordan:
And always validate the patient’s concerns. Even if it’s “just a migraine,” it can be disabling, and we need to treat it seriously. 

Dr Arreaza:
Thanks for listening! Stay tuned for our next episode!

_______________________

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________ 

References: 

1. International Headache Society. (2018). The International Classification of Headache Disorders, 3rd edition (ICHD-3). Retrieved fromhttps://ichd-3.org/ 

1. Dodick, D. W. (2003). Clinical clues and clinical rules: Approach to the diagnosis of secondary headache. Headache: The Journal of Head and Face Pain, 43(3), 282–292.https://doi.org/10.1046/j.1526-4610.2003.03057.x 

1. American College of Radiology. (2019). ACR Appropriateness Criteria® Headache. Journal of the American College of Radiology, 16(5S), S364–S377.https://doi.org/10.1016/j.jacr.2019.02.008 

1. Taylor, F. R., & Kaniecki, R. G. (2011). Symptomatic treatment of migraine: When to use NSAIDs, triptans, or opiates. Current Treatment Options in Neurology, 13(1), 15–27.https://doi.org/10.1007/s11940-010-0103-9 

1. Gilmore B, Michael M. Treatment of acute migraine headache. Am Fam Physician. 2011 Feb 1;83(3):271-80. Erratum in: Am Fam Physician. 2011 Oct 1;84(7):738. PMID: 21302868. https://pubmed.ncbi.nlm.nih.gov/21302868/

1. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased fromhttps://www.premiumbeat.com/. 

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:

1. Mechanical (like muscle strain or degenerative disc disease),
   
    
2. Radicular (nerve root involvement),
   
    
3. Referred pain (like from pelvic or abdominal organs),
   
    
4. Inflammatory (AS), and
   
    
5. 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.
  
   
• Constitutional symptoms like fever or weight loss raise red flags.
  
   
• Bladder/bowel changes or saddle anesthesia raise alarms for cauda equina.
  
   
• Pain that wakes patients up at night might point to malignancy.
  
   

Dr. Arreaza:
So when do we order labs or imaging?

Michael:
Not right away. For most patients with acute low back pain, imaging is not needed unless they have red flags. If infection is suspected, we’d get CBC, ESR, and CRP. For cancer, maybe PSA or serum protein electrophoresis. And if inflammatory back disease is suspected, HLA-B27 can be helpful.

Jordan:
Yes, imaging should be delayed for at least six weeks unless red flags or significant neurologic deficits are present. When we do image, MRI is our go-to especially for suspected radiculopathy or cauda equina. X-rays can help if we’re thinking about fractures, but they won’t show soft tissue or nerve root issues.

Michael:
In the example from our case, since the patient doesn’t have red flags, we’d go with conservative management: start NSAIDs and recommend activity modification. As this is the acute setting, physical therapy would not be recommended.

Jordan:
For the acute phase, research shows no serious difference between those with PT and those without in the long term. However, physical therapy is really the cornerstone of management for chronic back pain. It’s not just movement: it’s education, body mechanics, and teaching patients how to move safely. And PT can actually reduce opioid use, imaging, and injections down the line for patient struggling with long term back pain.

Dr. Arreaza:
Yes, and PT is not one-size-fits-all. PT might include McKenzie exercises, manual therapy, postural retraining, or even neuromuscular re-education. The goal is always to build core stability, promote healthy movement patterns, and reduce fear of motion.

Jordan:
Let’s take a minute to talk about the McKenzie Method, a physical therapy approach used to treat lumbar disc herniation by identifying a specific movement, (often spinal extension) that reduces or centralizes pain. A common exercise is the prone press-up, (cobra pose for yoga fans) where the patient lies face down and pushes the upper body upward while keeping the hips on the floor to relieve pressure on the disc. These exercises should be done carefully, ideally under professional guidance, and discontinued if symptoms worsen.

Michael:
For our case patient, our working diagnosis is mechanical low back pain with L5 radiculopathy. No imaging needed now, no red flags. We’ll treat conservatively and educate him about proper lifting, staying active, and recovery expectations.

Jordan:
We also emphasized to him that bed rest isn’t helpful. In fact, bed rest can make things worse. Keeping active while avoiding heavy lifting for now is key.

Dr. Arreaza:
Return-to-work recommendations should be individualized. For example, an office worker, positioning while working, or work hours may be able to return to work promptly. However, those with physically demanding jobs may need light duty or be off work.

Ice: no evidence of benefit. Heat: may reduce pain and disability in pain of less than 3 months, although the benefit was small and short.

And we should always teach safe lifting techniques: bend at the knees, keep the load close, avoid twisting. It's basic knowledge, but it is very effective in preventing recurrence.

Jordan:
Now, if a patient fails to improve after 6 weeks of conservative therapy, or if they develop new neurologic deficits, that’s when we think about referral to spine specialists or surgical consultation.

Michael:
And as previously mentioned: in cases where back pain becomes chronic (lasting more than 12 weeks) a multidisciplinary approach works best. That can include:

• Physical therapy,
  
   
• Cognitive behavioral therapy (CBT)
  
   
• And sometimes pain management interventions.
  
   

Jordan:
We can’t forget the psychological toll either. Chronic back pain is associated with depression, anxiety, and opioid dependence. Increased risk factors include obesity, smoking, sedentary lifestyle, and previous back injuries.

Dr. Arreaza:
Well said. So, let’s summarize. Michael?

Michael:
Sure! Low back pain is common, and most cases are benign. But we have to know the red flags that point to serious pathology. A focused history and physical exam are more powerful than many people realize. And the first step in treatment is almost always conservative, with a strong emphasis on maintaining physical activity.

Jordan:
And don’t underestimate the value of patient education. Helping patients understand their pain, set realistic expectations, and stay active is often just as important as the medications or therapies we offer.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

Chou, R., Qaseem, A., Snow, V., Casey, D., Cross, J. T., Shekelle, P., & Owens, D. K. (2007). Diagnosis and treatment of low back pain: A joint clinical practice guideline from the American College of Physicians and the American Pain Society. Annals of Internal Medicine, 147(7), 478–491. https://doi.org/10.7326/0003-4819-147-7-200710020-00006

Deyo, R. A., Mirza, S. K., Turner, J. A., & Martin, B. I. (2009). Overtreating chronic back pain: Time to back off? Journal of the American Board of Family Medicine, 22(1), 62–68. https://doi.org/10.3122/jabfm.2009.01.080102

National Institute for Health and Care Excellence. (2020). Low back pain and sciatica in over 16s: Assessment and management (NICE Guideline No. NG59). https://www.nice.org.uk/guidance/ng59

Qaseem, A., Wilt, T. J., McLean, R. M., & Forciea, M. A. (2017). Noninvasive treatments for acute, subacute, and chronic low back pain: A clinical practice guideline from the American College of Physicians. Annals of Internal Medicine, 166(7), 514–530. https://doi.org/10.7326/M16-2367

UpToDate. (n.d.). Evaluation and treatment of low back pain in adults. Wolters Kluwer. https://www.uptodate.com (Access requires subscription)

Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Jesica 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.

Definition

Gestational 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. 

Pathophysiology

GDM 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 GDM

Gestational 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 includes 75g after an overnight fast. Blood glucose is measured while fasting which should be less than 92, at 1 hour less than 180 and at 2 hours less than 153. If any one of these values is exceeded, the patient is diagnosed with GDM.

If the mother is found to be GDM positive during pregnancy she will also need continued screening post-partum to monitor for any development of overt diabetes. The testing is usually 75g 2-hour OGTT at 6-12 weeks postpartum. If this testing is normal, then they are tested using HbA1c every 3 years. If the post-partum testing shows pre-diabetes, annual testing is recommended using HbA1c measurements. 

Maternal complications 

Women with GDM are at an increased risk for future cardiovascular disease, T2DM, and chronic kidney disease. GDM is also associated with increased likelihood of developing pre-eclampsia following delivery. Pre-eclampsia is a complication seen in pregnancy characterized by high blood pressure, proteinuria, vision changes, and liver involvement (high LFTs). Pre-eclampsia can then progress to eclampsia or HELLP syndrome, both of which can include end organ damage. 

Additionally, she can develop polyhydramnios which leads to overstretching of the uterus and can induce pre-term labor, placental abruption, and or uterine atony, all of which additionally put the mother at increased risk for c-section. 

All of these maternal complications that stem from GDM lead to complications and extended hospitalization. 

Child’s complications 

Although there is an increased set of risks for the mother, the neonate can also develop a variety of risks due to the increased glucose while in utero. While the fetus is growing, the placenta is the source of nutrition for the fetus. As the levels of glucose in the mother increase so does the amount of glucose filtered through the placenta and into the fetal circulation. Over time the glucose leads to oxidative stress and inflammation with activation of TGF-b which leads to fibroblast activation and fibrosis of the placenta. This fibrosis decreases the nutrient and oxygen exchange for the fetus. As the fetus attempts to grow in this restrictive environment its development is affected. 

The fetus can develop IUGR (intrauterine growth restriction) leading to a small for gestation age newborn which can then lead to another set of complications. The low oxygen environment can lead to increased EPO production and polycythemia at birth which can then lead to increased clotting that can travel to the newborn brain. 

Newborns can also be born with fetal acidosis due to the anerobic metabolism and lactic acid buildup in fetal tissues which can cause fetal encephalopathy leading to cerebral palsy and developmental delay. 

And the most severe of newborn complications to gestational diabetes can lead to fetal demise. 

Furthermore, the increase of glucose can also lead to macrosomia in the infant which can often lead to a traumatic delivery and delivery complications such as shoulder dystocia and brachial plexus injury. 

Brachial plexus injury sometimes resolves without sequela, but other times can lead to permanent weakness or paralysis of the affected arm. 

The baby can be born too small or too big.

Additionally, once the fetus is born the cutting of the umbilical cord leads to a rapid deceleration in blood glucose in the fetal circulation and hypoglycemic episodes can occur, that often lead to NICU admission. 

The insulin that is created by the fetus in utero to accommodate the large quantities of glucose is known to affect lung maturation as well. The insulin produced inhibits surfactant production in the fetus. Upon birth some of the newborns also have to be placed on PEEP for ventilation and some children require treatment with surfactant to prevent alveolar collapse and/or progression to NRDS created by the low surfactant levels. 

Additionally, neonates who are macrosomic, which is usually seen in GDM mothers, are larger and stronger and when put on PEEP to help increase ventilation the newborn’s stronger respiratory effort can lead to higher pulmonary pressures and barotrauma such as neonatal pneumothorax.

Long term complications to the child of a mother with GDM also occur. As the child grows, they are also at an increased risk for developing early onset obesity because of the increased adipose storage triggered by the increase in insulin in response to the high glucose in utero. This then can lead to a higher chance of developing type 2 diabetes mellitus in the child. With diabetes, also comes an increase in cardiovascular risk as the child ages and becomes an adult. The effects of GDM go beyond the fetal life but continue through adulthood.

What can be done?

Gestational Diabetes Mellitus has many severe and lifelong consequences for both the mother and the child and prevention of GDM would help enhance the quality of life of both. 

Many of the ways to prevent GDM complications include patient education and dietary modifications with a diet rich in whole grains, fruits, vegetables and lean proteins. 

Benefits of some vegetables in the Mexican cuisine that may be beneficial: Nopales, Chayote, and Jicama. Those are good alternatives for highly processed carbs.

Mothers are usually offered nutritional counseling to help them develop a tailored eating plan. This and 30 minutes of moderate exercise daily is recommended to increase insulin sensitivity and lower the post-prandial glucose levels. If within 2 weeks of implementing lifestyle changes alone the glucose measurements remain high, then medications like insulin can be put onboard to manage the GDM. 

If they require insulin, I think it is time to refer to a higher level of care, if available, high risk OB clinic.

Conclusion: Now we conclude episode number ###, “[TITLE].” [summary here]. 

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References:

1. Eades CE, Burrows KA, Andreeva R, Stansfield DR, Evans JM. Prevalence of gestational diabetes in the United States and Canada: a systematic review and meta-analysis. BMC Pregnancy Childbirth. 2024 Mar 15;24(1):204. doi: 10.1186/s12884-024-06378-2. PMID: 38491497; PMCID: PMC10941381. https://pubmed.ncbi.nlm.nih.gov/38491497/
2. QuickStats: Percentage of Mothers with Gestational Diabetes,* by Maternal Age — National Vital Statistics System, United States, 2016 and 2021. Weekly / January 6, 2023 / 72(1);16. https://www.cdc.gov/mmwr/volumes/72/wr/mm7201a4.htm?utm
3. Akinyemi OA, Weldeslase TA, Odusanya E, Akueme NT, Omokhodion OV, Fasokun ME, Makanjuola D, Fakorede M, Ogundipe T. Profiles and Outcomes of Women with Gestational Diabetes Mellitus in the United States. Cureus. 2023 Jul 4;15(7):e41360. doi: 10.7759/cureus.41360. PMID: 37546039; PMCID: PMC10399637. https://pmc.ncbi.nlm.nih.gov/articles/PMC10399637/?utm
4. Perlman, J. M. (2006). Summary proceedings from the neurology group on hypoxic-ischemic encephalopathy. Pediatrics, 117(3), S28–S33.
   DOI: 10.1542/peds.2005-0620C.
5. Low, J. A. (1997). Intrapartum fetal asphyxia: definition, diagnosis, and classification. American Journal of Obstetrics and Gynecology, 176(5), 957–959.
   DOI: 10.1016/S0002-9378(97)70609-0.
6. Hallman, M., Gluck, L., & Liggins, G. (1985). Role of insulin in delaying surfactant production in the fetal lung. Journal of Pediatrics, 106(5), 786–790.
   DOI: 10.1016/S0022-3476(85)80227-0.
7. Sweet, D. G., Carnielli, V., Greisen, G., et al. (2019). European Consensus Guidelines on the Management of Respiratory Distress Syndrome – 2019 Update. Neonatology, 115(4), 432–450.
   DOI: 10.1159/000499361.
8. Raju, T. N. K., et al. (1999). Respiratory distress in term infants: when to suspect surfactant deficiency. Pediatrics, 103(5), 903–909.
   DOI: 10.1542/peds.103.5.903.
9. Burns, C. M., Rutherford, M. A., Boardman, J. P., & Cowan, F. M. (2008). Patterns of cerebral injury and neurodevelopmental outcomes after symptomatic neonatal hypoglycemia. Pediatrics, 122(1), 65–74.
   DOI: 10.1542/peds.2007-2822.
10. Dabelea, D., et al. (2000). Long-term impact of maternal diabetes on obesity in childhood. Diabetes Care, 23(10), 1534–1540.
    DOI: 10.2337/diacare.23.10.1534.
11. Dashe, J. S., et al. (2002). "Hydramnios: Etiology and outcome." Obstetrics & Gynecology, 100(5 Pt 1), 957–962.
    DOI: 10.1016/S0029-7844(02)02279-6.
12. Long-term cost-effectiveness of implementing a lifestyle intervention during pregnancy to prevent gestational diabetes mellitus: a decision-analytic modelling study. Diabetologia.
13. American College of Obstetricians and Gynecologists. (2018). Practice Bulletin No. 190: Gestational Diabetes Mellitus. Obstetrics & Gynecology, 131(2), e49–e64. https://doi.org/10.1097/AOG.0000000000002501
14. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

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 significant hyperactivity or sleep disturbances.

Non-pharmacologic treatments.

Behavioral therapy before age 6 is the first choice, after that, medications are more effective than BH only, and as adults again you use CBT.

Medication is often just one part of a broader treatment plan. Behavioral therapy, especially in children, plays a critical role. Parent-training programs, positive reinforcement systems, and structured routines can significantly improve functioning. And for adolescents and adults, cognitive-behavioral therapy (CBT) is particularly helpful. CBT can address issues like procrastination, time management, emotional regulation, and self-esteem which are areas that medication doesn’t always touch.

Using medications for ADHD can be faced with resistance by parents, and even children. There is stigma and misconceptions about mental health, there may be concerns about side effects, fear of addiction, negative past experiences, and some parents prefer to treat ADHD the “natural” way without medications or only with supplements. All those concerns are valid. Starting a medication for ADHD is the first line of treatment in children who are 6 years and older, but it requires a shared decision with parents and patients. 

Cardiac side effects are possible with stimulants. EKG may be needed before starting stimulants, but it is not required. Get a personal and family cardiac history, including a solid ROS. Benefits include control of current condition and treating comorbid conditions.

The presentation of ADHD changes as the person goes through different stages of life. For example, you may have severe hyperactivity in your school years, but that hyperactivity improves during adolescence and impulsivity worsens. 

It varies among sexes too. Women tend to present as inattentive, and men tend to be more hyperactive. ADHD is often underdiagnosed in adults, yet it can significantly impact job performance, relationships, and mental health. In adults, we often use long-acting stimulants to minimize the potential for misuse. And psychotherapy, particularly CBT or executive functioning coaching, can be life-changing when combined with pharmacologic treatment. 

There are several populations where treatment must be tailored carefully such as pregnant patients, individuals with co-occurring anxiety or depression, and those with a history of substance use. For example, atomoxetine may be preferred in patients with a history of substance misuse. And in children with coexisting oppositional defiant disorder, combined behavioral and pharmacologic therapy is usually more effective than either approach alone.

Comorbid conditions.

Depression and anxiety can be comorbid, and they can also mimic ADHD. Consult your DSM-5 to clarify what you are treating, ADHD vs depression/anxiety.

Treatment goes beyond the clinic. For school-aged children, we often work closely with schools to implement 504 plans or Individualized Education Programs (IEPs) that provide classroom accommodations. Adults may also benefit from workplace strategies like structured schedules, noise-reducing headphones, or even coaching support. Ongoing monitoring is absolutely essential. We assess side effects of medication, adherence, and symptom control. ***In children, we also monitor growth and sleep patterns. We often use validated rating scales, like the Vanderbilt questionnaire for children 6–12 (collect answers from two settings) or Conners questionnaires (collect from clinician, parents and teachers), to track progress. And shared decision-making with patients and families is key throughout the treatment process.

To summarize, ADHD is a chronic but manageable condition. Effective treatment usually involves a combination of medication and behavioral interventions, tailored to the individual’s needs. And early diagnosis and treatment can significantly improve quality of life academically, socially, and emotionally.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

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References:

1. American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders. 5th ed., text rev. (DSM-5-TR). Washington, DC: American Psychiatric Association; 2022.
   
    
2. CHADD (Children and Adults with Attention-Deficit/Hyperactivity Disorder). Understanding ADHD. Accessed May 2025. https://chadd.org
    
3. National Institute for Health and Care Excellence (NICE). Attention Deficit Hyperactivity Disorder: Diagnosis and Management. NICE guideline [NG87]. Updated March 2018. Accessed May 2025. https://www.nice.org.uk/guidance/ng87
    
4. Pliszka SR; AACAP Work Group on Quality Issues. Practice parameter for the assessment and treatment of children and adolescents with attention-deficit/hyperactivity disorder. J Am Acad Child Adolesc Psychiatry. 2007;46(7):894–921. doi:10.1097/chi.0b013e318054e724
    
5. Subcommittee on Children and Adolescents with Attention-Deficit/Hyperactivity Disorder, Steering Committee on Quality Improvement and Management. Clinical practice guideline for the diagnosis, evaluation, and treatment of attention-deficit/hyperactivity disorder in children and adolescents. Pediatrics. 2019;144(4):e20192528. doi:10.1542/peds.2019-2528
    
6. Texas Children’s Hospital. ADHD Provider Toolkit. Baylor College of Medicine. Accessed May 2025. https://www.bcm.edu
    
7. Wolraich ML, Hagan JF Jr, Allan C, et al. Attention deficit hyperactivity disorder in children and adolescents: Overview of treatment and prognosis. UpToDate. Published 2024. Accessed May 2025.https://www.uptodate.com
8. The History of ADHD and Its Treatments, https://www.additudemag.com/history-of-adhd/
9. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Future 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 that I will explain in just a bit. But overall the disorder is most simply characterized by a significant degree of difficulty in paying attention, controlling impulsive behaviors, or in being overly active in a way that the individual finds very difficult to control. (CDC)

Arreaza: How common is ADHD?

Steph: The most recently published data from The CDC estimates that 7 million (11.4%) of U.S. children between the ages of 3 and 17 have been diagnosed with ADHD. For adults, it is estimated that there are 15.5 million (6%) individuals in the U.S. who currently have ADHD. 

Arreaza: I suspected it would be more than that. [Anecdote about Boy Scout camp]. 

Steph: I totally agree. With short videos on TikTok, or paying high subscription fees to skip ads, it feels like as a society we all have a shorter attention span. 

Arreaza: Even churches are adapting to the new generation of believers: Shorter sermons and shorter lessons.

Steph: When it comes to better understanding these numbers, it's also important to know that there are three distinct presentations of ADHD recognized by The CDC and The World Health Organization. 

Arreaza: The DSM-5 TR no longer uses the word “subtypes” for ADHD. Instead, it uses the word "presentation" to describe the different ways that ADHD may manifest in a person. That reminded me to update my old DSM-5 manual and I ordered it while reading today about ADHD. This means people with ADHD are no longer diagnosed as having a “subtype”. Instead, they are diagnosed with ADHD and a certain “presentation” of symptoms.

Steph: These presentations are:

Inattentive Type

People often have difficulty planning or completing tasks

They find themselves easily distracted (especially when it comes to longer, focus-oriented tasks)

They can often forget details and specifics, even with things that are part of their daily routine

This used to be referred to as “ADD” (you’ll notice the absence of an “H”, segue).

Hyperactive-Impulsive Type

People often have a sense of intense “restlessness”, noticeable even in calm environments.

They tend to be noticeably more talkative, and might often be seen interrupting others, or finishing their sentences.

They find significant difficulty in being still for extended periods. Because of this, they are often unable to sit through a movie or class time, without fidgeting or getting up and moving around.

With this category of ADHD, we often see an impulsiveness that unwittingly leads to risky behavior. Because of this, accidents and bodily injury are more common in individuals with this type of ADHD.

Combined Type

These are individuals who exhibit symptoms from both “Inattentive” and “Hyperactive-Impulsive” ADHD equally.

Some listeners might have noticed that the categories are quite different, meaning that ADHD presents in different ways depending on the person! Two people who have ADHD can be in the same room and have vastly different presentations, whilst still having many of the same types of challenges. You also might have noticed what makes the discussion so interesting to the general public, which is also the thing that makes speaking to a professional to get formally tested so important:

The diagnostic criteria rely heavily on patterns of behavior, or external variables; rather than on how a person might feel, or certain measurements taken from lab tests.

Arreaza: Diagnosing ADHD requires evaluation by a professional who is properly trained for this. Fortunately, we have tools to assist with the diagnosis. The attention deficit must be noted in more than one major setting (e.g., social, academic, or occupational), that’s why the information should be gathered from multiple sources, including parents, teachers, and other caregivers, using validated tools, such as:

• The Neuropsychiatric EEG-Based ADHD Assessment Aid (NEBA), recommended by the American Academy of Neurology
• The Vanderbilt ADHD Diagnostic Parent Rating Scale (VADPRS) and the Vanderbilt ADHD Diagnostic Teacher Rating Scale (VADTRS), recommended by the Society for Developmental and Behavioral Pediatrics.
• For adults: The validated rating scales include the Adult ADHD Self-Report Scale (ASRS) and the Conners Adult ADHD Rating Scales (CAARS).

Steph: This is important because nearly everyone alive has experienced several, if not most, of these behavioral patterns at least once. Whether or not an individual has ADHD, I’m certain we could all think of moments we’ve had great difficulty focusing or sitting still. Perhaps some of us are incredibly forgetful, or act more impulsively than the average person might find typical. Getting a professional diagnosis is important because it is in skillfully assessing “the bigger picture” of a person’s life, or their patterns of behavior, that a skilled physician, who understands the nuances and complexities in these disorders, can properly tell each of us whether we have ADHD, or not.

Essentially, most of us could stand to use a bit more focus these days, but far fewer of us would meaningfully benefit from the kinds of treatments and therapies needed by individuals with ADHD to live healthier, more happy and regulated lives.

Arreaza: I had a mother who came to discuss the results of the Vanderbilt Questionnaire. I think she left a little disappointed when she heard that, based on the responses from her and the teacher, her son did not have ADHD. Some kids may have behaviors such as being distracted during a meeting, forgetting about homework or having a lot of energy, but that does NOT mean necessarily that they have ADHD, right?

Steph: Absolutely! The important thing to remember here is that these patterns of behavior outlined in the DSM-5 are merely an external gauge for a neurological reality. What the science is showing us is that the brains of people with ADHD are wired differently than that of the more “neurotypical” brain. Much like a check engine light would serve as a signal to a driver that something under the hood needs attention; these patterns of behavior, when they begin impeding our day to day lives, might tell us that it’s time to see a professional (whether it be an auto mechanic or a trained physician). I think we all know someone who drives with their check engine light and not a care in the world. 

Arreaza: How serious/urgent is ADHD? Why should we care to make the diagnosis?

Steph: Although we’ve yet to see anyone incur harm solely from having ADHD, it does lead to quite a range of more serious issues, some of which might prove more urgent. In the cases of ADHD, specifically, what we know is that there is a notable degree of dysregulation in some key neurotransmitters, like dopamine and norepinephrine. More plainly, what we are seeing in the brains of people with ADHD is a disruption, or alteration, of some of the brain’s key chemicals.

These neurotransmitters are largely responsible for much-needed processes like Motivation, Satisfaction, Focus, Impulse control, even things like energy and feelings of happiness. Many of these things serve as “fuel” for our day-to-day lives; things we’d call our “executive function”.  These are also what prove dysfunctional in those struggling with ADHD. It is in this sense that we might be able to bridge a meaningful gap between ADHD as being seen through 

patterns of behavior

that signal a 

real, neurological reality.

Steph: We often hear of the brain referenced as a kind of supercomputer. A more accurate assessment might be that the brain is more of a network of interconnected computers that run different processes and require continual communication with one another for our brain to function properly and seamlessly. What we’re seeing in members of the population with this diagnosis, is a significant disruption in these lines of communication. Although this is a very broad oversimplification, for the purposes of our metaphor is to think of it like our brain chemicals getting caught in a traffic jam, or parts of our brain attempting to communicate to one another with poor cell signal. 

Arreaza: Making the diagnosis is critical to start treatment because having that level of dysfunction sounds like having a very difficult life.

Steph: Yeah! I think that’s why this conversation matters so much. There’s a sense of urgency there, because much of life is, in fact, boring. Things like paying bills, exercising and eating well, work and school—these are all things that are vital to health and wellbeing in day-to-day life; and for the more neurotypical brain, these things might prove occasionally challenging. Yet, they are still doable. For those with ADHD however, this goes far beyond mere boredom or “laziness” (which proves to be a trigger term for many—more on that in just a bit).

For folks listening, I wanted to offer some statistics that show why this is such a big concern for the public, whether one has a formal ADHD diagnosis or not. 

The facts are figures are:

• Children with ADHD are more than five times as likely as the child without ADHD to have major depression.
• A significant increase in the prevalence of anxiety is seen in ADHD patients, ranging from 15% to 35%, when accounting for overlap in symptoms.
• There are significant correlations in youth diagnosed with ADHD, and those diagnosed with what are known as “externalizing disorders”. These are things like Conduct Disorder, Disruptive Mood Dysregulation Disorder, and Oppositional Defiant Disorder.
• We are seeing a much higher rate of academic problems in kids who have ADHD, like reading disorder, impaired verbal skills, and visual motor integration.

We’re finding that many, if not most, of these connections are being made after diagnosis. In the case of the “internalized disorders”, like depression and anxiety, we’re often seeing years between ADHD diagnoses and the diagnoses of major depressive disorder or anxiety disorders. Given this framework, much of the data is theorized to point towards what we call “negative environmental circumstances”, otherwise known as “ADHD-related demoralization”.

For children, this often looks like struggling with sitting still during class, failing to get homework done (because they forgot, or couldn’t focus on the tasks at hand), and struggling to focus their attention on what their teacher is saying during lecture. These things often lead to bad grades, discipline or forced time sitting still in detention. This can be seen in more problems at home, with children being disciplined often for behavior that they struggle immensely to control.

For adults, this can mean forgetting to pay your bills, missing work meetings, having trouble making appointments, or having difficulty with day-to-day tasks, really anything that requires sustained attention. We often see adults with ADHD who are chasing normalcy with caffeine addictions or even struggling with substance use. 

Arreaza: Substance use disorder actually can be a way for some people living with ADHD to self-treat their symptoms. 

Steph: These differences between the individual’s experience and the world around them can lead to really powerful feelings of failure or inadequacy. They can affect your social life, your sense of community, and even further limit your capacity to seek help.

Literacy in these things is so important—not just for the individual who feels that they may have ADHD, but also for those who are likely to encounter people with ADHD in their own lives. Understanding why some of these patterns pop up, even those who might not have a formal diagnosis, can go a long way to properly approaching these behaviors with success and with empathy.

Arreaza: Learning about ADHD is fundamental for primary care doctors. We talked about the high prevalence and the influence of the media in increasing awareness and sometimes increasing public panic. So, we have to be prepared to diagnose or undiagnosed ADHD. 

Steph: Whether we’re the physicians in the room, or the patient in the chair, I think it’s important to have a clear understanding of what ADHD is and how it can affect lives. Thanks for listening, I hope we were able to teach you a little more about ADHD. 

______________

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_______________

References:

1. NICHQ-Vanderbilt-Assessment-Scales PDF: https://nichq.org/wp-content/uploads/2024/09/NICHQ-Vanderbilt-Assessment-Scales.pdf
2. ADHD: The facts. ADDA - Attention Deficit Disorder Association. (2023, January 11). https://add.org/adhd-facts/
3. American Psychiatric Association, DSM-5 Task Force. (2013). Diagnostic and statistical manual of mental disorders: DSM-5™ (5th ed.). American Psychiatric Publishing, Inc. https://doi.org/10.1176/appi.books.9780890425596.
4. Gnanavel S, Sharma P, Kaushal P, Hussain S. Attention deficit hyperactivity disorder and comorbidity: A review of literature. World J Clin Cases. 2019 Sep 6;7(17):2420-2426. doi: 10.12998/wjcc.v7.i17.2420. PMID: 31559278; PMCID: PMC6745333.
5. Staley BS, Robinson LR, Claussen AH, et al. Attention-Deficit/Hyperactivity Disorder Diagnosis, Treatment and Telehealth Use in Adults — National Center for Health Statistics Rapid Surveys System, United States, October – November 2023. CDC.Gov, MMWR Morb Mortal Wkly Rep 2024;73:890-895.
6. Danielson ML, Claussen AH, Arifkhanova A, Gonzalez MG, Surman C. Who Provides Outpatient Clinical Care for Adults With ADHD? Analysis of Healthcare Claims by Types of Providers Among Private Insurance and Medicaid Enrollees, 2021. J Atten Disord. 2024 Jun;28(8):1225-1235. doi: 10.1177/10870547241238899. Epub 2024 Mar 18. PMID: 38500256; PMCID: PMC11108736. https://pubmed.ncbi.nlm.nih.gov/38500256/
7. Mattingly G, Childress A. Clinical implications of attention-deficit/hyperactivity disorder in adults: what new data on diagnostic trends, treatment barriers, and telehealth utilization tell us. J Clin Psychiatry. 2024;85(4):24com15592. https://www.psychiatrist.com/jcp/implications-adult-adhd-diagnostic-trends-treatment-barriers-telehealth/
8. Didier J. My four kids and I all have ADHD. We need telehealth options. STAT News. Published October 10, 2024. Accessed October 10, 2024. https://www.statnews.com/2024/10/10/adhd-medication-shortage-telehealth-dea-congress/.
9. Hong J, Mattingly GW, Carbray JA, Cooper TV, Findling RL, Gignac M, Glaser PE, Lopez FA, Maletic V, McIntyre RS, Robb AS, Singh MK, Stein MA, Stahl SM. Expert consensus statement for telepsychiatry and attention-deficit hyperactivity disorder. CNS Spectr. 2024 May 20:1-12. doi: 10.1017/S1092852924000208. Epub ahead of print. PMID: 38764385. https://pubmed.ncbi.nlm.nih.gov/38764385/
10. Gabor Maté: The Myth of Normal: Trauma, Illness, and Healing in a Toxic Culture. (2022). Youtube. Retrieved April 27, 2025, from https://www.youtube.com/watch?v=ttu21ViNiC0. 
11. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Future 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.

Epidemiology

Before 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.

Pathophysiology

The 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 Presentation

The classic presentation of measles can be remembered in three C’s:

● Cough

● Coryza (runny nose)

● Conjunctivitis

Course 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 individuals

Diagnosis

Clinical 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. 

Management

There 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 hypoxic

Vitamin 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 necessary for:

● Severe respiratory compromise

● Dehydration

● Neurologic complications

Prevention: We live in perilous times and vaccination is under scrutiny right now. Before the measles vaccine, about 48,000 people were hospitalized and 400–500 people died in the United States every year. Measles was declared eradicated in the US in 2000, but the vaccination coverage is no longer 95%. How do we prevent measles?

Vaccination is the cornerstone of prevention.

● MMR vaccine (Measles, Mumps, Rubella):

○ First dose at 12-15 months of age.

○ Second dose at 4-6 years of age.

○ 97% effective after 2 doses.

The Advisory Committee on Immunization Practices (ACIP) has noted that febrile seizures typically occur 7 to 12 days after vaccination with MMR, with an estimated incidence of 3.3 to 8.7 per 10,000 doses. The Centers for Disease Control and Prevention (CDC) states that febrile seizures following MMR vaccination are rare and not associated with any long-term effects. The risk of febrile seizures is higher when the MMR vaccine is administered as part of the combined MMRV (measles, mumps, rubella, and varicella) vaccine compared to the MMR vaccine alone.

Post-exposure prophylaxis:

● MMR vaccine within 72 hours of exposure (if possible).

● Immunoglobulin within 6 days for high-risk individuals (e.g., infants, pregnant women, immunocompromised).

Herd immunity requires at least 95% vaccination coverage to prevent outbreaks.

Key Takeaways

● Measles is a highly contagious viral illness that can lead to severe complications.

● Diagnosis is often clinical, but lab confirmation helps with public health tracking.

● Treatment is mainly supportive, with Vitamin A playing a critical role in reducing complications.

● Vaccination remains the most effective tool to eliminate measles worldwide.

While measles might seem like a disease of the past, it can make a dangerous comeback without continued vigilance and vaccination efforts.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. Centers for Disease Control and Prevention (CDC). Measles (Rubeola), Clinical Overview, July 15, 2024. Accessed on May 1, 2025. https://www.cdc.gov/measles/hcp/clinical-overview/index.html.
2. World Health Organization (WHO). Measles, November 14, 2024. https://www.who.int/news-room/fact-sheets/detail/measles
3. Gans, Hayley and Yvonne A. Maldonado, Measles: Clinical manifestations, diagnosis, treatment, and prevention, UpToDate, January 15, 2025. Accessed on May 1, 2025. https://www.uptodate.com/contents/measles-clinical-manifestations-diagnosis-treatment-and-prevention
4. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

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 Practice

Ramadan 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 fats
• Avoid greasy, heavy foods right after fasting
• Light exercise (such as a walk) after iftar is beneficial
• Review 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 Performance

Intermittent 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 IF

Hormonal Effects of IF: In addition to improving insulin sensitivity, IF also affects hormones such as ghrelin (which stimulates hunger, remember it as growling) and leptin (which signals fullness). Over time, IF may help the body regulate appetite better and reduce cravings. IF can also decrease morning cortisol levels, the stress hormone. That’s why it's important to monitor sleep, hydration, and stress levels when recommending IF.

Circadian Rhythm Alignment:

 Emerging research shows that aligning eating times with natural light/dark cycles—eating during the day and fasting at night—can improve metabolic outcomes. This practice, known as early time-restricted eating (eTRE), has been shown to lower blood glucose, reduce insulin levels, and improve energy use. Patients who eat earlier in the day tend to have better results than those who eat late at night.

Myths and Clarifications on IF:

-“Fasting slows metabolism” In fact, short-term fasting may boost metabolism slightly due to increased norepinephrine. 

-“You can’t exercise while fasting.” Many people can safely train during fasted states, especially for moderate cardio or strength training. 

-“Skipping breakfast is bad.” For some, skipping breakfast is a useful IF strategy—as long as total nutrition is maintained. You can break your fast at 2:00 pm, it does have to be at 7:00 AM.

What to Eat When Breaking a Fast

Breaking a fast properly is just as important as fasting itself. Whether it’s after a Ramadan fast or a 16-hour fast, the goal is to replenish energy gently and restore nutrients.

Ideal foods to break a fast:

• Dates and water: provide quick energy, potassium, and fiber
• Soups: lentil or broth-based soups are gentle on digestion
• Complex carbs: whole grains like brown rice or oats
• Lean proteins: chicken, fish, eggs, legumes
• Fruits and vegetables: hydrate and provide fiber
• Healthy fats: nuts, avocado, olive oil
• Probiotics: yogurt or kefir for gut support

Balanced meals with carbs, protein, and healthy fats help the body transition smoothly back to a fed state.

Using IF in Family Medicine and Community Health

Intermittent fasting can be a practical, cost-effective strategy in family medicine. In areas with high rates of obesity and diabetes, like Kern County, IF offers a lifestyle-based tool to improve metabolic health, especially in underserved populations. IF is free!

How IF can help in family medicine:

• Lower A1c levels: improves insulin sensitivity and glucose control
• Promote weight loss: decreases insulin resistance and inflammation
• Reduce medication dependence: fewer meds needed over time for some patients
• Encourage patient engagement: flexible and easier to follow than strict calorie counting
• Fit diverse lifestyles: aligns with religious and cultural practices
• Address food insecurity: structured eating windows can help patients stretch limited food resources

How to apply IF in clinic:

• Start the conversation by asking if the patient has heard of IF
• Recommend simple starting points: 12:12 or 14:10
• Emphasize hydration and nutrient-dense meals
• Monitor labs and symptoms, especially in diabetic patients
• Adjust medications to avoid hypoglycemia
• Provide follow-up and patient education handouts if possible

What if a patient isn't ready to try fasting?

• For those not ready to commit to intermittent fasting, one effective alternative is walking after meals. A simple 10–20 minute walk post-meal can help stimulate GLUT4 receptors in skeletal muscle, promoting glucose uptake independent of insulin. This reduces the demand on pancreatic beta cells and may help improve blood sugar control over time. This strategy is particularly useful for patients with insulin resistance or early-stage type 2 diabetes.

Conclusion: 

Intermittent fasting is not one-size-fits-all, but it can be a powerful tool for both individual and community health. From Ramadan to race day, IF has a place in family medicine when used thoughtfully. Encourage patients to work with their healthcare providers to find an approach that fits their lifestyle, medical needs, and personal values. IF is a cost-effective tool

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. American Academy of Family Physicians. (2022). "Intermittent Fasting: A Promising Treatment for Diabetes." AAFP Community Blog. https://www.aafp.org/pubs/afp/afp-community-blog/entry/intermittent-fasting-a-promising-treatment-for-diabetes.html
2. Healthline. (2023). "What Breaks a Fast? Foods, Drinks, and Supplements." https://www.healthline.com/nutrition/what-breaks-a-fast.
3. Sarri KO, Tzanakis NE, Linardakis MK, Mamalakis GD, Kafatos AG. Effects of Greek Orthodox Christian Church fasting on serum lipids and obesity. BMC Public Health. 2003 May 16;3:16. doi: 10.1186/1471-2458-3-16. PMID: 12753698; PMCID: PMC156653. https://pmc.ncbi.nlm.nih.gov/articles/PMC156653/.
4. Shang, Y., et al. (2024). "Effects of Intermittent Fasting on Obesity-Related Health Outcomes: An Umbrella Review." eClinicalMedicine.https://www.thelancet.com/journals/eclinm/article/PIIS2589-5370(24)00098-1.
5. Abaïdia AE, Daab W, Bouzid MA. Effects of Ramadan Fasting on Physical Performance: A Systematic Review with Meta-analysis. Sports Med. 2020 May;50(5):1009-1026. doi: 10.1007/s40279-020-01257-0. PMID: 31960369. https://pubmed.ncbi.nlm.nih.gov/31960369/.
6. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Dr. 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 RSV

Some 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 oxyhemoglobin saturation exceeds 90% in infants and children with a diagnosis of bronchiolitis (Evidence Quality: D; Recommendation Strength: Weak Recommendation [based on low level evidence and reasoning from first principles]).

-Clinicians should administer nasogastric or intravenous fluids for infants with a diagnosis of bronchiolitis who cannot maintain hydration orally (Evidence Quality: X; Recommendation Strength: Strong Recommendation).

How do we prevent RSV?

Infant Immuno-prophylaxis:

A clinical trial in 2022 demonstrated that a single injection of nirsevimab (Beyfortus®), administered before the RSV season, protected healthy late-preterm and term infants from RSV-associated lower respiratory tract that required medical treatment. Nirsevimab is a monoclonal antibody to the RSV fusion protein that has an extended half-life.

Additionally, on August 3, 2023, the Advisory Committee on Immunization Practices (ACIP) recommended nirsevimab for all infants younger than 8 months who are born during or entering their first RSV season and for infants and children between 8-19 months who are at increased risk for severe RSV disease and are entering their second RSV season. On the basis of pre-COVID-19 pandemic patterns, nirsevimab could be administered in most of the continental United States from October through the end of March.

Maternal Vaccination: 

The CDC recommends the administration of the RSVPreF vaccine to pregnant women between 32 0/7 and 36 6/7 weeks of gestation. This vaccination aims to reduce the risk of RSV-associated lower respiratory tract infection in infants during the first 6 months of life.

At this time, if a pregnant woman has already received a maternal RSV vaccine during any previous pregnancy, CDC does not recommend another dose of RSV vaccine during subsequent pregnancies.

Older individuals: 

-Each year in the U.S., it is estimated that between 60,000 and 160,000 older adults are hospitalized and between 6,000 and 10,000 die due to RSV infection

-ABRYSVO’s approval will help offer older adults protection in the RSV season.

-On June 26, 2024, ACIP voted to give these recommendations: all adults older than 75 years and adults between 60–74 years who are at increased risk for severe RSV disease should receive a single dose of RSV vaccine (Abrysvo®).

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. Hamid S, Winn A, Parikh R, et al. Seasonality of Respiratory Syncytial Virus — United States, 2017–2023. MMWR Morb Mortal Wkly Rep 2023;72:355–361. DOI: http://dx.doi.org/10.15585/mmwr.mm7214a1
2. Hammitt LL, Dagan R, Yuan Y, Baca Cots M, Bosheva M, Madhi SA, Muller WJ, Zar HJ, Brooks D, Grenham A, Wählby Hamrén U, Mankad VS, Ren P, Takas T, Abram ME, Leach A, Griffin MP, Villafana T; MELODY Study Group. Nirsevimab for Prevention of RSV in Healthy Late-Preterm and Term Infants. N Engl J Med. 2022 Mar 3;386(9):837-846. doi: 10.1056/NEJMoa2110275. PMID: 35235726.
3. Ralston SL, Lieberthal AS, Meissner HC, Alverson BK, Baley JE, Gadomski AM, Johnson DW, Light MJ, Maraqa NF, Mendonca EA, Phelan KJ, Zorc JJ, Stanko-Lopp D, Brown MA, Nathanson I, Rosenblum E, Sayles S 3rd, Hernandez-Cancio S; American Academy of Pediatrics. Clinical practice guideline: the diagnosis, management, and prevention of bronchiolitis. Pediatrics. 2014 Nov;134(5):e1474-502. doi: 10.1542/peds.2014-2742. Erratum in: Pediatrics. 2015 Oct;136(4):782. doi: 10.1542/peds.2015-2862. PMID: 25349312.
4. CDC, per their published article Seasonality of Respiratory Syncytial Virus — United States for 2017–2023, in the United States
5. What U.S. Obstetricians Need to Know About Respiratory Syncytial Virus.Debessai H, Jones JM, Meaney-Delman D, Rasmussen SA. Obstetrics and Gynecology. 2024;143(3):e54-e62. doi:10.1097/AOG.0000000000005492.
6. Maternal Respiratory Syncytial Virus Vaccination and Receipt of Respiratory Syncytial Virus Antibody (Nirsevimab) by Infants Aged <8 Months - United States, April 2024.Razzaghi H, Garacci E, Kahn KE, et al. MMWR. Morbidity and Mortality Weekly Report. 2024;73(38):837-843. doi:10.15585/mmwr.mm7338a2. 
7. Use of Nirsevimab for the Prevention of Respiratory Syncytial Virus Disease Among Infants and Young Children: Recommendations of the Advisory Committee on Immunization Practices - United States, 2023.Jones JM, Fleming-Dutra KE, Prill MM, et al. MMWR. Morbidity and Mortality Weekly Report. 2023;72(34):920-925. doi:10.15585/mmwr.mm7234a4.
8. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Future 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' thoughts and feelings.

- Nonverbal communicative behaviors to socialize, such as using aspects with eye contact, facial expressions, gestures, and tone of voice, which makes communication more difficult.

- Difficulty developing, understanding, and maintaining relationships: This could manifest as difficulty adjusting behavior to social settings, an inability to show expected social behaviors, a lack of interest in socializing, or difficulty making friends despite wanting to.

Two or more of the following Cluster B symptoms:

- Stereotyped or repetitive movements, use of objects, or speech: Echolalia or flapping the hands repeatedly.

- Persistent sameness, where patients require adherence to routines or ritualized patterns of behavior, such as difficulty with transitions or a need to eat the same food each day.

- Highly restricted, fixated interests: This may include an intense focus on specific objects (trains) or topics (such as dinosaurs or natural disasters).

- Sensory response variations, including heightened or diminished responses to sensory input, such as adverse reactions to sounds, indifference to temperature, or excessive touching/smelling of objects.

Additionally, the symptoms must:

- Significantly impair social, academic/occupational, and daily functioning,

- Not be better explained by intellectual disability or global developmental delay, and

- Be present in early childhood. (However, symptoms may only become apparent when social demands exceed the child's capacity; in later life, they may be masked by learned strategies.)

How can we go about managing autism?

There is no "cure" for Autism. However, various therapies can help manage the condition. Treatment tailors to the individual's age, strengths, and weaknesses. Our main goal is to maximize function, encourage independence, and improve the patient's overall quality of life.

During office visits as primary care doctors, we have to use different strategies to make the visits more focused on individual needs, making sure the caregivers are involved as well as the patient. 

We communicate with caregivers before and during the visit to optimize patient compliance, allow enough time for the family/caregiver to talk about the patient's history, allow the patient to play with instruments/materials provided, and use simple instructions. Sometimes, the physical exam can be the most challenging aspect of the exam because it is so overstimulating for the patient. Hence, allowing enough time for the patient to be comfortable is key.

This is a multidisciplinary management that includes, family med, pediatricians, social workers, behavioral health, etc.

Personal experiences interacting and managing patients with autism in the clinic or in the hospital:

Dr. Arreaza: I have seen a lot of adult patients with autism.I see a challenge commonly found is agitation and the use of medications. I prefer to defer any prescriptions to psychiatry, if needed, but behavioral concerns can be successfully managed by behavioral health with participation of family, caregivers, and especial education.

TJ:  Personal story with Auditory Processing Disorder (APD).

Conclusions: 

Dr. Arreaza: Autism is a spectrum, not all persons with ASD are the same. They are not all geniuses, and they are not all developmentally delayed, they are not just black or white, but there are several shades of gray in between. 

TJ:  Not one doctor or one family will take care all responsibility, it requires a multifaceted approach.People with autism can live a long and meaningful lives.

Thank you for listening to this week’s episode on Autism. We will see you next time.  Have a nice day.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. Centers for Disease Control and Prevention. Data and statistics on autism spectrum disorder. CDC.gov. Accessed on March 13, 2025. https://www.cdc.gov/autism/data-research/index.html
2. Weissman Hale, Laura, “Autism spectrum disorder in children and adolescents: Overview of management and prognosis,” UpToDate, accessed on March 13, 2025. https://www.uptodate.com/contents/autism-spectrum-disorder-in-children-and-adolescents-overview-of-management-and-prognosis.
3. Volkers, N. (2016). Early Signs. The ASHA Leader.https://doi.org/10.1044/leader.ftr1.21042016.44
4. Urquhart-White, Alaina, “'The Good Doctor' Puts The Spotlight On A Rare, Mysterious Syndrome,” Bustle, September 25, 2017. https://www.bustle.com/p/whats-real-about-savant-syndrome-is-something-the-good-doctor-should-explore-2439405
5. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Dr. 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 Prescription

Arreaza: 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 Exercise

Arreaza: 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 Exercise

Arreaza: 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 can adapt exercises—low-impact options like swimming or chair exercises work well.

No access to a gym: Many exercises require no equipment—walking, stair climbing, bodyweight exercises.

Ranbir: As physicians, we need to normalize movement as part of daily life rather than an all-or-nothing approach.

Segment 5: The Role of Healthcare Providers in Exercise Counseling

Arreaza: We often focus on medications and procedures, but exercise is one of the best treatments we have. What role should physicians play in promoting physical activity?

Ranbir: Our role is critical! Exercise is preventive medicine and can reduce the risk of heart disease, diabetes, obesity, and even depression. As physicians, we can:

-Ask about exercise levels at routine visits.

-Provide specific, personalized exercise prescriptions rather than just saying 'you should exercise more.'

-Address patient concerns by modifying recommendations to their abilities.

-Follow up and reinforce progress like we would with any other treatment.

-Even a brief conversation about physical activity can significantly impact patient motivation and adherence.

Arreaza: Exercise vs physical activity. Ask your patients as a routine. 

Closing Thoughts & Call to Action

Arreaza: Ranbir andWessam, this has been a fantastic discussion. Any final thoughts for our listeners?

Ranbir: My biggest takeaway is that any movement is better than none. Exercise doesn’t have to be perfect—it just has to be consistent. Start small, find an activity you enjoy, and build from there!

Arreaza: Any take-home message, Wes?

Wes: Same for me, find an activity you enjoy, start where you are, and keep moving!

Arreaza: Great advice! If you found this episode helpful, share it with your colleagues and patients. 

Ranbir: Until next time—stay active and stay healthy!

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

Sources:

1. Some information in this podcast was inspired by conferences from the Obesity Medicine Association, https://obesitymedicine.org/.
2. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

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.

Interview

Arreaza: Question 1: 

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:

1. 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 the community’s location and interests. 

But in the long run, education and motivation will be the biggest interventions. People need to know more about their bodies over time, because preparing for aging takes knowledge and starts in one’s thirties or forties. This means establishing an exercise habit which will endure for decades and is consistent with one’s responsibilities to one’s family and one’s job. It must work and be doable over time. 

Arreaza: So, we must develop an exercise routine that we enjoy, it’s challenging, and sustainable over decades. Brain exercise also works (new ways to go to work, learning a new language, etc.)

Schlaerth: -Eating habits must be changed, which will involve less eating out and more home cooking. 

TJ: [As much as I enjoy a good In-N-Out burger, nothing beats a home cooked meal. Aside from controlling the ingredients for individualized diets/spice levels, cooking for me is therapeutic and helps relieve stress, especially when I cook Indian food (my specialty).] 

Schlaerth: Choosing the right lifelong partner and staying married is a big help. That may also require a bit of education, starting in childhood! All studies show that being married prolongs life!

Tongue in cheek, I would suggest choosing the right location to settle down. Los Angeles and New York City don’t currently look like stress free places to live. That may change though.

Arreaza: I guess if you have a good social support in those cities, it may work. What else can we recommend our patients?

Schlaerth: People who are happy and optimistic and have lots of friends and family statistically do well. Join your local church, synagogue, temple, mosque, etc. Living according to your code of ethics and beliefs with others who share these is always reinforcing and offers support in times of trouble. 

One recently widowed octogenarian who had had a very strong and fulfilling marriage knew that she had to reinvent purpose in her life. So, she became the neighborhood unofficial social worker. Did a friend’s child need a place to stay until he or she got their own apartment? Come on over, there’s an extra bedroom. Was a trip to the doctor needed by someone who couldn’t drive? Let’s go! 

Another widow opened her home to students at a university, charging rent and becoming a “mother hen” to her student lodgers.

A man who loved aeronautics served as a docent for a local museum and became a fount of information about the intricacies of World War II planes right down to structural details. 

All of these and similar strategies kept people interested and interesting, promoted exercise and took a bit of creativity and yes, energy.

Arreaza: So, to slow down aging, stay physically, spiritually, and mentally active. Question 3:

1. Why are people so afraid of aging? 

(TJ: There are some concepts we can introduce for discussion: 
-Gerascophobia is an abnormal or incessant fear of growing older or ageing. 
-Gerontophobia is the hatred or fear of the elderly. 
-Ageism refers to age discrimination) 

Schlaerth: There are very personal and idiosyncratic reasons for a fear of aging. 

One gentleman saw his wife die a painful death from cancer and this triggered his fear.

Another saw his grandparents age and had to help care for them. Sometimes this kind of experience can engender love and respect for one’s older family members, and sometimes the opposite. 

-One’s teeth leave, food is no longer palatable, balanced precludes getting a kid’s ball off your roof, constipation and aches are a daily struggle, even the TV shows you loved are now old reruns. You no longer feel welcome in this new world. And anyway, you can’t drive at night, and you can’t hear well enough in a crowd to join in a restaurant conversation.

-But probably the biggest reasons include a loss of function and autonomy (the Bible even alludes to this fear!), loss of employment and loneliness when one’s friends and especially one’s lifelong partner are no longer there.

-Cultural change can also be a factor. The community one grew up in no longer exists. Communication is by computer or cell phone and much too complicated to learn. The old lot where baseball was played so long ago is now a derelict and abandoned shopping center! 

-You don’t look beautiful anymore.

-A strong religious faith often mitigates a lot of these fears. 

TJ: Question 4:

1. How can we fight age discrimination (ageism) in our clinics, hospitals, and society?

Schlaerth: The humanity of each person needs to be recognized. It is said that people feel about 20 years younger than their chronologic age. This may not be true for children, teenagers, or young adults though. 

When interacting with older folk, the need for environmental issues like good illumination, comfort, clear and low-pitched speech, the absence of extraneous noise, eye contact should be addressed to facilitate communication. If a younger person accompanies the older person, address at least some comments specifically to the older person. 

Allow time for a slower gait or response to questions. 

If possible, add a small complement that acknowledges the senior’s personality or accomplishment. For example, an older lady with her daughter was left out of a conversation about her health because she was deaf, spoke a language other than English, and couldn’t recall the particulars of a recent visit to a specialist. However, she’d raised 13 children who were all gainfully employed raising their own children and assets to society. When she was praised for this monumental accomplishment in the face of scanty resources, she brightened up like a wilted flower given water. 

-In society, again let older people perform when they have the capacity, be this in the workplace, the home, or in a social situation. Recognize everyone’s humanity, even if it means just smiling at an elderly man in a wheelchair. And if the old lady can cross the street by herself, let her do so, even if you are a boy scout!

Arreaza: In summary, treat your elderly patients with dignity and acknowledge them. Question 5.

1. Give us three fundamentals of aging for primary care.

Schlaerth:

• Help people in their thirties and forties prepare for old age by evaluating genetic and other risk factors, attacking the early stages of chronic diseases, encouraging lifelong good habits and working on eliminating bad ones, and vaccinate early.
• Help people maintain function as long as possible, even if total cure is no longer possible.
• Recognize the humanity and need for recognition in every person no matter how old and frail.

TJ: Let’s talk about your book: What was your motivation to write it? 

Arreaza: What is the basic message of your book? 

TJ: Give advice to new or aspiring writers or medical authors. 

Arreaza: The book can be found in Amazon: The Ways our Bodies Age by Katherine Schlaerth, MD.

Conclusions:

Arreaza: My take-home point for this episode is that aging is a physiologic process that takes place at a different pace in every individual. We can slow down or speed up the process depending on many factors, such as genetics, diet, occupation, and physical activity. We all will undergo the process of aging. So, let’s be prepared and prepare our patients for that process with the advice given by Dr. Schlaerth.

TJ: I want to have smooth conversation with our patients about aging.

_____________________

References:

1. Schlaerth, Katherine R., The Ways Our Bodies Age, Archway Publishing, 2025. Available for purchase at Amazon.com.
2. Theme song, Works All The Time, by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Sub-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 <10 g/dL, or more than 2g/dL below normal, and 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 presentations are weakness, fatigue, increased bruising under the skin, reduced urine output, weakened bones that is likely prone to fractures, etc. And if multiple myeloma is highly suspected, a Bone Marrow biopsy should be done with testing for flow cytometry and fluorescent in situ hybridization (FISH). Actually, if any of the “Biomarkers of malignancy (SLIM)” is met we can also diagnose multiple myeloma even without the CRAB criteria. 

Jessica: The diagnosis is made if one or more of the following is found: >= 60% of clonal plasma cells on bone marrow biopsy, > 1 lytic bone lesion on MRI that is at least 5mm in size, or a biopsy confirmed plasmacytoma. 

Di: Imaging comes in at the final step especially if we able to find one or more sites of osteolytic bone destruction > 5mm on an MRI scan.

Jessica: What if the bone marrow biopsy returns > 10% of monoclonal plasma cells, but our patient doesn't have either the CRAB or the Biomarker criteria? 

Di: That’s actually a very good question, since Multiple Myeloma is part of a spectrum of plasma cell disorders. That’s when smoldering myeloma comes into play. It is a precursor of active multiple myeloma. Smoldering myeloma is further categorized as high-risk or low-risk based on specific criteria.

A less severe form is called Monoclonal Gammopathy of Undetermined Significance, or simply MGUS, with < 10% bone marrow involvement. Those are diagnoses we give once we rule out actual multiple myeloma, which are defined by the amount of M-protein in the serum.

Jessica:  When to get started on treatment? Multiple Myeloma is on a spectrum of plasma cells proliferative disorders, starting from MGUS to Smoldering Myeloma, to Multiple Myeloma and to  Plasma Cell Leukemia.  Close supervision/active watching is enough for MGUS and low risk Smoldering Myeloma. But once it has progressed to high-risk smoldering myeloma or to active Multiple Myeloma, chemotherapy is usually required. Some situations may require emergent treatment to improve renal function, reduce hypercalcemia, and to prevent potential infections.

Di: As of 2024, treatment of Multiple Myeloma comprises the Standard-of-Care approved by the FDA. In fact, the quadruple therapy is a combination of 4 different class of drugs that include a monoclonal antibody, a proteasome inhibitor, an immunomodulatory drug, and a steroid. 

Jessica: They are Darzalex (daratumumab), Velcade (bortezomib), Revlimid (lenalidomide) and dexamethasone.  Other treatment plans for Multiple Myeloma include chemotherapy, immunotherapy, radiation therapy (for plasmacytomas) and stem cell transplants. The patient will also be on prophylaxis acyclovir and Bactrim while on chemotherapy. Sometimes anticoagulants are also considered because the chemo increases the risk of venous thromboembolic events.

Di: Although the disease is incurable, but with the advancing of novel therapies and clinical trials patients with multiple myeloma are able to live longer.  Problem is the majority of patients diagnosed with Multiple Myeloma are older adults (>65), the risk of falling is adding to multiple complications of the disease itself, such as bone density loss, pain, neurological compromises, distress and weakness.  Palliative care may come in help at any point in time throughout the course of treatment but is most often needed at the very end of the course. Jessica, can you give us a conclusion for this episode?

Jessica: Multiple Myeloma may not be the most common cancer, but we have to be aware of the symptoms and keep it in our differential diagnosis for patients with bone pain, easy bruising, persistent severe headaches, unexplained renal dysfunction, and remember the CRAB: HyperCalcemia, Renal impairment, Anemia and Bone lesions.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. International Myeloma Foundation. (n.d.). International Myeloma Working Group (IMWG) criteria for the diagnosis of multiple myeloma. https://www.myeloma.org/international-myeloma-working-group-imwg-criteria-diagnosis-multiple-myeloma 
2. Laubach, J. P. (2024, August 28). Patient education: Multiple myeloma symptoms, diagnosis, and staging (Beyond the Basics). UpToDate. https://www.uptodate.com/contents/multiple-myeloma-symptoms-diagnosis-and-staging-beyond-the-basics.
3. University of California San Francisco. (n.d.). About multiple myeloma. UCSF Helen Diller Family Comprehensive Cancer Center. https://cancer.ucsf.edu/research/multiple-myeloma/about 
4. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Future 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.

Introduction

Jessica: 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 Boseman

Jessica: 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. 

Epidemiology

Jessica: 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 Factors

Jessica: 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 only 20% of early-onset CRC cases are linked to hereditary syndromes such as Lynch syndrome and familial adenomatous polyposis (FAP), individuals with a first-degree relative with CRC are at a significantly higher risk and should undergo earlier and more frequent screening (Stoffel & Murphy, 2023).

Arreaza: Also, there is a difference in incidence per gender assigned at birth, which is also not modifiable. The rate in the US was 33% higher in men (41.5 per 100,000) than in women (31.2 per 100,000) during 2015-2019. So, if you are a man, your risk for CRC is slightly higher. Protective factors, according to the ACS, are physical activity (no specification about how much and how often) and dairy consumption (400g/day). Jessica, let’s talk about how colon cancer presents in our younger patients.

Clinical Presentation and Challenges in Diagnosis

Jessica: Young-onset CRC is often diagnosed at advanced stages due to delayed recognition of symptoms. Common symptoms include:

• Rectal bleeding (often mistaken for hemorrhoids)
• Young individuals may ignore it, believe they do not have time to address it, or lack insurance to cover a comprehensive evaluation.
• Unexplained weight loss
• Fatigue or weakness
• Changes in bowel habits (persistent diarrhea or constipation)
• This may also be rationalized by dietary habits.
• Abdominal pain or bloating
• Iron deficiency anemia.

Arreaza: All those symptoms can also be explained by benign conditions, and colorectal cancer can often be present without clear symptoms in its early stages. 

Jessica: Yes, in young adults, symptoms may be dismissed by healthcare providers as benign conditions such as irritable bowel syndrome (IBS), hemorrhoids, or dietary intolerance, leading to significant diagnostic delays. 

Arreaza: We must keep a low threshold for ordering a colonoscopy, especially in patients with the risks we mentioned previously. 

Jessica: We may also be concerned about the risk/benefit of colonoscopy or diagnostic methods in younger adults, given the traditional low likelihood of CRC. Approximately 58% of young CRC patients are diagnosed at stage III or IV, compared to 43% of older adults (American Gastroenterological Association, 2024). Early recognition and prompt evaluation of persistent symptoms are crucial for improving outcomes. Empowering and informing young adults about concerning symptoms is the first step in better recognition and better outcomes for these individuals.

Arreaza: This is when the word “follow up” becomes relevant. I recommend you leave the door open for patients to return if their common symptoms worsen or persist. Let’s talk about screening. 

Screening and Prevention

Jessica: Due to the trend of CRC being identified in younger populations, the U.S. Preventive Services Task Force (USPSTF) lowered the recommended screening age for CRC from 50 to 45 in 2021 (USPSTF, 2021). Off the record, some Gastroenterologists also foresee the USPSTF lowering the age to 40. 

Arreaza: That is correct, it seems like everyone agrees now that the age to start screening for average-risk adults is 45. It took a while until everyone came to an agreement, but since 2017, the US Multi-Society Task Force had recommended screening at age 45, the American Cancer Society recommended the same age (45) in 2018, and the USPSTF recommended the same age in 2021. This podcast is a reminder that the age of onset has been decreased from 50 to 45, for average-risk patients, according to major medical associations.

Jessica: For individuals with additional risk factors, including a family history of CRC or chronic gastrointestinal symptoms, screening starts at age 40 or 10 years before the diagnosis of colon cancer in a first-degree relative. Dr. Arreaza, who has the lowest and the highest rate of screening for CRC in the US? 

Arreaza: The best rate is in Massachusetts (70%) and the lowest is California (53%). Let’s review how to screen:

Jessica: Recommended Screening Methods:

• Colonoscopy: Considered the gold standard for CRC detection and prevention, colonoscopy allows for identifying and removing precancerous polyps.
• Fecal Immunochemical Test (FIT): A non-invasive stool test that detects hidden blood, recommended annually.
• Stool DNA Testing (e.g., Cologuard): This test detects genetic mutations associated with CRC and is recommended every three years.

Arreaza: Computed tomographic colonography (CTC) is another option, it is less common because it is not covered by all insurance plans, it examines the whole colon, it is quick, with no complications. 

Conclusion:

Colorectal cancer is rapidly emerging as a serious health threat for young adults. The increase in cases over the past three decades highlights the urgent need for increased awareness, early symptom detection, and proactive screening. While healthcare providers must weigh the risk/benefit of testing for CRC in younger adults, patients must also be equipped with knowledge of concerning signs so that they may also advocate for themselves. Early detection remains the most effective tool in preventing and treating CRC, emphasizing the importance of screening and risk factor modification.

Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at RioBravoqWeek@clinicasierravista.org, or visit our website riobravofmrp.org/qweek. See you next week! 

_____________________

References:

1. American Cancer Society. (2024). Colorectal Cancer Statistics, 2024. Retrieved fromhttps://www.cancer.org
2. American Gastroenterological Association. (2024). Delays in Diagnosis of Young-Onset Colorectal Cancer: A Systemic Issue. Gastroenterology Today.
3. Brennan, C. A., & Garrett, W. S. (2023). Gut Microbiota and Colorectal Cancer: Advances and Future Directions. Gastroenterology.
4. Dekker, E., et al. (2023). Colorectal Cancer in Adolescents and Young Adults: A Growing Concern. The Lancet Gastroenterology & Hepatology.
5. Siegel, R. L., et al. (2023). Colorectal Cancer Statistics, 2023. CA: A Cancer Journal for Clinicians.
6. Stoffel, E. M., & Murphy, C. C. (2023). Genetic and Environmental Risk Factors in Young-Onset Colorectal Cancer. JAMA Oncology.
7. U.S. Preventive Services Task Force. (2021). Colorectal Cancer Screening Guidelines.
8. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.

Future 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.