Rio Bravo qWeek

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 [email protected], 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/.

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 [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

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 [email protected], 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/.

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 [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

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 [email protected], 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/.

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 [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

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 [email protected], 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/.

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 [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

Episode 197: Continuous Glucose Monitoring

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 [email protected], 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/.

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 [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

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.

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 [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

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 [email protected], 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/. 

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 [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

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 [email protected], 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/.

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 [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

Episode 193: Gestational Diabetes Intro

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]. 

_____________________

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/.

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 [email protected], or visit our website riobravofmrp.org/qweek. See you next week!

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 [email protected], 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/.

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 [email protected], or visit our website riobravofmrp.org/qweek. See you next week!