Episode 172: NAFLD and Obesity

28 juin · Rio Bravo qWeek

00:27:52

Future Dr. Nguyen explains the pathophysiology of non-alcoholic fatty liver disease and how it relates to obesity. Dr. Arreaza gives information about screening and diagnosis of NAFLD.

Written by Ryan Nguyen, MS4, Ross University School of Medicine. Comments by Hector Arreaza, MD.

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

Introduction/Pathophysiology
Nonalcoholic fatty liver disease (NAFLD) refers to the buildup of excess fat in liver cells, occurring without the influence of alcohol or drugs. Nonalcoholic steatohepatitis (NASH) represents a more severe form of NAFLD, characterized by inflammation and liver cell injury due to fat accumulation. If left untreated, NASH can progress to liver fibrosis or cirrhosis. Typically, NAFLD/NASH is diagnosed after other liver conditions are ruled out, making it a diagnosis of exclusion.

NAFLD -> NASH -> Cirrhosis -> Liver failure. Another term for NAFLD is metabolic dysfunction-associated steatotic liver disease.

Fatty liver disease is identified when more than 5% of liver weight consists of fat, whereas, NASH is diagnosed when this fat accumulation is accompanied by inflammation and liver cell injury, sometimes leading to fibrosis. Understanding these distinctions is crucial in recognizing and managing the spectrum of liver conditions associated with obesity and metabolic syndrome.

BMI serves as a tool to gauge body fat levels: individuals are categorized as normal weight if their BMI falls between 18.5 and 24.9, overweight if it ranges from 25 to 29.9. Class I obesity is diagnosed with a BMI of 30 to 34.9, class II obesity between 35 and 39.9, and class III obesity when BMI exceeds 40.

Obesity puts you at risk of NAFLD, but you can also see NAFLD in non-obese patients, but the prevalence is very low, about 5%. What did you learn about the demographics of NAFLD?

NAFLD is most widespread in regions like South Asia, the Middle East, Mexico, Central and South America, with prevalence rates exceeding 30%. In the United States, prevalence varies with approximately 23-27%, notably higher among Asians at 30%, followed by Hispanic individuals at 21%, White individuals at 12.5%, and Black individuals at 11.6%.

Across all racial groups, obesity plays a significant role, affecting more than two-thirds of individuals diagnosed with NAFLD. Understanding these demographics underscores the global impact of obesity on NAFLD prevalence.

Diagnosis: Screening/Labs/Imaging/Tools

The American Association for the Study of Liver Diseases does not recommend screening for NAFLD, but if it is discovered an appropriate workup is warranted.

AST/ALT Ratio

Liver health can be assessed by a series of tests aimed at assessing fat accumulation, inflammation, and fibrosis. Initial screening often includes laboratory tests such as measuring the ratio between aspartate transaminase (AST) and alanine transaminase (ALT), where a ratio less than 1 may suggest possible NAFLD, although it is not diagnostic on its own. Normally, AST is slightly more elevated than ALT. So, if the AST/ALT ratio is lower, then means that ALT is higher than AST.

FibroSure®.

Additionally, you can measure indirect markers of fibrosis with tests such as FibroSure or FibroTest blood tests that combine several biomarkers including age, sex, gamma-glutamyl-transferase (GGT), total bilirubin, alpha-2-macroglobulin, apolipoprotein A1, haptoglobin, and ALT to provide insights into liver health.

Some people may be more familiar with FibroSure before Hepatitis C treatment. You can get a fibrosis score (F0-F4), and it is considered significant fibrosis if the score is > or equal to F2. Imaging plays a crucial role in diagnosing NAFLD without the need for invasive procedures like liver biopsy. Vibration-controlled transient elastography (Fibroscan) uses ultrasound to measure liver stiffness, indicating potential fibrosis and inflammation. While noninvasive and portable, it focuses solely on liver ultrasound and may not be universally accessible. MRI with proton density fat fraction (MRI-PDFF) offers a comprehensive assessment of liver fat content, commonly used in clinical and research settings for NAFLD and NASH evaluation.

For evaluating hepatic fibrosis in patients with suspected NAFLD, tools like the Fibrosis-4 Index (FIB-4) incorporate age, AST, ALT, and platelet count to estimate the likelihood of liver disease progression. These screening methods collectively aid in diagnosing and monitoring NAFLD, particularly in individuals at risk due to factors like prediabetes, type 2 diabetes, obesity, and abnormal liver enzyme ratios.

With the FIB-4 you can get a faster answer than FibroSure because you only need 4 elements: Age, platelet count, AST and ALT. Cirrhosis is less likely if FIB-4 is 3.25. Understanding these diagnostic approaches is essential for early detection and management of NAFLD in clinical practice.

Some researchers are invested in diagnosis and treating NAFLD while others recommend against labeling patients with NAFLD. A 2018 Lancet article concluded that the risks of over-diagnosing and overtreating NAFLD exceed the benefits of screening or periodic imaging because of “the low hepatic mortality, high false-positive rate of ultrasonography, selection bias of current studies, and lack of viable treatment.” However, patients who suffer from metabolic syndrome should be counseled about dietary modification and physical activity regardless of their liver condition.

NAFLD and obesity

Fatty liver disease is often caused by multiple insults towards either genetically or environmentally predisposed individuals. Family history of NAFLD and having specific genetic variants are important risk factors for NAFLD. Those with prior health conditions can have increased susceptibility to NAFLD including T2DM leading to insulin resistance, metabolic syndrome, sleep apnea, hepatitis C, and cardiovascular or chronic kidney disease.

A sedentary lifestyle and unhealthy nutrition (especially high intake of processed carbohydrates) cause an increase in free fatty acids leading to hepatic fat deposition → ballooning of hepatocytes → leading to hepatocyte injury/death → inflammation with fibroblast recruitment → end result of fibrosis/cirrhosis. Just a quick reminder, NAFLD is defined as fatty liver with >5% hepatic fat and NASH is defined as fatty liver with >5% hepatic fat with inflammation, hepatocyte injury, with or without fibrosis that we can determine through imaging.

A leading concern for the development of NAFLD is the consumption of high fructose corn syrup. High fructose corn syrup (HFCS), commonly found in candy, processed sweets, soda, fruit juices, and other processed foods, is linked to non-alcoholic fatty liver disease (NAFLD). Unlike natural whole fruits, which contain fiber and are generally healthier due to their slower absorption, HFCS lacks fiber and is quickly absorbed, leading to rapid transport to the liver. This process contributes to NAFLD by increasing the hepatic synthesis of lipids and interfering with insulin signaling. To avoid HFCS, individuals are encouraged to consume whole fruits rather than fruit juices and adopt diets rich in whole grains, lean meats, plant-based proteins, fruits, and vegetables, such as the Mediterranean or DASH diets, which are less likely to promote NAFLD, especially in those with healthy body weight.

NAFLD treatment.

Avoiding alcohol seems very obvious, but we need to mention it. Avoiding heavy alcohol consumption is recommended and complete abstinence is suggested.

Weight loss is crucial; even a modest reduction of 3–5% in body weight can alleviate hepatic steatosis, with greater improvements typically seen with 7–10% weight loss, particularly beneficial for addressing histopathological features of NASH, such as fibrosis. We must focus on tailored medical nutrition therapy and regular physical activity.

A strategic meal plan is essential, emphasizing achieving a healthy body weight while limiting trans fats and ultra-processed carbohydrates. Options like the Mediterranean diet, which balances lean proteins and restricts processed carbohydrates have shown promise.

Dynamic aerobic and resistance exercises play a significant role in managing NAFLD. They help maintain a healthy weight and enhance peripheral insulin sensitivity, reduce circulating free fatty acids and glucose levels, and boost intrahepatic fatty acid oxidation while curbing fatty acid synthesis. These benefits contribute to mitigating liver damage associated with NAFLD, offering therapeutic advantages beyond mere weight reduction.

Exercise may not be a great tool for weight loss, but it is a great tool for weight maintenance, liver health, and overall health as well. “Most patients with NAFLD die from vascular causes, but NAFLD puts patients at increased risk of cardiovascular death”.

Medications for NAFLD.

Regarding pharmacotherapy, while no medications are currently FDA-approved specifically for NAFLD treatment, some options show promise in clinical settings. Vitamin E supplementation at 800 IU (international units) daily has demonstrated biochemical and histological improvements in NASH cases without diabetes or cirrhosis, though long-term use may elevate prostate cancer risks. It is important to make a shared decision with the patient before starting Vitamin E supplementation.

Medications like pioglitazone can reduce liver fat and improve NASH, even as they may increase body weight. But our favorite, GLP-1 receptor agonists, such as liraglutide and semaglutide, also show potential in reducing liver fat and improving NASH symptoms, and this is an emerging therapeutic option for managing this condition.

If you decide to treat, then you should monitor as part of the treatment. An aminotransferase check is recommended 6 months after starting a weight loss program. If levels do not improve or do not return to normal after 5-7% of weight loss, another cause of elevated transaminases needs to be investigated.

You also need to monitor fibrosis in patients with >F2. If fibrosis has been proven by liver biopsy, you can order FibroSure every 3-4 years.

Having a fatty liver may be a red flag that your patient has a metabolic problem. If you discover it, start interventions that would benefit not only the liver but the whole metabolic profile of your patient. The Obesity Medicine Association (OMA) issued a Clinical Practice Statement (CPS) regarding NAFLD and obesity stating that patients with obesity are at increased risk for NAFLD and NASH. It recommends that clinicians strive to understand the etiology, diagnosis, and optimal treatment of NAFLD with a goal to prevent NASH in their patients.

Regular exercise, even walking 30 minutes a day can show many benefits in curbing fatty accumulation in the liver. Having a proper diet with avoidance of high fructose corn syrup can overall help in reducing NAFLD/NASH.

_____________________

Conclusion: Now we conclude episode number 172, “NAFLD and Obesity.” Future Dr. Nguyen explained that NAFLD and obesity are closely related and NAFLD can lead to NASH and cirrhosis in some patients. Dr. Arreaza explained that screening may not be recommended by some medical societies, but others are in favor of screening and treating this disease. However, most people agree that NAFLD is a sign of metabolic disease and a good reason to talk about healthy eating and physical activity with our patients. There are no FDA-approved medications to treat NAFLD, but some evidence suggests that Vitamin E can improve it and GLP-1 receptor agonists are a promising option.

This week we thank Hector Arreaza and Ryan Nguyen. Audio editing by Adrianne Silva.

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:

Karjoo S, Auriemma A, Fraker T, Edward H. Nonalcoholic fatty liver disease and obesity: An Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) 2022. https://doi.org/10.1016/j.obpill.2022.100027.Curry M, Afdhal N. Noninvasive assessment of hepatic fibrosis: Overview of serologic tests and imaging examinations. https://www.uptodate.com/contents/noninvasive-assessment-of-hepatic-fibrosis-overview-of-serologic-tests-and-imaging-examinationsRoyalty-free music used for this episode: Cool Groove (Alt-Mix) by Videvo, downloaded on Nov 06, 2023, from https://www.videvo.net

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Episodes

Episode 179: Impact of intermittent fasting on T2DM.
27 oct.· Rio Bravo qWeek
Episode 179: Impact of intermittent fasting Impact on T2DM
Future Dr. Carlisle explains the physiology of fasting and how it can help revert type 2 diabetes. Dr. Arreaza adds details on how to do intermittent fasting.
Written by Cameron Carlisle, MSIV, Ross University School of Medicine. Comments and edits by Hector Arreaza, MD, FAAFP.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
What is type 2 Diabetes Mellitus (T2DM)?
-Type 2 Diabetes Mellitus (T2DM) is a metabolic disorder characterized by insulin resistance and impaired glucose regulation.
-This impaired regulation can lead to hyperglycemia, contributing to complications in a myriad of organs: heart, kidneys, eyes, nerves, etc. (target organs). According to the CDC, more than 38 million Americans have T2DM (about 1/10 people).
-Multiple mechanisms are believed to contribute to insulin resistance in obese patients with T2DM, such as increased lipid deposition throughout the body and systemic inflammation.
What is Intermittent Fasting (IF)?
Intermittent fasting (IF) has recently gained popularity as a dietary approach for health benefits, but it has been around for thousands of years. IF is an eating pattern that alternates between eating and fasting (no calories consumed) over a specific period of time. When you are fasting, you are allowed and encouraged to keep drinking water and non-caloric drinks, like coffee, tea, and even homemade bone broth.
-According to the International Food Information Council Foundation (IFIC), 10% of Americans engage in IF daily.
-According to Mark Mattson, a neuroscientist and IF expert for over 25 years, a mechanism called “metabolic switching” is seen with IF. This is when your body runs out of glucose and starts burning fat (i.e., fatty oxidation). These metabolic changes can help protect your organs and reduce the risk of chronic conditions, like T2DM.
Common IF methods:
Time-restricted eating: Most common method, involves eating within a specific time frame (e.g., the 16:8, 18:6, 12:12 method is also common. [16:8 means you have 16 hours of fasting and 8 hours of eating.]Alternate-day fasting: Alternating between fasting days and normal eating days. [Find more info in The Complete Guide to Fasting, by Jason Fung, who is a nephrologist, he explains that alternate-day is basically eating every other day, which would give 36 hours of fasting, but if you are a beginner you can try a 24 hours fasting, in short, not eating breakfast any day of the week and having lunch 4 days a week, and dinner every night.]5:2 diet (aka periodic fasting): Maintaining a normal diet for 5 days, with 2 days (usually non-consecutive) of caloric restriction (25% of normal caloric intake; e.g., 500 calorie meal).
IF is strongly believed to improve metabolic health in individuals with T2DM by reducing insulin resistance via increasing insulin sensitivity, promoting weight loss (patients with obesity and DM… AKA patients with diabesity), and enhancing lipolysis via fat oxidation.
While fasting, the body goes through several phases that affect how energy is metabolized. Between 0 and 4 hours after eating, the body enters a feeding state, using glucose as its main energy source. After fasting for 12-16 hours, the body enters ketosis and starts to use fat for energy. Within 24-36 hours, autophagy begins, a process that recycles damaged cells and allows for cellular repair. This process can have great benefits for people with T2DM, such as improved insulin sensitivity and glucose regulation.
Pathophysiology of Implementing IF in T2DM.
-IF is thought to increase insulin sensitivity by decreasing fatty tissue in the body (i.e., visceral adipose tissue), which is correlated to insulin resistance. Insulin resistance is defined as higher than normal circulating insulin levels needed for a glucose lower response, which is thought to be the culprit for the generation of T2DM. It means you need high levels of insulin to keep glucose normal.
-Obesity is an important risk factor for T2DM. Visceral adipose tissue functions as an organ via the secretion of adipokines (cytokines or cellular messengers produced by adipose tissue): leptin and adiponectin.
Leptin: proinflammatory, leading to chronic inflammation. Patients with higher BMI levels and increased insulin resistance were found to have increased leptin levels.
[Leptin is a good hormone at normal levels, but there is leptin resistance]
Adiponectin: anti-inflammatory and antidiabetic effects. Higher adiponectin levels result in decreased hepatic gluconeogenesis, enhanced glucose absorption, and enhanced skeletal muscle and hepatic fatty acid oxidation. Levels drop as visceral fat increases.
-Dr. López-Jaramillo, a Colombian endocrinologist and researcher, and colleagues published a review in 2014 examining the imbalance in the levels of leptin and adiponectin in individuals with metabolic syndrome. This imbalance (increase in leptin and decrease in adiponectin) is linked to obesity and insulin resistance, which has been shown to increase the risk of T2DM. It has been shown that IF has resulted in the reduction of leptin levels and increased levels of adiponectin, which leads to decreased insulin resistance and increased insulin sensitivity.
-IF allows pancreatic beta-cells to rest by not having to secrete insulin constantly. This allows the beta-cells of the pancreas to improve in function over time. In addition, IF has been shown to lead to noticeable weight loss and loss in body fat, both of which play an important contribution in managing T2DM. Research demonstrates that this weight loss increases insulin sensitivity and decreases the need for insulin therapy, making IF a powerful approach for improving metabolic health.
AMP-Activated Protein Kinase (AMPK) and Its Role in IF and T2DM
Recent research has highlighted an important enzyme seen in IF, AMP-activated protein kinase (AMPK), which plays a vital role as an important energy sensor in cells. It is activated when cellular energy levels are low, such as during IF. A 2020 research study in Nature Reviews Endocrinology explains that activation of AMPK aids in suppressing gluconeogenesis and stimulates fatty acid oxidation, leading to optimal energy balance and reduction of visceral adipose tissue accumulation, a major contributor to insulin resistance and T2DM progression. AMPK is upregulated during fasting, which enhances glucose metabolism and reduces insulin resistance. This is imperative in managing T2DM, as it counters the effects of insulin resistance associated with T2DM.
Exercise, which also promotes AMPK activation, complements IF and can promote a synergistic effect in improving insulin sensitivity and promoting fat burning,
New Research Findings on IF and T2DM
-The EARLY (Exploration of Treatment of Newly Diagnosed Overweight/Obese Type 2 Diabetes Mellitus) study is a randomized clinical trial published in JAMA Network Open (2024). Findings In this randomized clinical trial study found that a time-restricted eating window significantly improved fasting glucose levels and HbA1c levels in individuals with T2DM. The study examined the effect of a 16-week 5:2 meal replacement (5:2 MR) fasting plan that consisted of five days of normal eating and 2 days, nonconsecutive of restricted diet (500-600 calories). This group was examined alongside a group of patients who took metformin 0.5 g BID and empagliflozin 10 mg QD. The study wanted to investigate the changes in HbA1c in Chinese adults with early T2DM.
-The study was a randomized clinical trial of 405 adults, and a study showed that the 5:2 MR approach led to better glycemic control at 16 weeks compared to the counter treatments with metformin and empagliflozin. The 5:2 MR group had the greatest reduction in HbA1c (-1.9%), followed by metformin (-1.6%), and empagliflozin (-1.5%). The 5:2 MR plan also revealed the greatest weight loss (-9.7 kg), followed by empagliflozin (-5.8 kg), and metformin (-5.5 kg).
-This research suggests IF, such as 5:2 MR, can be a powerful tool in the management of T2DM and improving metabolic health. This study can potentially open doors for healthcare providers to provide the 5:2 MR approach for individuals as an effective initial lifestyle intervention. However, follow-up studies are needed to assess the effectiveness and durability of the 5:2 MR.
Safety and Risks of IF in T2DM.
-IF when combined with glucose-lowering medications (e.g., insulin, sulfonylureas, GLP-1 agonists) can increase the risk of hypoglycemia. Also, prolonged fasting can lead to nutrient deficiencies if not planned carefully. Patients should be counseled on maintaining a balanced, nutritious diet during non-fasting days.
-IF is not suitable for everyone. Children under the age of 18 should not try IF due to needing proper calories for adequate development and proper growth. Also, it is recommended that pregnant or breastfeeding women do not undergo IF. It is advised that people with eating disorders should not try IF.
-Individuals with certain medical conditions, such as kidney stones or gastroesophageal disease should speak with their doctor before trying IF. Also, patients on insulin or other glucose-lowering medications should adjust their dose and talk with their healthcare providers to prevent hypoglycemia during fasting. It is recommended that each person speak with their doctor to discuss the safety and risks of IF and see if it would benefit the individual before starting IF.
-Many studies have explored the benefits of IF at the micro level revealing its cellular benefits and on a macro level of the body as a whole. However, more research is needed to confirm the long-term effects of IF on glycemic control and its sustainability as a therapeutic approach for T2DM.
Conclusion:
-IF shows potential for improving glycemic control, promoting weight loss, and enhancing metabolic health in individuals with T2DM. Despite its benefits, IF may present with risks, such as hypoglycemia, nutrition deficiencies, or dehydration in certain patients. Therefore, it may not be suitable for all individuals. It’s important to monitor patients who engage in IF, especially for patients with T2DM. Patients should follow up with their doctor for individualized IF plans in patients with T2DM.
______________
This week we thank Hector Arreaza and Cameron Carlisle. Audio editing by Adrianne Silva.
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:
Albosta, Michael, and Jesse Bakke. “Intermittent Fasting: Is There a Role in the Treatment of Diabetes? A Review of the Literature and Guide for Primary Care Physicians - Clinical Diabetes and Endocrinology.” BioMed Central, BioMed Central, 3 Feb. 2021, doi.org/10.1186/s40842-020-00116-1.Blumberg, Jack, et al. “Intermittent Fasting: Consider the Risks of Disordered Eating for Your Patient - Clinical Diabetes and Endocrinology.” BioMed Central, BioMed Central, 21 Oct. 2023, https://clindiabetesendo.biomedcentral.com/articles/10.1186/s40842-023-00152-7.De Cabo, Rafael, and Mark P. Mattson. “Effects of intermittent fasting on health, aging, and disease.” New England Journal of Medicine, vol. 381, no. 26, 26 Dec. 2019, pp. 2541–2551, https://doi.org/10.1056/nejmra1905136.Guo, Lixin, et al. “A 5:2 intermittent fasting meal replacement diet and glycemic control for adults with diabetes.” JAMA Network Open, vol. 7, no. 6, 21 June 2024, https://doi.org/10.1001/jamanetworkopen.2024.16786.Herz, Daniel, et al. “Efficacy of Fasting in Type 1 and Type 2 Diabetes Mellitus: A Narrative Review.” Nutrients, U.S. National Library of Medicine, 10 Aug. 2023, www.ncbi.nlm.nih.gov/pmc/articles/PMC10459496/. Herzig, S., & Shaw, R. J. (2018). AMPK: Guardian of metabolism and mitochondrial homeostasis. Nature Reviews Molecular Cell Biology, 19(2), 121-135.Longo, V. D., & Mattson, M. P. (2014). Fasting: Molecular mechanisms and clinical applications. Cell Metabolism, 19(2), 181-192. https://doi.org/10.1016/j.cmet.2013.12.008López-Jaramillo P, Gómez-Arbeláez D, López-López J, et al. The role of leptin/adiponectin ratio in metabolic syndrome and diabetes. Hormone Molecular Biology and Clinical Investigation. 2014;18(1):37–45.Mattson, Mark P., et al. “Impact of intermittent fasting on health and disease processes.” Ageing Research Reviews, vol. 39, Oct. 2017, pp. 46–58, https://doi.org/10.1016/j.arr.2016.10.005. Patikorn, Chanthawat, et al. “Intermittent fasting and obesity-related health outcomes.” JAMA Network Open, vol. 4, no. 12, 17 Dec. 2021, https://doi.org/10.1001/jamanetworkopen.2021.39558.Sharma, Suresh K, et al. “Effect of Intermittent Fasting on Glycaemic Control in Patients with Type 2 Diabetes Mellitus: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.” TouchREVIEWS in Endocrinology, U.S. National Library of Medicine, May 2023, www.ncbi.nlm.nih.gov/pmc/articles/PMC10258621/#:~:text=In%20IF%2C%20eating%20habits%20are,the%20risk%20of%20developing%20T2DM.Xiaoyu, Wen, et al. “The effects of different intermittent fasting regimens in people with type 2 diabetes: A network meta-analysis.” Frontiers in Nutrition, vol. 11, 25 Jan. 2024, https://doi.org/10.3389/fnut.2024.1325894. Theme song, Works All The Time by Dominik Schwarzer, YouTube ID: CUBDNERZU8HXUHBS, purchased from https://www.premiumbeat.com/.
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Episode 178: Social Media in Medicine
18 oct.· Rio Bravo qWeek
Episode 178: Social Media in Medicine
Dr. De Luna and Dr. Song explain the role of social media in medical education and how online journal clubs have become more useful in recent years. Dr. Arreaza offers insights into our role as educators and sources of truth.
Written by Patrick De Luna, MD. Comments by David Zheng Song, MD, and Hector Arreaza, 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.
Intro to episode (voiceover): Get ready to listen to a great conversation between three doctors diving into the impact of social media on medicine. It’s no secret that social media shapes our lives—not just as professionals, but also as humans and members of our society. Every second, new information floods our feeds, and with the rise of artificial intelligence, it’s becoming harder to separate fact from fiction. As doctors, we have a crucial role in clearing up confusion and supporting evidence-based practices. You’ll hear insightful tips from Dr. De Luna, Dr. Song, and Dr. Arreaza—but remember, you also have a role in spreading the truth, you must be a reliable source of online truth and correct misinformation quickly. Also, use reliable sources, recommend fact-check websites, including Snopes, and FactCheck.org, and avoid “back-and-forth” arguing about fake news online, because as you keep arguing, fake news will continue to spread.
Social Media in Medicine.
Patrick: Social media has helped both physicians and patients obtain and expand their knowledge of medicine. This role in medical knowledge expansion has been more prevalent since the COVID-19 pandemic, especially in the form of podcasts (like this one), medical content creators, and personalities. This growing medium has helped physicians to deliver medical knowledge in an efficient, but layman, format which can become a great outreach and educational tool.
Arreaza: This podcast was created 3 days before the lockdown. It has been an educational tool for those who record and hopefully for those who listen to us.
Patrick: In today’s episode, we will explore a little about how this more accessible approach to medical learning has shaped our medical education landscape. We’ll explore a recent study that shows the breakdown of how social media is used among medical professionals and the concerns that physicians have about medical education through social media. We will discuss how platforms such as X/Twitter have “Journal Club” threads and their implications. Furthermore, will discuss how online personalities have been able to bring medical education discussion to the broader population, and what we can learn from their work.
David: Who is your favorite medical educator?
Patrick: Dr. Mike (YouTube FM), Dr. Glaucomflecken (ophthalmologist comedian), and HealthyGamerGG (gamer), and yours?
David: Curbsiders (THE internal medicine podcast)
Arreaza: I like Dr. Glaucomflecken as well. He is a comedian but he is becoming a little more political. The AFP podcast is my favorite.
David: We will explore and discuss how we could make quality and accurate medical education content and, hopefully, mitigate concerns about creating future educational content for physicians and patients alike.
Analysis of Healthcare Professional Social Media Use
Patrick: Social media has traditionally been used to share about your social life (posting pictures of your cat and family vacation), stay up to date on news and what is happening among your peers, as well as (for some select folks) a platform for content creation and a means of a career. Healthcare professionals also participate in social media in the same manner.
David: Some social media users are called “influencers”.
Arreaza: The term “influencer” is becoming a somewhat negative term online because many “influencers” are giving a bad reputation to that term, to the point that many prefer to be called “content creator.”
Patrick: In a recent study published in Taylor and Francis’ Medical Education Online, 72.1% of the participants reported use of social media to some degree. Out of the 72%, 11.5% of the surveyed report using social media sites exclusively for professional purposes, 22.8% for strictly personal use, and 65.7% for both.
David: The most used social media platforms among healthcare workers were Facebook at 70%, YouTube 58%, LinkedIn 52%, Instagram 42%, Twitter (now called X) 27%, TikTok 10%, and Reddit at 5% among those surveyed. Those are 6 different media, which ones do you currently use, Patrick?
Patrick: [Add response]. 20.4% of the surveyed indicated they use clinically focused social media platforms as well. This same survey found that respondents specializing in addiction medicine, family medicine, pediatrics, and psychiatry were more likely to use social media for continued professional development as compared to other specialties.
David: Social media among the participants was highly used for staying informed with medical news and actively participating in medical discussions online, especially about medical management and treatments. Of note, the data is based on a population that skews more toward physicians and medical professionals who have practiced for more than 15 years.
Arreaza: Doximity is one of those platforms that I have used in the past, and it contains interesting articles but they have to be read “with a grain of salt,” because they are editorials.
The “New Journal Club” Online
Patrick: Multiple residency programs report using social media as a form of engagement about published journal articles and updates to medical practice. Medical education may benefit from the implementation of social media and similar platforms as a medium for professional development, according to an analysis performed by Medical Education Online. The use of social media among many physicians has changed from content consumption (passive) to active participation in furthering medical education.
David: This is reflected heavily in how platforms such as X (formerly known as Twitter), have become a forum towards a new form of “Journal Club”.Tweet Threads can now be utilized for further publication discussion in an open online space. Good examples of this can be found among Twitter feeds from publication sites like the New England Journal of Medicine or #IDJClub (Before their move to Meta’s Threads in November 2023). The Infectious Disease Journal Club, using the handle @IDJClub, published a study in May 2022 highlighting the impact of 20 months of journal club hosting through Twitter.
Patrick: The authors of the study state that it may be harder for physicians outside of academic circles to have opportunities for well-scaffolded discussions and continued maintenance of critical appraisal skills. Due to an explosion of questionable medical literature during to COVID-19 pandemic (AKA fake news), they report a higher need for avenues to keep the practice of critical appraisal, thus we need to expand journal club access outside of academic sites.
Arreaza: From May 19, 2019 – August 7, 2021, the @IDJClub account was followed by almost 9,500 followers from 114 countries and hosted 31 journal club posts and discussions. During the study, they found data that shows a decrease in participation in journal clubs use in residencies, as well as a lack of expert hosts to lead those discussions.
Patrick: In addition to the increased accessibility, the survey makes a case that online interdisciplinary journal clubs can be an effective tool to update medical professionals and for practicing critical appraisal of the research studies. 75% of respondents believed that they learned more from these #IDJClub discussions than in their traditional journal club forums (if such forums were available to their respective programs). A case is made where it could be reflective of easier access, the make-up of how the publication is presented, and how the overall journal club is run.
Concerns and Challenges to Avoid
David: As well-intended and useful as these platforms for medical education can be, some authors from AAFP recommend that we be mindful of problems that can occur from misapplied use.
Patrick: One problem that has been brought to the AAFPs' attention is potential society and licensing board actions. Medical boards, such as our own California Medical Board, can sanction physicians, uphold practice restrictions, or even take away physician licenses due to unprofessional behavior in social media content creation. This is especially worrisome if posting scientifically misleading or untrue claims.
David: One example was an incident here in Bakersfield where 2 physicians used YouTube to post the results of COVID-19 tests at their urgent care during the peak of the pandemic. They misled the public in stating the disease did not have serious ramifications as the CDC stated. Due to the large number of viewers, the physicians were censured by medical societies due to their distribution of biased and unfounded information to the public.
Patrick: AAFP authors suggest that for medical statements and discussions posted on social media for general patient education, it is recommended to add hyperlinks or direct sources with any online interaction in-so-that it better qualifies accuracy. If it’s unverifiable, it would be best to add written caveats about the information’s non-verifiability or that it is in the process of continued research.
Patrick: At this time, there is some effort made by social media platforms to help indicate that the post is made by a reputable source. For example, when a licensed medical professional posts on YouTube, there are information panels that appear that will give context to the health content that is viewed. At the time of this episode, YouTube also currently allows channels to apply to be indicated as a licensed medical professional in the channel's posts. The applicants are examined by three different medical societies: the Council of Medical Specialty Societies (CMSS), the National Academy of Medicine (NAM), and the World Health Organization (WHO) to standardize how health education should be shared online.
David: An example being Dr. Lin of Common Sense Family Doctor, an online medical blog for patients and physician education. In his statement to AAFP, he states that he wanted to post educational content twice a week, however, it required 3 to 4 hours a week to create. This can be time-consuming and distracting from other responsibilities.
Arreaza: Social media can change mind. What other concerns do you think should be considered when physicians try to educate patients in an online environment?
Social Media Platforms to Teach Medicine to the Greater Public
Patrick: In general, social media platforms can be used to educate the public. One AAFP panel of authors wrote that some key points are important to consider when creating online content that is meant for public use.
We must define our goals toward the subset population we are directing the education towards. Is it providing general health education? Is it promoting a practice? Is this used to advocate for a cause?We must consider who our audience is. For example, if our goal is to create a professional message to incite political or societal change towards public health policy, it would be best to utilize platforms that involve policymakers, political leaders, and/or patients that can inform them of what we want to achieve. Focus on general topics. These can include topics such as viral medical discussion trends on platforms like TikTok (ex. Ozempic), fitness and wellness, nutrition, or topics that you yourself have interest or expertise in. This can lead to the production of original content such as informatic YouTube series’, podcasts such as this one, or discussion threads. AAFP recognizes that this can become a creative outlet for physicians and can reduce burnout.
Conclusion
Patrick: We can see the transformative impact of social media on medical education, and how it’s further evolved since the COVID-19 pandemic. We explored how platforms like Twitter have redefined traditional journal clubs, making scholarly discussions more accessible across global medical communities. Moreover, we examined the role of influential medical content creators in bridging the gap between healthcare professionals and the general public.
Patrick: While social media presents unprecedented opportunities for disseminating medical knowledge, our discussion also highlighted the challenges, including the need for accuracy in content, navigating professional conduct, and addressing algorithmic biases that can influence online interactions.
Patrick As we conclude, it's evident that social media has revolutionized medical education by fostering broader engagement and democratizing access to knowledge. However, both physicians and content creators must uphold ethical standards and ensure the accuracy of information shared online. By navigating these challenges thoughtfully, we can harness its full potential as a powerful tool for advancing medical education and improving health outcomes in our local communities.
____________________
This week we thank Hector Arreaza, Patrick De Luna, and David Zeng Song. Audio editing by Adrianne Silva. Intro by Raj Ajudia, MSIII.
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!
_____________________
Links:
Topf, Joel M., Introduction: Social Media and Medical Education Come of Age, Seminars in Nephrology, Volume 40, Issue 3, 247 – 248. https://www.seminarsinnephrology.org/article/S0270-9295(20)30043-7/fulltextNguyen BM, Lu E, Bhuyan N, Lin K, Sevilla M. Social Media for Doctors: Taking Professional and Patient Engagement to the Next Level. Fam Pract Manag. 2020;27(1):19-14. https://www.aafp.org/pubs/fpm/issues/2020/0100/p19.htmlIserson KV, Derse AR, Delpier M. Navigating the Hazards of Social Media. Fam Pract Manag. 2022;29(3):15-20. https://www.aafp.org/pubs/fpm/issues/2022/0500/p15.htmlVan Ravenswaay L, Parnes A, Nisly SA. Clicks for credit: an analysis of healthcare professionals' social media use and potential for continuing professional development activities. Med Educ Online. 2024 Dec 31;29(1):2316489. doi: 10.1080/10872981.2024.2316489. Epub 2024 Feb 15. PMID: 38359156; PMCID: PMC10877644. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10877644/Doctor Mike, YouTube Channel, https://www.youtube.com/@DoctorMikeDr. Glaucomflecken, YouTube Channel, https://www.youtube.com/@DGlaucomfleckenHealthyGamerGG, YouTube Channel, https://www.youtube.com/@HealthyGamerGGGet info on health-related content, Google Support, https://support.google.com/youtube/answer/9795167Apply to be a source in YouTube health features, YouTube Help, https://support.google.com/youtube/answer/12796915Theme Song: Works All The Time by Dominik Schwarzer, License #5924333, PremiumBeat.com.
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Episode 177: Urinary Incontinence in Older Adults
13 sept.· Rio Bravo qWeek
Episode 177: Urinary Incontinence in Older Adults
Future Dr. Nguyen explains the evaluation and treatment of older adults with urinary incontinence. Dr. Arreaza adds insights into the conservative management of urinary incontinence.
Written by Vy Nguyen, MSIV, Western University of Health Sciences, College of Osteopathic Medicine of the Pacific-Northwest. Editing and comments by Hector Arreaza, MD.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
Definition of urinary incontinence.
The International Continence Society (ICS) defines it as any involuntary urine leakage.
Epidemiology of urinary incontinence.
Data analysis from the National Health and Nutrition Examination Survey (NHANES) from 2015 to 2018 shows that more than 60% of adult women which is equivalent to around 78,000,000 females living in the United States experience urinary incontinence with 32.4% reporting symptoms monthly. More data analysis shows the strongest association with urinary incontinence include age greater than 70, prior vaginal delivery, and BMI of 40 or greater.
Despite urinary incontinence commonly affecting the senior population, this medical condition can also affect the quality of life of younger adult females and males. On top of that, urinary incontinence is often underestimated due to the low report level for various reasons and the obtained data might not accurately reflect the true prevalent rate.
Types and etiology.
Urinary incontinence is divided into 5 categories: stress, urge, mixed, overflow, and functional.
Stress urinary incontinence has the highest prevalence of 37.5% followed by mixed urinary incontinence at 31.3%, urgency at 22%, and unspecified urinary incontinence at 9.2%. Due to time constraints, we will discuss the most prevalent type which is stress urinary incontinence.
In females, stress urinary incontinence is often due to urethral sphincter hypermobility caused by weakened pelvic floor muscles. It can also be caused by dysfunction of the sphincter muscle that is exacerbated by increased intraabdominal pressure from coughing, sneezing, or physical exertion. This type of incontinence is commonly seen in pregnant women, those who experienced childbirth, and young women active in sports.
In males, the most common etiology for stress urinary incontinence in males is prostate surgery such as radical prostatectomy which can damage the external urethral sphincter. Another cause is spinal cord injury or disease that can interfere with sphincter function.
Evaluation.
Urinary incontinence is first evaluated by a thorough history taking that includes inquiries about the type, severity, burden, and duration of incontinence. The initial evaluation includes a voiding diary that can provide clarity and help distinguish between the different types of incontinence or identify the dominating type in the case of mixed incontinence.
Examples of voiding diary can be found on the websites of International Urogynecological Association (IUGA). Medical conditions such as COPD and asthma can induce cough; heart failure can cause volume overload; neurological disorders and musculoskeletal conditions can interfere with bladder emptying and urinary retention and thus should also be investigated. It is also helpful to ask about medication and substance use as the adverse effects can directly or indirectly contribute to urinary incontinence. For our female-identifying patients, a gynecological and obstetrical history such as birth history (vaginal versus c-section), current pregnancy as well as low estrogen (menopause) can contribute to reversible urinary incontinence.
Management.
There are various treatment modalities for stress urinary incontinence ranging from conservative to more invasive surgical management.
Conservative treatment:
-Initial treatment includes pelvic floor strengthening exercises and bladder training with scheduled void.
-Pelvic floor muscle training (PFMT) is very effective, and it is proven to help achieve cure and improve the quality of life in women with ALL types of urinary incontinence.
-For stress urinary incontinence, the median cure rate is around 58.8% for women after 12 months and 78.8% for men at 6 months of supervised pelvic floor muscle training (PFMT).
-Certain behavioral modifications such as fluid intake management (
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Episode 176: Self-sampling for HPV screening
6 sept.· Rio Bravo qWeek
Episode 176: Self-sampling for HPV screening
Future Dr. Markarian explains the importance of HPV screening for the prevention of cervical cancer. Dr. Arreaza adds some insight about cervical cancer.
Written by Chantal Markarian, MSIV, American University of the Caribbean. Editing and comments by Hector Arreaza, MD.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
Insights into Cervical Cancer.
Chantal: Cervical cancer stands as the most prevalent form of cancer in women globally costing the lives of approximately 350,000 women annually. About 4,000 women die of cervical cancer a year in the US.
Cervical cancer is initially asymptomatic, allowing it to advance to a more severe stage if not detected early. The positive news is that cervical cancer is highly preventable through screening for precancerous lesions or the presence of HPV —the primary culprit behind most cases.
The role of HPV: Human Papilloma Virus, according to the World Health Organization, caused an estimated 620,000 cancer cases in women and 70,000 cancer cases in men.
Cervical cancer is more prevalent in certain regions. In regions with established screening initiatives, the incidence rate and mortality rate of cancer are lower than in resource-limited areas. This highlights that resource-constrained countries continue to bear a burden of this disease. In nations like the United States, access to the HPV vaccine along with routine screenings, like Pap smears and HPV tests has significantly decreased the prevalence of cervical cancer.
Screening recommendations from the US Preventive Services Task Force (USPSTF) and the American Cancer Society (ACS).
The U.S Preventive Services Task Force advises that women aged 21 to 29 undergo a Pap test every three years while those aged 30 to 65 should opt for co-testing (Pap and HPV tests) every five years. These examinations are usually conducted in outpatient facilities, where a medical professional collects a sample of cervical cells that are later examined under a microscope.
A normal result states that the sample was adequate for evaluation, in other words, that endocervical/transformation zone components are present, and that the patient is “Negative for intraepithelial lesion or malignancy.”
ACS recommends cervical cancer screening begin at age 25 for women and people with a cervix. Those aged 25 to 65 should have a primary HPV test every 5 years. (A primary HPV test means the HPV test is done without cytology; follow-up screening can be done with a Papanicolaou (Pap) test if needed.) If primary HPV testing is not available, screening may be done with either a co-test every 5 years, which combines an HPV test with a Papanicolaou (Pap) test, or a Pap test alone every 3 years.
How is Cervical Cancer Classified?
Two systems categorize lesions: the Cervical Intraepithelial Neoplasia (CIN) scale and the Bethesda system.
The CIN scale categorizes lesions based on the degree of involvement of the cervical lining ranging from mild (CIN I) to moderate (CIN II) to severe dysplasia (CIN III).The Bethesda system emphasizes cytological findings organizing results into categories such as atypical squamous cells, low-grade lesions (LSIL), and high-grade lesions (HSIL).
ASCUS (Atypical Squamous Cells of Undetermined Significance) is the most common abnormality seen in pap smears. It may or may not indicate a problem, you have to make a decision based on the patient.
Cervical cancer is largely linked to high-risk HPV (hrHPV), mostly HPV 16 and 18, and scientists are investigating tests that identify hrHPV DNA or RNA. These tests may provide a more accurate evaluation of cancer risk compared to traditional cytology. Examples include DNA amplification tests like Cobas test and the Xpert HPV test.
Obstacles to Screening.
Despite the efficacy of cervical cancer screening, many women face many obstacles to testing. In regions with limited resources, fear, embarrassment, lack of awareness, and restricted healthcare access pose challenges to screening.
In Nigeria, a study revealed that women often avoid Pap smears due to a lack of awareness. Similarly, healthcare providers in Ecuador highlighted issues like the absence of screening programs and inadequate health promotion efforts. Women in Peru face obstacles such as long waiting times preferences for female healthcare providers and limited access to health facilities.
In 2022, 31% of minority women in the US did not undergo Pap smears in the past three years; many of these women were uninsured, unemployed, or low-income. These challenges contribute to higher rates of cervical cancer among women who do not follow recommended screening guidelines.
We must mention the cultural obstacle as well. Some cultures do not allow any kind of pelvic exams before marriage. They put a major emphasis on being a “virgin,” and placing a speculum in the vagina may be considered culturally unacceptable. In those cases, the doctor has to use their best persuasion skills to accomplish the goals of care. For example, they may suggest having the mother in the room during the pap smear, using the smallest speculum possible, or other techniques.
Self-sampling.
In 2020, the World Health Organization (WHO) introduced a global initiative to combat cervical cancer worldwide. The initiative aims to:
Vaccinate 90% of girls by age 15.Screen 70% of women by age 35.Treat 90% of women with lesions and invasive cancer by 2030.
To achieve these goals, self-sampling for HPV testing has been introduced as a viable option for cervical cancer screening.
Self-sampling for HPV testing is seen as an alternative for cervical cancer screening that addresses barriers associated with traditional methods. This approach enables women to take samples themselves using swabs or brushes removing the necessity for a pelvic examination. The option to mail in samples and receive results within two weeks enhances the convenience, privacy, and accessibility of the process giving individuals control over their health.
While self-sampling for hrHPV detection is not currently standard practice in the United States, it has been successfully implemented in countries across Europe, Africa, and South America. Pilot studies are ongoing in nations like Canada and New Zealand to assess its effectiveness offering promise for its impact.
In May 2024, the Food and Drug Administration (FDA) approved primary HPV self-collection for cervical cancer screening in a health-care setting. That means, the patient still has to go to a clinic to self-collect her sample.
How Effective is HPV Self-Sampling?
Research supports the accuracy of HPV self-sampling. A study conducted by Polman et al., which involved a randomized controlled trial, demonstrated that HPV tests on self-collected samples were just as precise as those done on samples collected by clinicians in detecting high-grade lesions (CIN II and CIN III). Similarly, a meta-analysis conducted by Arbyn et al. showed no difference in sensitivity or specificity between self-sampled and clinician-sampled tests for detecting CIN grade II or higher.
These results indicate that self-sampling could be an adequate screening method for cervical cancer. This reassurance may motivate women to partake in screenings knowing they have a convenient and effective option. Ok, let’s say a patient has collected her sample or the sample was collected by a clinician, what is next?
Management of Cervical Cancer Screening Results.
The process of managing cervical cancer screening results involves evaluating a patient’s immediate and five-year risk of developing cervical abnormalities (CIN 3+) following guidelines from the American Society for Colposcopy and Cervical Pathology (ASCCP).
The ASCCP app is the best investment you can make in primary care. It is only $9.99, but it can save you a lot of time in clinic. Estimating risk is a process that considers factors such as current HPV test results, past screening outcomes, the patients' age, and whether they’ve had a hysterectomy or not.
When Risk is Elevated, Prompt Action.
If a patient’s immediate risk of developing CIN 3 exceeds 4%, expedited treatment is typically recommended. This treatment may entail one of several procedures aimed at removing abnormal cervical tissue.
Loop Electrosurgical Excision Procedure (LEEP): A common method that removes tissue using an electric wire loop. Cold Knife Conization: In this procedure, a scalpel removes a cone-shaped section of the cervix.Laser Cone Biopsy: This technique involves removing a cone-shaped section of tissue using a laser.
Alternatively, healthcare providers may opt for treatment methods such, as cryotherapy, thermos-ablation, and laser ablation to eliminate abnormal tissue.
And those procedures are typically out of the scope of family medicine, but many family doctors may perform them with the proper training and experience.
When the risk is deemed low, Surveillance.
Patients with a risk of CIN 3 below 4% are typically advised to undergo surveillance with HPV testing every 1-5 years. If HPV testing is not available cytology alone (Pap test) is considered acceptable.
Special considerations for women.
For women under 25, a cautious approach is taken. If a low-grade lesion (LSIL) is identified through cytology, it is recommended to repeat the test annually for two years. If two consecutive tests show normal results the patient can resume screening intervals based on age. However, if a high-grade lesion (HSIL) is detected, a colposcopy and biopsy are recommended. It should be noted that expedited treatment is generally not advised for this age group since many high-grade lesions may resolve spontaneously.
For women over 25, the presence of low-grade lesions or persistent high-risk HPV often leads to recommendations for colposcopy and cervical biopsy.
When a cervical biopsy shows adenocarcinoma in situ it is suggested to perform an excisional procedure to rule out invasive cancer. The next steps depend on the margins of the excised tissue; If the margins show positive results (indicating abnormal tissue remains) further excision is necessary to ensure clear margins. This may be followed by a hysterectomy due to the risk of residual disease.
For individuals who have been treated for high-grade lesions there is still a risk of developing cervical cancer. Therefore, long-term surveillance is essential. Women over 25 should undergo HPV testing six months after treatment, then annually until three consecutive negative tests are obtained. Subsequently testing every three years is advised for 25 years. As for women under 25, cervical cytology should be done six months post-treatment. Then at six-month intervals until three consecutive negative results are achieved. Once they reach 25 years old, they should switch to HPV testing.
As summary, HPV is the most common cause of cervical cancer, and screening must be implemented no matter what your zip code is because adequate screening can lead to a lower mortality. Remember that self-collection is an alternative for your patients, and it is FDA-approved if it is done in a healthcare setting. The ASCCP guidelines are very useful but difficult to memorize, so you can invest in the ASCCP phone app to provide accurate care for your patients. Thanks!
References:
1. World Health Organization. HPV and Cervical Cancer Fact Sheet. 2024. Available online: https://www.who.int/en/news-room/fact-sheets/detail/human-papillomavirus-(hpv)-and-cervical-cancer (accessed on 10 August 2024).
2. Arbyn M, Weiderpass E, Bruni L, et al. Estimates of incidence and mortality of cervical cancer in 2018: a worldwide analysis. Lancet Glob Health. 2020;8(2):e191-e203.
3. Serrano B, Ibáñez R, Robles C, Peremiquel-Trillas P, de Sanjosé S, Bruni L. Worldwide use of HPV self-sampling for cervical cancer screening. Preventive Medicine. 2022;154:106900.
4. Gupta S, Palmer C, Bik EM, et al. Self-sampling for human papillomavirus testing: increased cervical cancer screening participation and incorporation in international screening programs. Front Public Health. 2018;6:345033.
5. Ubah C, Nwaneri AC, Anarado AN, Iheanacho PN, Odikpo LC. Perceived barriers to cervical cancer screening uptake among women of an urban community in South-eastern Nigeria. Asian Pac J Cancer Prev. 2022;23(6):1959-1965.
6. Vega Crespo, B., Neira, V.A., Ortíz Segarra, J. et al.Barriers and facilitators to cervical cancer screening among under-screened women in Cuenca, Ecuador: the perspectives of women and health professionals. BMC Public Health 22, 2144 (2022). https://doi.org/10.1186/s12889-022-14601-y
7.Olaza-Maguiña AF, De la Cruz-Ramirez YM. Barriers to the non-acceptance of cervical cancer screenings (Pap smear test) in women of childbearing age in a rural area of Peru. Ecancermedicalscience. 2019;13:901.
8. Sharma M, Batra K, Johansen C, Raich S. Explaining correlates of cervical cancer screening among minority women in the United States. Pharmacy. 2022 Feb 15;10(1):30.
9. Polman NJ, Ebisch RMF, Heideman DAM, et al. Performance of human papillomavirus testing on self-collected versus clinician-collected samples for the detection of cervical intraepithelial neoplasia of grade 2 or worse: a randomised, paired screen-positive, non-inferiority trial. The Lancet Oncology. 2019;20(2):229-238.
10. Costa S, Verberckmoes B, Castle PE, Arbyn M. Offering HPV self-sampling kits: an updated meta-analysis of the effectiveness of strategies to increase participation in cervical cancer screening. British Journal of Cancer. 2023 Mar 23;128(5):805-13.
11. Perkins RB, Guido RS, Castle PE, et al. 2019 ASCCP risk-based management consensus guidelines for abnormal cervical cancer screening tests and cancer precursors. J Low Genit Tract Dis. 2020;24(2):102-131.
12. Straughn, Jr, J Michael, and Catheryn Yashar. “Management of Early-Stage Cervical Cancer.” Www.uptodate.com, 2 Aug. 2024, https://www.uptodate.com/contents/management-of-early-stage-cervical-cancer. Accessed 13 Aug. 2024.
13. AMBOSS GmbH.Cervical cancer screening. https://amboss.com/. Accessed August 18, 2024.
14. Royalty-free music used for this episode: Lofi-Chilly by Gushito, downloaded on Nov 06, 2023, from https://www.videvo.net
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Episode 175: Alcohol Use Disorder Basics
30 août· Rio Bravo qWeek
Episode 175: Alcohol Use Disorder Basics
Future Dr. Sangha explains the clinical presentation, diagnosis, and fundamentals of the treatment of alcohol use disorder (AUD). Dr. Arreaza offers insights about the human aspect of the treatment of AUD.
Written by Darshpreet Sangha, MS4, Ross University School of Medicine. Editing and comments by Hector Arreaza, MD.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
What is Alcohol Use Disorder?
AUD is characterized as the inability to stop or control alcohol use despite adverse physical, social and occupational consequences.
According to DSM-5, it is a pattern of alcohol use that, over 12 months, results in at least two of the following symptoms, indicating clinically substantial impairment or distress:
Alcohol is frequently used in higher quantities or for longer periods than planned.There is a persistent desire or unsuccessful attempt to reduce or manage alcohol use.Activities that are required to get alcohol, consume alcohol, or recuperate from its effects take up a lot of time.A strong need or desire to consume alcohol—a craving.A pattern of drinking alcohol that prevents one from carrying out important responsibilities at work, school, or home.Sustained alcohol consumption despite ongoing or recurring interpersonal or social issues brought on by or made worse by alcohol's effects.Alcohol usage results in the reduction or cessation of important social, professional, or leisure activities.Frequent consumption of alcohol under risky physical circumstances.Continuing to drink even when one is aware of a chronic or recurrent health or psychological issue that may have been brought on by or made worse by alcoholTolerance: requiring significantly higher alcohol intake to produce the same intended effect. Withdrawal: Characterized by the typical withdrawal symptoms or a noticing relief after taking alcohol or a closely related substance, such as benzodiazepine.
How can we determine the severity of AUD?
Mild: 2–3 symptomsModerate: 4–5 symptomsSevere: >/= 6 symptoms
Who is at risk for AUD?
Note: Ancestry offers a DNA analysis to find out about your heritage. You can also send that DNA to a third party to learn about your risks for diseases and conditions (for example, Prometheus.) Anyone can find out about their risk for alcoholism by doing a DNA test.
The risk factors for AUD are:
Male genderAges 18-29Native American and White ethnicitiesHaving Significant disabilityHaving other substance use disorderMood disorder (MDD, Bipolar)Personality disorder (borderline, antisocial personality)
What is heavy drinking?
According to the National Institute of Alcohol Abuse and Alcoholism (NIAAA), heavy alcohol use is characterized as:
Males who drink > 4 drinks daily or > 14 drinks per week Females who drink > 3 drinks on any given day or > 7 drinks per week
Pathophysiology of AUD.
The pathogenesis of AUD is not well understood, but factors that may play a role are genetics, environmental influences, personality traits, and cognitive functioning. Also, genetic factors may decrease the risk of AUD, i.e., the flushing reaction, seen in individuals who are homozygous for the gene that encodes for aldehyde dehydrogenase, which breaks down acetaldehyde.
Who should be screened?
A person with AUD may not be easy to diagnose in a simple office visit, but some clues may point you in that direction. First of all, patients with AUD may present to you during their sober state, that´s why ALL adults (including pregnant patients) must be screened for AUD in primary care )Grade B recommendation). The frequency has not been determined but as a general rule, at least in Clinica Sierra Vista, we screen once a year. The USPSTF has concluded that there is insufficient evidence to recommend screening adolescents between 12-17 years old.
What are the clinical manifestations of AUD?
Some symptoms may be subtle, including sleep disturbance, GERD, HTN, but some may be obvious, such as signs of advanced liver disease (ascites, jaundice, bleeding disorders, etc.)
If you draw routine labs, you may find abnormal LFTs (AST:ALT ratio >2:1), macrocytic anemia (MCV >100 fL), and elevated Gamma-glutamyl transferase (GGT). All these findings are highly suggestive of AUD.
Patients with AUD may present in either an intoxication or withdrawal state.
Signs and symptoms of acute intoxication may include “slurred speech, nystagmus, disinhibited behavior, incoordination, unsteady gait, hypotension, tachycardia, memory impairment, stupor, or coma.”
Signs and symptoms of withdrawal range from tremulousness to hallucinations, seizures, and death. They are seen between 4 and 72 hours after the last drink, peaking at 48 hours, and can last up to 5 days. Alcohol withdrawal is one of the few fatal withdrawal syndromes that we know in medicine, and the symptoms can be assessed using a CIWA assessment.
Treatment of AUD.
There are factors to consider before starting treatment:
Evaluating the severity of AUD Establishing clear treatment goals is associated with better treatment outcomesAssessing readiness to change: It can be done by motivational interviewing and using the stages of change model, which are, Pre-contemplation, contemplation, preparation, action, maintenance, and relapse.Discussing treatment of withdrawal.
Treatment may be done as outpatient or it may require hospitalization. Dr. Beare sent an email with this information: “The approach to treating patients with AUD can be broken into two parts - the first is withdrawal management and the second is the long-term maintenance part. You MUST have a good plan for withdrawal treatment as it can be fatal if it's not addressed properly.”
“Patients with any history of seizures due to withdrawal or a history of delirium tremens need inpatient management. If their withdrawal symptoms are typically mild (agitation, tremors, sleeplessness, anxiety) then outpatient management may be appropriate, typically with a long-acting benzodiazepine such as Librium or Ativan.”
According to Dr. Beare, “the human aspect isa key element in treating alcohol use disorder. These patients arrive with tremendous amounts of suffering, shame, guilt, and fear. The relationship between the patient and provider needs to be built with compassion and understanding that this disease is horrible from the patient's perspective and using an algorithmic and calculated approach can cause significant harm to the rapport-building process, leading to lower success rates.”
Treatment requires a lot of motivation and willpower. Hopefully, we can use some tools to assist our patients to be successful.
-For mild disorder, Psychosocial interventions like motivational interviewing and mutual help groups like AA meetings may be enough to help our patient quit drinking.
-For moderate or severe disorder:
1st line treatment is Meditation and structured, evidence-based psychosocial interventions (CBT, 12-step facilitation); which leads to better outcomes
For patients who lack motivation, motivational interviewing can be a useful initial interventionFor motivated patients: medical management, combined behavioral intervention, or a combination of both can be utilizedFor patients with limited cognitive abilities, 12-step facilitation, or contingency management can be helpful For patients who have an involved partner: Behavioral couples therapy can be utilized
Medications for AUD.
The first-line pharmacological treatment is Naltrexone. It is given as a daily single dose and can be started while the patient is still actively drinking. There is a monthly dose of long-acting injectable naltrexone as well. Naltrexone is contraindicated in individuals taking opioids, and patients with acute hepatitis or hepatic failure. Alternative 1st line treatment is Acamprosate which can be used in people with contraindications to Naltrexone.
AUD is a chronic problem and requires a close follow-up to evaluate response to treatment and complications. Medications need to be used along with psychotherapy and support, and medications may need to be changed or adjusted depending on the patient. It is an individualized therapy that requires full engagement of the doctor, the patient, and their families or social support.
In conclusion, I would just like to add that, be compassionate because AUD is not a choice. AUD is a chronic problem like diabetes and HTN and may require a long road to recovery. Treatment includes psychotherapy, medications, and regular follow-up.
Thank you for listening!
Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!
_____________________
References:
Risky drinking and alcohol use disorder: Epidemiology, clinical features, adverse consequences, screening, and assessment, https://www.uptodate.com/contents/risky-drinking-and-alcohol-use-disorder-epidemiology-clinical-features-adverse-consequences-screening-and-assessment, accessed on August 18, 2024.Hasin DS, Stinson FS, Ogburn E, Grant BF. Prevalence, correlates, disability, and comorbidity of DSM-IV alcohol abuse and dependence in the United States: results from the National Epidemiologic Survey on Alcohol and Related Conditions. Arch Gen Psychiatry, Accessed on August 18, 2024.Alcohol use disorder: Treatment overview, https://www.uptodate.com/contents/alcohol-use-disorder-treatment-overview, assessed on August 18, 2024. Royalty-free music used for this episode, Grande Hip-Hop by Gushito, downloaded on Nov 06, 2023, from https://www.videvo.net
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Episode 174: GERD in Adults
19 juil.· Rio Bravo qWeek
Episode 174: GERD in Adults
Common and atypical symptoms are presented. Pathophysiology, diagnosis, and management are discussed. H. pylori's role is discussed during this episode.
Written by Jacquelyn Garcia MS4 Ross University School of Medicine. Comments by Hector Arreaza, MD.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
Definitions:
Gastroesophageal reflux (GER): occasional backflow of stomach acid into the esophagus. It's a common physiological process that happens to many people, especially after meals. Occurs less than twice a week. Associated with mild and temporary symptoms such as heartburn or regurgitation.
Gastroesophageal reflux disease (GERD): a chronic and more severe form of GER. It occurs when acid reflux happens frequently, typically more than twice a week, and/or causes esophageal injury/complications.
-Non-erosive reflux disease (NERD)= GER without evidence of esophageal injury on endoscopy.
-Erosive reflux disease (ERD)= GER with evidence of esophageal injury on endoscopy.
AFP Journal, January 2024: “Nonerosive GERD does not increase the likelihood of esophageal cancer. However, erosive GERD is associated with a doubled, but still low, risk of developing cancer, with the likelihood increasing over time.”
Pathophysiology:
The main pathophysiology behind GERD is lower esophageal sphincter (LES) dysfunction which can occur due to the following:
-LES Pressure: The LES is a muscular ring at the junction of the esophagus and stomach. It normally maintains a high-pressure zone to prevent reflux. In GERD, the intragastric pressure is higher than the pressure created by the LES. The tone of the LES can be reduced by caffeine, nitroglycerin, and scleroderma.
-Transient LES Relaxations (TLESRs): These are normal relaxations of the LES that occur independently of swallowing. In GERD, these relaxations are more frequent or prolonged, allowing acid to reflux into the esophagus.
-Anatomic abnormalities: A hiatal hernia occurs when a portion of the stomach protrudes through the diaphragm into the chest cavity. This disrupts the normal anatomy of the gastroesophageal junction, reducing the pressure barrier and promoting reflux.
Epidemiology:
It affects 10-20% of adults in Western cultures and less than 5% in Asia. Prevalence in the US ranges from 18.1% to 27.8% with a slightly higher rate in men.
Risk factors:
-Obesity, pregnancy, scleroderma, hiatal hernia; smoking, caffeine, alcohol, stress, fatty/fried/spicy foods. Spicy foods can be a challenge in some cultures (e.g. Mexican and Indian.) Sometimes, patients may ask for “something” to stop GERD but all they may need is dietary modification.
-Medications:
-aspirin, ibuprofen, clindamycin, tetracycline, bisphosphonates (irritate the esophagus and cause heartburn pain similar to GERD)
-anticholinergics, TCA’s, CCB’s, ACEi, statins, benzodiazepines, theophylline, opioids, progesterone (increase acid reflux and worsen GERD)
Clinical features:
Typical symptoms:
-heartburn (burning retrosternal pain)
-regurgitation (acidic stomach contents)
Atypical symptoms:
-chest pain (can mimic angina pectoris, squeezing/burning substernal, radiates to back/neck/jaw/arm)
-water brash (hypersalivation)
-globus sensation (lump in throat)
-nausea
-belching
-bloating
Alarm features in GERD:
-dysphagia
-odynophagia (pain with swallowing)
-new onset of dyspepsia in ≥60yo
-weight loss
-GI bleeding
-vomiting
-anemia
Diagnosis:
-There is no gold standard test
-Patient with typical symptoms: diagnosis can be based on clinical symptoms alone
-Patient with atypical symptoms: these symptoms can be seen in GERD but are not sufficient for diagnosis of GERD in the absence of typical symptoms. Need to rule out other disorders before associating the symptoms with GERD. (ex: chest pain r/o other causes such as MI with ECG)
-Patient with alarm features: refer to GI for upper GI endoscopy.
Complications:
-Esophagitis: Erosive reflux disease (ERD) = GER with evidence of esophageal distal injury on endoscopy; in untreated GERD 30% have esophagitis.
-Iron deficiency anemia: due to mucosal ulcerations -> chronic bleeding.
-Esophageal stricture: narrowing near GE junction, solid food dysphagia.
-Barrett Esophagus: intestinal metaplasia of esophagus due to chronic GERD (stratified squamous epithelium replaced by columnar epithelium)
-Risk factors: GERD for 5-10 years, >50yo, males, obesity, Caucasian, Tobacco use, family history
-Predisposes to esophageal adenocarcinoma
Role of H. pylori.
Sometimes we tend to think that H. pylori is the cause of GERD. “H. pylori infection appears to protect the esophagus from gastroesophageal reflux disease, Barrett's esophagus, dysplasia in Barrett's esophagus, and esophageal adenocarcinoma, perhaps by causing chronic gastritis that interferes with acid production.”
It is unclear whether long-term use of PPIs heightens the risk of atrophic gastritis in patients with H. pylori. Consequently, routine screening for H. pylori infection and empiric eradication of H. pylori are NOT advised for patients with GERD. However, if H. pylori is diagnosed in the setting of GERD, eradication of H. pylori has been associated with an improvement of symptoms in patients with antral-predominant gastritis.
Treatment:
Two categories:
Mild/intermittent symptoms (
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Episode 173: Acute Osteomyelitis
5 juil.· Rio Bravo qWeek
Episode 173: Acute Osteomyelitis
Future Dr. Tran explains the pathophysiology of osteomyelitis and describes the presentation, diagnosis and management of acute osteomyelitis. Dr. Arreaza provides information about
Written by Di Tran, MSIII, Ross University School of Medicine. Editing and comments by Hector Arreaza, MD.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
What is osteomyelitis?
Osteomyelitis, in simple terms, is an infectious disease that affects both bone and bone marrow and is either acute or chronic. According to archaeological findings of animal fossils with a bone infection, osteomyelitis was more than likely to be known as a “disease for old individuals”.Our ancestors over the years have used various vocabulary terms to describe this disease until a French surgeon, Dr. Nelaton, came up with the term “Osteomyelitis” in 1844.
This is the beauty of medical terms, Latin sounds complicated for some people, but if you break up the term, it makes sense: Osteo = bone, myelo = marrow, itis = inflammation. So, inflammation of the bone marrow.
Traditionally, osteomyelitis develops from 3 different sources:
First category is the “hematOgenous” spread of the infection within the bloodstream, as in bacteremia. It is more frequent in children and long bones are usually affected. [Arreaza: it means that the infection started somewhere else but it got “planted” in the bones]Second route is “direct inoculation” of bacteria from the contiguous site of infection “without vascular insufficiency”, or trauma, which may occur secondary to fractures or surgery in adults. In elderly patients, the infection may be related to decubitus ulcers and joint replacements.And the third route is the “contiguous” infection “with vascular insufficiency”, most seen in a patient with a diabetic foot infection.
Patients with vascular insufficiency often have compromised blood supply to the lower extremities, and poor circulation impairs healing. In these situations, infection often occurs in small bones of the feet with minimal to no pain due to neuropathy.They can have ulcers, as well as paronychia, cellulitis, or puncture wounds.
Thus, the importance of treating onychomycosis in diabetes because the fungus does not cause a lot of problems by itself, but it can cause breaks in the nails that can be a port of entry for bacteria to cause severe infections. Neuropathy is an important risk factor because of the loss of protective sensation. Frequently, patients may step on a foreign object and not feel it until there is swelling, purulent discharge, and redness, and they come to you because it “does not look good.”
Acute osteomyelitis often takes place within 2 weeks of onset of the disease, and the main histopathological findings are microorganisms, congested blood vessels, and polymorphonuclear leukocytes, or neutrophilic infiltrates.
What are the bugs that cause osteomyelitis?
Pathogens in osteomyelitis are heavily depended on the patient’s age. Staph. aureus is the most common culprit of acute hematogenous osteomyelitis in children and adults. Then comes Group A Strep., Strep. pneumoniae, Pseudomonas, Kingella, and methicillin-resistant Staph. aureus. In newborns, we have Group B Streptococcal.
Less common pathogens are associated with certain clinical presentations, including Aspergillus, Mycobacterium tuberculosis, and Candida in the immunocompromised.Salmonella species can be found in patients with sickle cell disease, Bartonella species in patients with HIV infection, and Pasteurella or Eikenella species from human or animal bites.
It is important to gather a complete medical history of the patient, such as disorders that may put them at risk of osteomyelitis, such as diabetes, malnutrition, smoking, peripheral or coronary artery disease, immune deficiencies, IV drug use, prosthetic joints, cancer, and even sickle cell anemia. Those pieces of information can guide your assessment and plan.
What is the presentation of osteomyelitis?
Acute osteomyelitis may present symptoms over a few days from onset of infection but usually is within a 2-week window period. Adults will develop local symptoms of erythema, swelling, warmth, and dull pain at the site of infection with or without systemic symptoms of fever or chills.Children will also be present with lethargy or irritability in addition to the symptoms already mentioned.
It may be challenging to diagnose osteomyelitis at the early stages of infection, but you must have a high level of suspicion in patients with high risks. A thorough physical examination sometimes will show other significant findings of soft tissue infection, bony tenderness, joint effusion, decreased ROM, and even exposed bone.
Diagnosis.
As a rule of thumb, the gold standard for the diagnosis of osteomyelitis is bone biopsy with histopathology findings and tissue culture. There is leukocytosis, but then WBC counts can be normal even in the setting of acute osteomyelitis.Inflammatory markers (CRP, ESR) are often elevated although both have very low specificity.
Blood cultures should always be obtained whenever osteomyelitis is suspected. A bone biopsy should also be performed for definitive diagnosis, and specimens should undergo both aerobic and anaerobic cultures. In cases of osteomyelitis from diabetic foot infection, do the “probe to bone” test. What we do is we use a sterile steel probe to detect bone which is helpful for osteomyelitis confirmation.
Something that we can’t miss out on is radiographic imaging, which is quite important for the evaluation of osteomyelitis. Several modalities are useful and can be used for the work-up plan; plain radiographs often are the very first step in the assessment due to their feasibility, low cost, and safety. Others are bone scintigraphy, CT-scan, and MRI. In fact, the MRI is widely used and provides better information for early detection of osteomyelitis than other imaging modalities. It can detect necrotic bone, sinus tracts, and even abscesses. We look for soft tissue swelling, cortical bone loss, active bone resorption and remodeling, and periosteal reaction. Oftentimes, plain radiography and MRI are used in combination.
Treatment:
Treatment of osteomyelitis actually is a teamwork effort among various medical professionals, including the primary care provider, the radiologist, the vascular, the pharmacist, the podiatrist, an infectious disease specialist, orthopedic surgeons, and the wound care team.
Something to take into consideration, if the patient is hemodynamically stable it is highly recommended to delay empirical antibiotic treatment 48-72 hours until a bone biopsy is obtained. The reason is that with percutaneous biopsy ideally done before the initiation of antibiotic treatment, “the microbiological yield will be higher”.We’ll have a better idea of what particular bugs are causing the problem and guide the treatment appropriately.
The choice of antibiotic therapy is strongly determined by susceptibilities results. The antibiotic given will be narrowed down only for the targeted susceptible organisms. In the absence of such information, or when a hospitalized patient presents with an increased risk for MRSA infection, empiric antibiotic coverage is then administered while awaiting culture results.
It should be broad-spectrum antibiotics and include coverage for MRSA, broad gram-negative and anaerobic bacteria. For example, vancomycin plus piperacillin-tazobactam, or with broad-spectrum cephalosporin plus clindamycin. Treatment will typically be given for 4 to 6 weeks.
The duration between 4-6 weeks is important for complete healing, but a small study with a small sample showed that an even shorter duration of 3 weeks may be effective, but more research is needed.
In certain situations, surgery is necessary to preserve viable tissue and prevent recurrent infection, especially when there are deep abscesses, necrosis, or gangrene, amputation or debridement is deemed appropriate.
If the infected bone is completely removed, patients may need a shorter course of antibiotics, even a few days only. Amputation can be very distressing, especially when we need to remove large pieces of infected bone, for example, a below-the-knee amputation. We need to be sensitive to the patient’s feelings and make a shared decision about the best treatment for them.
In patients with diabetes, additional care must be taken seriously, patient education about the need for compliance with treatment recommendations, with careful wound care, and good glycemic control are all beneficial for the healing and recovery process.
Because this is a very common problem in the clinic and at the hospital, we must keep our eyes wide open and carefully assess patients with suspected osteomyelitis to detect it promptly and start appropriate treatment. Adequate and timely treatment is linked to fewer complications and better outcomes.
_________________________
Conclusion: Now we conclude episode number 173, “Acute Osteomyelitis.” Future Dr. Tran explained the pathophysiology, diagnosis, and management of osteomyelitis. A bone biopsy is the ideal method of diagnosis. Delaying antibiotic treatment a few days until you get a biopsy is allowed if the patient is stable, but if the patient is unstable, antibiotics must be started promptly. Dr. Arreaza mentioned the implications of amputation and that we must discuss this treatment empathically with our patients.
This week we thank Hector Arreaza and Di Tran. Audio editing by Adrianne Silva.
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:
Bury DC, Rogers TS, Dickman MM. Osteomyelitis: Diagnosis and Treatment. Am Fam Physician. 2021 Oct 1;104(4):395-402. PMID: 34652112.Cunha BA. Osteomyelitis in elderly patients. Clin Infect Dis. 2002 Aug 1;35(3):287-93. doi: 10.1086/341417. Epub 2002 Jul 11. PMID: 12115094.Fritz JM, McDonald JR. Osteomyelitis: approach to diagnosis and treatment. Phys Sportsmed. 2008 Dec;36(1):nihpa116823. doi: 10.3810/psm.2008.12.11. PMID: 19652694; PMCID: PMC2696389.Hatzenbuehler J, Pulling TJ. Diagnosis and management of osteomyelitis. Am Fam Physician. 2011 Nov 1;84(9):1027-33. PMID: 22046943.Hofstee MI, Muthukrishnan G, Atkins GJ, Riool M, Thompson K, Morgenstern M, Stoddart MJ, Richards RG, Zaat SAJ, Moriarty TF. Current Concepts of Osteomyelitis: From Pathologic Mechanisms to Advanced Research Methods. Am J Pathol. 2020 Jun;190(6):1151-1163. doi: 10.1016/j.ajpath.2020.02.007. Epub 2020 Mar 16. PMID: 32194053.Momodu II, Savaliya V. Osteomyelitis. [Updated 2023 May 31]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2024 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532250/Royalty-free music used for this episode: Trap Chiller by Gushito, downloaded on Nov 06, 2023, from https://www.videvo.net
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Episode 172: NAFLD and Obesity
28 juin· Rio Bravo qWeek
Episode 172: NAFLD and Obesity
Future Dr. Nguyen explains the pathophysiology of non-alcoholic fatty liver disease and how it relates to obesity. Dr. Arreaza gives information about screening and diagnosis of NAFLD.
Written by Ryan Nguyen, MS4, Ross University School of Medicine. Comments by Hector Arreaza, MD.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
Introduction/Pathophysiology
Nonalcoholic fatty liver disease (NAFLD) refers to the buildup of excess fat in liver cells, occurring without the influence of alcohol or drugs. Nonalcoholic steatohepatitis (NASH) represents a more severe form of NAFLD, characterized by inflammation and liver cell injury due to fat accumulation. If left untreated, NASH can progress to liver fibrosis or cirrhosis. Typically, NAFLD/NASH is diagnosed after other liver conditions are ruled out, making it a diagnosis of exclusion.
NAFLD -> NASH -> Cirrhosis -> Liver failure. Another term for NAFLD is metabolic dysfunction-associated steatotic liver disease.
Fatty liver disease is identified when more than 5% of liver weight consists of fat, whereas, NASH is diagnosed when this fat accumulation is accompanied by inflammation and liver cell injury, sometimes leading to fibrosis. Understanding these distinctions is crucial in recognizing and managing the spectrum of liver conditions associated with obesity and metabolic syndrome.
BMI serves as a tool to gauge body fat levels: individuals are categorized as normal weight if their BMI falls between 18.5 and 24.9, overweight if it ranges from 25 to 29.9. Class I obesity is diagnosed with a BMI of 30 to 34.9, class II obesity between 35 and 39.9, and class III obesity when BMI exceeds 40.
Obesity puts you at risk of NAFLD, but you can also see NAFLD in non-obese patients, but the prevalence is very low, about 5%. What did you learn about the demographics of NAFLD?
NAFLD is most widespread in regions like South Asia, the Middle East, Mexico, Central and South America, with prevalence rates exceeding 30%. In the United States, prevalence varies with approximately 23-27%, notably higher among Asians at 30%, followed by Hispanic individuals at 21%, White individuals at 12.5%, and Black individuals at 11.6%.
Across all racial groups, obesity plays a significant role, affecting more than two-thirds of individuals diagnosed with NAFLD. Understanding these demographics underscores the global impact of obesity on NAFLD prevalence.
Diagnosis: Screening/Labs/Imaging/Tools
The American Association for the Study of Liver Diseases does not recommend screening for NAFLD, but if it is discovered an appropriate workup is warranted.
AST/ALT Ratio
Liver health can be assessed by a series of tests aimed at assessing fat accumulation, inflammation, and fibrosis. Initial screening often includes laboratory tests such as measuring the ratio between aspartate transaminase (AST) and alanine transaminase (ALT), where a ratio less than 1 may suggest possible NAFLD, although it is not diagnostic on its own. Normally, AST is slightly more elevated than ALT. So, if the AST/ALT ratio is lower, then means that ALT is higher than AST.
FibroSure®.
Additionally, you can measure indirect markers of fibrosis with tests such as FibroSure or FibroTest blood tests that combine several biomarkers including age, sex, gamma-glutamyl-transferase (GGT), total bilirubin, alpha-2-macroglobulin, apolipoprotein A1, haptoglobin, and ALT to provide insights into liver health.
Some people may be more familiar with FibroSure before Hepatitis C treatment. You can get a fibrosis score (F0-F4), and it is considered significant fibrosis if the score is > or equal to F2. Imaging plays a crucial role in diagnosing NAFLD without the need for invasive procedures like liver biopsy. Vibration-controlled transient elastography (Fibroscan) uses ultrasound to measure liver stiffness, indicating potential fibrosis and inflammation. While noninvasive and portable, it focuses solely on liver ultrasound and may not be universally accessible. MRI with proton density fat fraction (MRI-PDFF) offers a comprehensive assessment of liver fat content, commonly used in clinical and research settings for NAFLD and NASH evaluation.
For evaluating hepatic fibrosis in patients with suspected NAFLD, tools like the Fibrosis-4 Index (FIB-4) incorporate age, AST, ALT, and platelet count to estimate the likelihood of liver disease progression. These screening methods collectively aid in diagnosing and monitoring NAFLD, particularly in individuals at risk due to factors like prediabetes, type 2 diabetes, obesity, and abnormal liver enzyme ratios.
With the FIB-4 you can get a faster answer than FibroSure because you only need 4 elements: Age, platelet count, AST and ALT. Cirrhosis is less likely if FIB-4 is 3.25. Understanding these diagnostic approaches is essential for early detection and management of NAFLD in clinical practice.
Some researchers are invested in diagnosis and treating NAFLD while others recommend against labeling patients with NAFLD. A 2018 Lancet article concluded that the risks of over-diagnosing and overtreating NAFLD exceed the benefits of screening or periodic imaging because of “the low hepatic mortality, high false-positive rate of ultrasonography, selection bias of current studies, and lack of viable treatment.” However, patients who suffer from metabolic syndrome should be counseled about dietary modification and physical activity regardless of their liver condition.
NAFLD and obesity
Fatty liver disease is often caused by multiple insults towards either genetically or environmentally predisposed individuals. Family history of NAFLD and having specific genetic variants are important risk factors for NAFLD. Those with prior health conditions can have increased susceptibility to NAFLD including T2DM leading to insulin resistance, metabolic syndrome, sleep apnea, hepatitis C, and cardiovascular or chronic kidney disease.
A sedentary lifestyle and unhealthy nutrition (especially high intake of processed carbohydrates) cause an increase in free fatty acids leading to hepatic fat deposition → ballooning of hepatocytes → leading to hepatocyte injury/death → inflammation with fibroblast recruitment → end result of fibrosis/cirrhosis. Just a quick reminder, NAFLD is defined as fatty liver with >5% hepatic fat and NASH is defined as fatty liver with >5% hepatic fat with inflammation, hepatocyte injury, with or without fibrosis that we can determine through imaging.
A leading concern for the development of NAFLD is the consumption of high fructose corn syrup. High fructose corn syrup (HFCS), commonly found in candy, processed sweets, soda, fruit juices, and other processed foods, is linked to non-alcoholic fatty liver disease (NAFLD). Unlike natural whole fruits, which contain fiber and are generally healthier due to their slower absorption, HFCS lacks fiber and is quickly absorbed, leading to rapid transport to the liver. This process contributes to NAFLD by increasing the hepatic synthesis of lipids and interfering with insulin signaling. To avoid HFCS, individuals are encouraged to consume whole fruits rather than fruit juices and adopt diets rich in whole grains, lean meats, plant-based proteins, fruits, and vegetables, such as the Mediterranean or DASH diets, which are less likely to promote NAFLD, especially in those with healthy body weight.
NAFLD treatment.
Avoiding alcohol seems very obvious, but we need to mention it. Avoiding heavy alcohol consumption is recommended and complete abstinence is suggested.
Weight loss is crucial; even a modest reduction of 3–5% in body weight can alleviate hepatic steatosis, with greater improvements typically seen with 7–10% weight loss, particularly beneficial for addressing histopathological features of NASH, such as fibrosis. We must focus on tailored medical nutrition therapy and regular physical activity.
A strategic meal plan is essential, emphasizing achieving a healthy body weight while limiting trans fats and ultra-processed carbohydrates. Options like the Mediterranean diet, which balances lean proteins and restricts processed carbohydrates have shown promise.
Dynamic aerobic and resistance exercises play a significant role in managing NAFLD. They help maintain a healthy weight and enhance peripheral insulin sensitivity, reduce circulating free fatty acids and glucose levels, and boost intrahepatic fatty acid oxidation while curbing fatty acid synthesis. These benefits contribute to mitigating liver damage associated with NAFLD, offering therapeutic advantages beyond mere weight reduction.
Exercise may not be a great tool for weight loss, but it is a great tool for weight maintenance, liver health, and overall health as well. “Most patients with NAFLD die from vascular causes, but NAFLD puts patients at increased risk of cardiovascular death”.
Medications for NAFLD.
Regarding pharmacotherapy, while no medications are currently FDA-approved specifically for NAFLD treatment, some options show promise in clinical settings. Vitamin E supplementation at 800 IU (international units) daily has demonstrated biochemical and histological improvements in NASH cases without diabetes or cirrhosis, though long-term use may elevate prostate cancer risks. It is important to make a shared decision with the patient before starting Vitamin E supplementation.
Medications like pioglitazone can reduce liver fat and improve NASH, even as they may increase body weight. But our favorite, GLP-1 receptor agonists, such as liraglutide and semaglutide, also show potential in reducing liver fat and improving NASH symptoms, and this is an emerging therapeutic option for managing this condition.
If you decide to treat, then you should monitor as part of the treatment. An aminotransferase check is recommended 6 months after starting a weight loss program. If levels do not improve or do not return to normal after 5-7% of weight loss, another cause of elevated transaminases needs to be investigated.
You also need to monitor fibrosis in patients with >F2. If fibrosis has been proven by liver biopsy, you can order FibroSure every 3-4 years.
Having a fatty liver may be a red flag that your patient has a metabolic problem. If you discover it, start interventions that would benefit not only the liver but the whole metabolic profile of your patient. The Obesity Medicine Association (OMA) issued a Clinical Practice Statement (CPS) regarding NAFLD and obesity stating that patients with obesity are at increased risk for NAFLD and NASH. It recommends that clinicians strive to understand the etiology, diagnosis, and optimal treatment of NAFLD with a goal to prevent NASH in their patients.
Regular exercise, even walking 30 minutes a day can show many benefits in curbing fatty accumulation in the liver. Having a proper diet with avoidance of high fructose corn syrup can overall help in reducing NAFLD/NASH.
_____________________
Conclusion: Now we conclude episode number 172, “NAFLD and Obesity.” Future Dr. Nguyen explained that NAFLD and obesity are closely related and NAFLD can lead to NASH and cirrhosis in some patients. Dr. Arreaza explained that screening may not be recommended by some medical societies, but others are in favor of screening and treating this disease. However, most people agree that NAFLD is a sign of metabolic disease and a good reason to talk about healthy eating and physical activity with our patients. There are no FDA-approved medications to treat NAFLD, but some evidence suggests that Vitamin E can improve it and GLP-1 receptor agonists are a promising option.
This week we thank Hector Arreaza and Ryan Nguyen. Audio editing by Adrianne Silva.
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:
Karjoo S, Auriemma A, Fraker T, Edward H. Nonalcoholic fatty liver disease and obesity: An Obesity Medicine Association (OMA) Clinical Practice Statement (CPS) 2022. https://doi.org/10.1016/j.obpill.2022.100027.Curry M, Afdhal N. Noninvasive assessment of hepatic fibrosis: Overview of serologic tests and imaging examinations. https://www.uptodate.com/contents/noninvasive-assessment-of-hepatic-fibrosis-overview-of-serologic-tests-and-imaging-examinationsRoyalty-free music used for this episode: Cool Groove (Alt-Mix) by Videvo, downloaded on Nov 06, 2023, from https://www.videvo.net
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Episode 171: Postpartum Blues, Depression, and Psychosis
21 juin· Rio Bravo qWeek
Episode 171: Postpartum Blues, Depression, and Psychosis
Future Dr. Nguyen defines and explains the difference between baby blues, depression, and psychosis. Dr. Arreaza added comments about screening and management of these conditions.
Written by Vy Nguyen, OMSIII, Western University of Health Sciences, College of Osteopathic Medicine of the Pacific. 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.
Pregnancy is one of the most well-celebrated milestones in one’s life. However, once the baby is born, the focus of the family and society quickly shifts to the new member. It is important to continue to care for our mothers and offer them support physically and mentally as they begin their transition into their role. Peripartum mood disorders affect both new and experienced mothers as they navigate through the challenges of motherhood.
The challenges of motherhood are not easy to spot, and they include sleep deprivation, physical exhaustion, dealing with pain, social isolation, and financial pressures, among other challenges. Let’s focus on 3 aspects of the postpartum period: Postpartum Blues (PPB), Post-partum Depression (PPD) and Post-partum Psychosis (PPP). By the way, we briefly touched on this topic in episode 20, a long time ago.
Postpartum blues (PPB) present as transient and self-limiting low mood and mild depressive symptoms that affect more than 50% of women within two or three days of childbirth and resolve within two weeks of onset. Symptoms vary from crying, exhaustion, irritability, anxiety, appetite changes, and decreased sleep or concentration to mood lability.
Women are at risk for PPB.
Several factors are thought to contribute to the increased risk of postpartum blues including a history of menstrual cycle-related mood changes, mood changes associated with pregnancy, history of major depression, number of lifetime pregnancies, or family history of postpartum depression.
Pathogenesis of PPB: While pathogenesis remains unknown, hormonal changes such as a dramatic decrease in estradiol, progesterone, and prolactin have been associated with the development of postpartum blues. In summary, PPB is equivalent to a brief, transient “sad feeling” after the delivery.
Peripartum depression (PPD) occurs in 20% of women and is classified as depressive symptoms that appear within six weeks to 1 year after childbirth. Those with baby blues have an increased risk of developing postpartum depression. About 50% of “postpartum” major depressive episodes begin before delivery, thus the term has been updated from “postpartum” to “peripartum” depressive episodes.
Some risk factors include adolescent patients, mothers who deliver premature infants, and women living in urban areas. Interestingly, African American and Hispanic mothers are reported to have onset of symptoms within two weeks of delivery instead of six like their Caucasian counterparts.
Additional risks include psychological risks such as a personal history of depression, anxiety, premenstrual syndrome, and sexual abuse; obstetric risks such as emergency c-sections and hospitalizations, preterm or low birth infant, and low hemoglobin; social risks such as lack of social support, domestic violence in form of spousal physical/sexual/verbal abuse; lifestyle risks such as smoking, eating sleep patterns and physical activities. Peripartum depression can present with or without psychotic features, which may appear between 1 in 500 or 1 in 1,000 deliveries, more common in primiparous women.
Pathogenesis of PPD: Much like postpartum blues, the pathogenesis of postpartum depression is unknown. However, it is known that hormones can interfere with the hypothalamic-pituitary-adrenal axis (HPA) and lactogenic hormones. HPA-releasing hormones increase during pregnancy and remain elevated up to 12 weeks postpartum. The body receptors in postpartum depression are susceptible to the drastic hormonal changes following childbirth which can trigger depressive symptoms. Low levels of oxytocin and prolactin also play a role in postpartum depression causing moms to have trouble with lactation around the onset of symptoms.
The USPSTF recommends screening for depression in the adult population, including pregnant and postpartum persons, as well as older adults. Edinburgh Postnatal Depression Scale (EPDS) can be used in postpartum and pregnant persons (Grade B recommendation).
Postpartum psychosis (PPP) is a psychiatric emergency that often presents with confusion, paranoia, delusions, disorganized thoughts, and hallucinations. Around 1-2 out of 1,000 new moms experience postpartum psychosis with the onset of symptoms as quickly as several days and as late as six weeks after childbirth. Given the high risk of suicide and harm, individuals with postpartum psychosis require immediate evaluation and treatment.
Postpartum psychosis is considered multifactorial, and the single most important risk factor is first pregnancy with family or personal history of bipolar 1 disorder. Other risk factors include a prior history of postpartum psychosis, family history of psychosis, history of schizoaffective disorder or schizophrenia, or discontinuation of psychiatric medications.
Studies show that patients with a history of decreased sleep due to manic episodes are twice as likely to have postpartum psychosis at some point in their lives. However, approximately 50% of mothers who experience psychosis for the first time do not have a history of psychiatric disorder or hospitalization.
Evaluation.
Symptoms of postpartum blues should not meet the criteria for a major depressive episode and should resolve in 2 weeks. The Edinburg Postpartum Depression Scale which is a useful tool for assessing new moms with depressive symptoms.
Postpartum depression is diagnosed when the patient presents with at least five depressive symptoms for at least 2 weeks. According to the DSM5, postpartum depression is defined as a major depressive episode with peripartum onset of mood symptoms during pregnancy or in the 4 weeks following delivery. Symptoms for diagnosis include changes in sleep, interest, energy, concentration, appetite, psychomotor retardation or agitation, feeling of guilt or worthlessness, and suicidal ideation or attempt. These symptoms are not associated with a manic or hypomanic episode and can often lead to significant impediments in daily activities.
Peripartum-onset mood episodes can present with or without psychotic features. The depression can be so severe that the mother commits infanticide. Infanticide can happen, for example, with command hallucinations or delusions that the infant is possessed.
While there are no standard screening criteria in place of postpartum psychosis, questionnaires mentioned earlier such as the Edinburg Postpartum Depression Scale can assess a patient’s mood and identify signs of depression and mania.
It is important after a thorough history and physical examination to order labs to rule out other medical conditions that can cause depressive and psychotic symptoms. Disorders like electrolyte imbalance, hepatic encephalopathy, thyroid storm, uremia, substance use, infections, and even stroke can mimic a psychiatric disorder. So, How can we treat patients who are diagnosed with a peripartum mood disorder?
Management.
On the spectrum of peripartum mood disorders, postpartum blues are the least severe and should be self-limiting by week 2. However, patients should be screened for suicidal ideation, paranoia, and homicidal ideation towards the newborn. Physicians should provide validation, education, and resources especially support with sleep and cognitive therapy and/or pharmacotherapy can be recommended if insomnia persists.
Regarding postpartum depression, the first-line treatment includes psychotherapy and antidepressants. For those with mild to moderate depression or hesitant to start on medications, psychosocial and psychotherapy alone should be sufficient. However, for those with moderate to severe symptoms, a combination of therapy and antidepressants, such as selective serotonin reuptake inhibitors, is recommended. Once an effective dose is reached, patients should be treated for an additional 6 to 12 months to prevent relapse. In severe cases, patients may need to be hospitalized to treat their symptoms and prevent complications such as self-harm or infanticide.
Most SSRIs can be detected in breast milk, but only 10 percent of the maternal level. Thus, they are considered safe during breastfeeding of healthy, full-term infants. So, you mentioned SSRIs, but also SNRIs, bupropion, and mirtazapine are reasonable options for treatment. In patients who have never been treated with antidepressants, zuranolone (a neuroactive steroid) is recommended. Zuranolone is easy to take, works fast, and is well tolerated. Treatment with zuranolone is consistent with practice guidelines from the American College of Obstetricians and Gynecologists.
While there are no current guidelines to manage postpartum psychosis, immediate hospitalization is necessary in severe cases. Patients can be started on mood stabilizers such as lithium, valproate, and lamotrigine, and atypical antipsychotics such as quetiapine, and olanzapine, to name a few. Medications like lithium can be eliminated through breast milk and can expose infants to toxicity.
The use of medications such as SSRIs, carbamazepine, valproate, and short-acting benzodiazepines are relatively safe and can be considered in those with plans to breastfeed. Ultimately, it is a decision that the patient can make after carefully discussing and weighing the pros and cons of the available medical management.
While the prognosis of peripartum mood disorders is relatively good with many patients responding well to treatments, these disorders can have various negative consequences. Individuals with a history of postpartum blues are at increased risk of developing postpartum depression. Similarly, those with a history of postpartum psychosis are at risk of experiencing another episode of psychosis in future pregnancies. Additionally, postpartum depression can have a detrimental effect on mother-infant bonding and affect the growth and development of the infant. These children may have difficulties with social interactions, cognitive development, and depression.
In summary, following the birth of a baby can pose new challenges and often is a stressful time for not only the mother but also other family members. Validation and reassurance from primary care physicians in an empathetic and understanding manner may offer support that many mothers may not have in their close social circle. As the first contact, primary care physicians can identify cues and offer support promptly that will not only improve the mental well-being of mothers but also that of the growing children.
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Conclusion: Now we conclude episode number 171, “Postpartum blues, depression, and psychosis.” These conditions may be more common than you think. So, be alert during your prenatal and postpartum visits and start management as needed. Psychotherapy and psychosocial therapy alone may be effective but do not hesitate to start antidepressants or antipsychotics when necessary. Make sure you involve the family and the patient in the decision-making process to implement an effective treatment.
This week we thank Hector Arreaza and Vy Nguyen. Audio editing by Adrianne Silva.
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:
Raza, Sehar K. and Raza, Syed. Postpartum Psychosis. National Library of Medicine. Last updated Jun 26, 2023. https://www.ncbi.nlm.nih.gov/books/NBK544304/Balaram, Kripa and Marwaha, Raman. Postpartum Blues. National Library of Medicine. Last updated Mar 6, 2023. https://www.ncbi.nlm.nih.gov/books/NBK554546/Mughal, Saba, Azhar, Yusra, Siddiqui, Waquar. Postpartum Depression. National Library of Medicine. Last updated Oct 7, 2022. https://www.ncbi.nlm.nih.gov/books/NBK519070/Royalty-free music used for this episode: Good Vibes by Simon Pettersson, downloaded on July 20, 2023, from https://www.videvo.net/royalty-free-music/.
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Episode 170: Schizophrenia: An Overview
10 mai· Rio Bravo qWeek
Episode 170: Schizophrenia: An Overview
Future Dr. Chng explains the diagnostic criteria and describes how to treat schizophrenia. Dr. Arreaza mentions additional risk factors and social aspects of schizophrenia.
Written by Tiffanny Chng, MSIV, Ross University School of Medicine. Comments by Hector Arreaza, MD.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
Schizophrenia may be an intriguing disease for many, even for health care providers. Schizophrenia is frequently misunderstood and stigmatized. Receiving a diagnosis of schizophrenia can be life-altering and cause significant distress in patients and their families, but it can also impact their work, relationships, and even their communities.
Epidemiology of schizophrenia:
Schizophrenia has a prevalence of about 1% worldwide, and a prevalence of about 0.6% in the US. Although the distribution between males and females is comparable, males will typically present with their first episode, sometimes known as a “psychotic break” in the early 20’s as opposed to women who may present in their late 20s or early 30s. Despite having a low prevalence, the NIH lists schizophrenia as one of the top 15 leading causes of disability and disease burden in the world.
In 2019 the economic burden of schizophrenia in the US was $343 billion. For comparison, in 2019, diabetes had an economic burden of $760 billion in the US, however, the prevalence of diabetes that year was 11.6%, more than 10 times that of schizophrenia.
Patients who are diagnosed with schizophrenia are also at increased risk of a multitude of co-occurring medical conditions: alcohol and substance abuse disorders, mood disorders, and metabolic disturbances (diabetes, hyperlipidemia, and obesity, which may be exacerbated with the use of antipsychotics). These patients have a two-to-four-fold increased risk of premature mortality with an estimated potential life loss of ~28.5 years. Of note, 4-10% of patients with schizophrenia die secondary to suicide.
Pathogenesis:
The exact pathogenesis of schizophrenia is unknown, but we do know that it is a combination of genetic, neurological, and environmental factors.
Genetics: Twin studies conducted in mono and dizygotic twins have shown that schizophrenia is highly inheritable (~80%). Although there are no specific genes that directly cause the disease state, genome-wide association studies have shown polygenic additive effects of 108 single nucleotide polymorphisms. This includes genes involved in the dopaminergic and glutamate pathways, which are the basis of antipsychotic medications.
Epigenetics: Studies have also shown that epigenetics is a potential factor that plays into the risk of developing schizophrenia. Having a history of obstetric complications, for example, has an almost two-fold increased risk of schizophrenia in the child during early adulthood. Such complications include maternal infections, preterm labor, and fetal hypoxia. Certain infections and pro-inflammatory disease states, such as Celiac and Graves’ disease have also been associated with schizophrenia. The suggested pathophysiology is thought to involve pro-inflammatory cytokines crossing the blood-brain barrier inducing or exacerbating psychosis or cognitive impairment.
Trauma: As in many other psychiatric conditions, childhood trauma or severe childhood adversities, especially emotional neglect, have also been shown to increase the risk of schizophrenia later in life.
Cannabis and Immigration: So, you mentioned the role of genetics, epigenetics, and inflammation. I’d like to mention the use of cannabis as a risk factor for developing psychosis as well, more specifically the THC component of cannabis. Something to keep in mind during these times when cannabis is being studied in more detail. Also, this is interesting: immigration puts you at risk for schizophrenia, and the risk can be as high as four-fold, depending on the study. Some explanations for this are increased discrimination, stress, and even low vitamin D. Tiffany, how do we diagnose schizophrenia?
DSM-5 Diagnostic Criteria:
The DSM-5 identifies 5 diagnostic criteria for schizophrenia:
Patient must have two or more active phase symptoms for one month or longer: (1) Delusions, (2) Hallucinations (auditory, visual, or tactile) (3) Disorganized speech, (4) Negative symptoms (flat affect, avolition, social withdrawal, anhedonia), or (5) Catatonic behavior (which can be a collection of abnormal physical movements, the lack of movement or resistance to movement, psychomotor agitation). For the first criterion to be met, the patient must have delusions, hallucinations, or disorganized speech as one of their two presenting symptoms. Arreaza: The 1-month duration can be less if the patient is successfully treated.The symptoms experienced by the patient must impair their level of functioning in one or more major areas (professional career, relationships, and self-care). In addition, the disruption must be present most of the time since the onset of symptoms. There must be continuous signs of disturbance for at least 6 months. Within these 6 months, there must be at least 1 month where the patient experiences symptoms mentioned in the first criteria (delusions, hallucinations, disorganized speech, negative symptoms, or catatonic behavior). The disturbance may only be negative symptoms or attenuated positive symptoms (unusual perceptual experiences, odd beliefs, etc.)Mood disorders must be ruled out. This includes bipolar disorder with psychotic features, depressive disorder with psychotic features, and schizoaffective disorder. The behavioral disturbances must not be attributable to any substance use or medical conditions.
After the diagnosis of schizophrenia has been made for 1 year or more, specifiers can be added to further categorize the disease state, according to the DSM-V:
Acute episode: a period in which all symptomatic criteria are met.Partial remission: a period in which symptomatic criteria are only partially met and symptoms are improved from a previous episode.Full remission: a period in which no symptomatic criteria are met (for a minimum of 6 months).Continuous: symptoms prevalent for the majority of the illness course.
Goals of Treatment:
Reduce acute symptoms to allow patients to return to their baseline level of functioning. Prevent recurrence and maximize a patient’s quality of life using maintenance therapy.
There are 2 components of treatment: Pharmacotherapy and Psychosocial Intervention.
Pharmacotherapy.
Pharmacotherapy is initiated with second-generation antipsychotics as first-line agents due to their decreased risk of extrapyramidal side effects, compared to our first-generation antipsychotics. Commonly used medications include aripiprazole (Abilify), lurasidone (Latuda), risperidone (Risperdal), and quetiapine (Seroquel). These antipsychotics also have a more favorable side effect profile, showing a lower incidence of seizures, orthostatic hypotension, QT prolongation, weight gain, impaired glucose metabolism, and hyperlipidemia.
Of note, younger patients being treated for their first psychotic episode are more likely to experience metabolic side effects while on antipsychotics. Hence, it is important to start at lower doses in these patients and slowly titrate to a therapeutic dose.
Antipsychotics are implicated in the development of obesity, and obesity is one of my favorite topics. As a PCP, you need to have close communication with the psychiatrist before you change any doses of any antipsychotics, in my case, I just avoid making changes.
Older patients, who are likely on other medications should be started at doses that are ¼ to ½ the adult dose initially to monitor for any potential drug interactions. After therapy initiation, routine monitoring for symptomatic response is done weekly for the first 3 months. Signs of any extrapyramidal symptoms should also be evaluated at each visit.
Special care must be taken to patients with risk factors, for example, a metabolic profile should be ordered every 6 to 12 weeks depending on a patient’s comorbidities, and an EKG should be done before and 3 months after therapy initiation to monitor for QT prolongation.
QT prolongation is higher with ziprasidone, quetiapine, chlorpromazine, and intravenous (IV) haloperidol. Normal QTc intervals: Before puberty: NORMAL
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Episode 169: Food insecurity and Obesity in Kern County
3 mai· Rio Bravo qWeek
Episode 169: Food insecurity and Obesity in Kern County
Future Dr. Kim presents the problem of food insecurity in Kern County and how it is linked to obesity and liver disease. She shared several resources available to address food insecurity. Dr. Arreaza reminds us of the importance of improving access to fresh and healthy foods.
Written by Judy Kim, OMS3; Mira Patel, OMS3; and Vy Nguyen, OMS3. Western University of Health Sciences. Editing and comments by Hector Arreaza, MD.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
Arreaza: Why did you pick this topic?
Judy: While Kern County is known as one of the top-producing agricultural counties in the country, food insecurity is a major health disparity within this county. In order to dissect the problem of food insecurity in Kern County, we must first discuss the demographics and significance of this current topic. Among residents of Kern County, 23.1% are at or below 100% of the federal poverty level (FPL) and 47.7% are low-income (200% of FPL or below), which is higher than that of California.
Arreaza: What is food insecurity? In February 2023, we discussed the definition in Episode 128, but it is important to remember what it is. “Food insecurity is having limited, uncertain, or inconsistent access to the food necessary for a healthy life.” Another interesting fact is that it is estimated that 45% of undocumented immigrants in California are affected by food insecurity, including 64% of undocumented children (Source: 2021 CHIS).
Judy: Food insecurity is strongly tied to numerous conditions such as hypertension, coronary artery disease, diabetes, hepatitis, stroke, cancer, asthma, arthritis, chronic obstructive pulmonary disease, and kidney disease. Thus, this problem must be explored and discussed to find ways to improve health outcomes. However, the first steps must focus on bridging gaps in accessing healthy and affordable foods. For example, consumers have consistently noted that reliable transportation is a barrier when even applying for assistance before accessing their benefits. Oftentimes, families experiencing poverty, a large number of residents in Kern County, are part of the migrant community, move frequently, and experience difficulties even completing the necessary paperwork for programs such as the Migrant Childcare Alternative Payment program.
Arreaza: It may be off-topic, but I had to search what MCAP is. The Migrant Childcare Alternative Payment (MCAP) Program provides childcare services to migrant farm worker families in Kern and other counties in California, such as Merced and Fresno. MCAP allows parents to work while children are taken care of by licensed childcare centers, licensed family childcare homes, license-exempt (relatives), and in-home providers. I think many families may not be aware of this program. This is a reminder for our residents and students that this is available for your patients.
Judy: Going back to food insecurity, when looking at the distribution and locations of large supermarkets in the greater Bakersfield area, such as Albertsons, Smart & Final, and Vallarta, the northwest area has many large stores and without a high density of households in poverty. In contrast, Oildale, the southwest and southeast areas do not have many large markets nearby. Thus, it is also important to examine how and where our patients can access healthy and affordable food.
Obesity and Fatty Liver Disease in Kern County.

Judy: I would like to describe the relationship between food insecurity with liver disease. The food insecurity that is prevalent in Kern County contributes to the increasing number of overweight and obese populations we see here. Almost 78% of adults in Kern County are considered either overweight or obese. This is concerning because increased rates of obesity are correlated with higher rates of liver disease. As we know, the liver is responsible for breaking down fats, creating new small and medium-chain fatty acids, and transporting fats. With obesity, fat tends to accumulate in the liver since it is unable to properly break down the fat. This leads to steatosis. Short-term fatty liver disease does not have many clinical findings associated with it, but long term if left uncontrolled it can lead to cirrhosis and death.
Arreaza: According to a review of the liver transplant list done in 2022, Non-alcoholic steatohepatitis (NASH) is currently the second leading cause of liver transplant overall, and in females, it is the number-one cause. In California, we see about 13.8 deaths per 100,000 persons from liver-related disease, but Kern County has a high 15.9 deaths per 100,000 persons, which exceeded the Healthy People 2020 objective for liver disease deaths of 8.2 per 100,000 persons.
Judy: This was found in Kern Medical Community Needs assessments so these deaths could be correlated to NAFLD, NASH, fatty liver, autoimmune hepatitis, etc. but it is still concerning that the number of deaths from liver disease is about 2x the goal of maximum deaths we would want.
Arreaza: So, you are linking food insecurity to obesity, and obesity to fatty liver disease, I see the correlation. Tell us about the local resources to address the problem of food insecurity.
Local Resources
Judy: As patients walk through our doors, we recognize the social determinants for health and quality of life of our patients. Besides providing affirmations and words of encouragement, it’s helpful for the physician and medical staff to offer specific local resources that one can refer to. We collected a list of available resources, please keep in mind that this is not an exhaustive list of the support available in Kern County. Rely on resources around you such as local organizations like Community Action Partnership of Kern (CAPK) and social workers in conjunction with your research to have a comprehensive understanding of what’s available for your patients.
Arreaza: The first notable resource you guys found is the Commodity Supplemental Food Program, for our unique population– the elderly. It’s a USDA-sponsored program that provides a 30-lb monthly food box for seniors 60 years and older who also fall below the federal income guidelines.
Judy: The Golden Empire Gleaners also offer support to eligible seniors via a program called Senior Sack, which has established over 20 sites throughout Kern County. Twice a month, each registered senior will pick up 10-12 items of fresh fruits, vegetables, canned food, bread, and boxed staples at a local site. Upon arrival, they also engage in interactive activities with the staff and learn more about other local services available.
Arreaza: Another resource is the Food Bank, provided by several nonprofit organizations such as Community Action Partnership of Kern, Golden Empire Gleaners, where individuals of any age can come and receive nutritious food every month. Home delivery and emergency food boxes for seniors are also available.
Judy: There are also farmers markets such as F Street Farmers Market, which operates year-round every Saturday from 7:45 am to noon. What’s unique about F Street is they offer Market Match which matches program assistance’s benefits such as that of CalFresh and eWIC to the farmers' markets and other farm-directed sites. How it works is when individuals use their benefits, Market Match will match that fund so the person can buy even more fruits and vegetables.
For example, if I use $10 of CalFresh benefits at the farmers’ market, I will also receive another $10 for a total of $20 to spend on any fresh produce. F Street Farmers Market will match up to $20 per visit year-round which increases access to fresh fruits and vegetables, as well as provides an incentive for the locals to support family farms and their businesses. To find other farmers' markets that offer other benefits, please visit Farmers Market Finder by Ecology Center or call CAPK for other free food distribution sites.
Arreaza: I have to mention this wonderful initiative which I have participated in many times. It is called the bishop’s storehouse, sponsored by The Church of Jesus Christ of Latter-day Saints. It is a place where those in need can go to obtain food and other supplies at the recommendation of their bishop. So, it requires a “ticket” from a bishop, who is the leader of a congregation, to receive goods for free. People of any faith can request this help by going to any church location. So, we mentioned the Commodity Supplemental Food Program, Golden Empire Gleaners, Food Bank, F Street Farmers Market, and the bishop’s storehouse. Judy, thanks for sharing this relevant information. Please give us a conclusion to wrap up this episode.
Judy: As primary care doctors we are in a special position to prevent and treat many diseases. By addressing food insecurity, you may have a significant impact on your community. By providing appropriate nutrition, we can fight and prevent many diseases, such as fatty liver disease among others. We should share these resources with patients to improve their access to healthy food.
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Conclusion: Now we conclude episode number 169, “Food Insecurity and Obesity in Kern County.” Future Dr. Kim explained that food insecurity is linked to multiple chronic conditions, and she mentioned particularly obesity and fatty liver disease. Food insecurity can be partially addressed by sharing with our patients the resources in our community, and today you heard some of them, but we encourage you to keep looking for many others and share them with your patients.
This week we thank Hector Arreaza, Judy Kim, Vy Nguyen, and Mira Patel. Audio editing by Adrianne Silva.
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:
Food Bank - CAPK: Community Action Partnership of Kern. CAPK. (2024, February 27). https://www.capk.org/seniorfood/Kern Food Insecurity Needs Assessment. CAPK. (2023, August). https://feedingkern.org/wp-content/uploads/2023/09/CAPK-Food-Insecurity-Needs-Assessment-Report-revised-with-copyedits-9-11-2023.pdfMarket Match Program Helps Residents Double Their CalFresh Dollars. Department of Public Social Services. (n.d.)https://dpss.lacounty.gov/en/news/2021/05/calfresh-market-match.htmlSenior Sack. Golden Empire Gleaners. (n.d.). https://www.goldenempiregleaners.com/programsSenior food program - CAPK: Community Action Partnership of Kern. CAPK. (2024, February 27). https://www.capk.org/seniorfood/Fabbrini E, Sullivan S, Klein S. Obesity and nonalcoholic fatty liver disease: biochemical, metabolic, and clinical implications. Hepatology. 2010 Feb;51(2):679-89. doi: 10.1002/hep.23280. PMID: 20041406; PMCID: PMC3575093.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3575093/Know your numbers. Kern County Public Health. (2024, April 1). https://kernpublichealth.com/knowyournumbers/CAPK feeding Kern - feeding Kern. CAPK Food Assessment Report. (2024, March 15). https://feedingkern.org/Community Health Needs Assessment. (n.d.). https://www.kernmedical.com/documents/Kern-Medical-2019-CHNA-Report-Final.pdfDepartment of Health & Human Services. (2007, November 28). Liver - fatty liver disease. Better Health Channel. https://www.betterhealth.vic.gov.au/health/conditionsandtreatments/liver-fatty-liver-disease#Noureddin M, Vipani A, Bresee C, et al. NASH Leading Cause of Liver Transplant in Women: Updated Analysis of Indications For Liver Transplant and Ethnic and Gender Variances. Am J Gastroenterol. 2018;113(11):1649-1659. doi:10.1038/s41395-018-0088-6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9083888/The Bishops’ Storehouse, Provident Living, The Church of Jesus Christ of Latter-day Saints, https://providentliving.churchofjesuschrist.org/bishops-storehouse?lang=eng.Royalty-free music used for this episode: Good Vibes by Simon Pettersson, downloaded on July 20, 2023, from https://www.videvo.net/royalty-free-music
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Episode 168: UTI in Males
26 avril· Rio Bravo qWeek
Episode 168: UTI in Males
Future Dr. Tran gives a summary of UTIs in Males, including epididymitis, orchitis, urethritis, prostatitis, and pyelonephritis. Diagnosis and treatment were briefly described and some differences with female patients were mentioned by Dr. Arreaza.
Written by Di Tran, MS-3, Ross University School of Medicine. Editing and comments by Hector Arreaza, MD.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
WHAT ARE URINARY TRACT INFECTIONS?
Urinary Tract Infection (UTI) is an infection of any part of the urinary tract system. It may involve any part of the renal system, the kidneys, the ureters, the bladder, the prostate, and the urethra. Different from men, a woman may get a UTI more easily due to their anatomical difference. A woman’s urethra is shorter and lies close in proximity to both the vagina and the anus, which allows easy access for bacteria to travel up to the bladder.
UTI is further subdivided into two different categories, depending on where the infection takes place within the urinary tract:
Lower Tract Infection – cystitis and urethritis when the infection occurs on the bladder and the urethra, respectively. Common infections are a result of bacteria migrating from the skin (and also from sexual organs) to the urethra and ending up in the bladder.In males, other forms of lower tract infection can result in prostatitis, epididymitis, and orchitis.Upper Tract Infection - aka pyelonephritis, is a more concerning infection that involves the upper parts of the urinary system, in other words, the ureters, and kidneys.
AGE DIFFERENCES IN UTI FOR MEN:
For men, the incidence of UTI increases with age. Dr. John Brusch reports UTI rarely develops in young males and the prevalence of bacteriuria is 0.1% or less. Men who are 15-50 years of age often have urethritis due to sexually transmitted infection (STI), mainly by Neisseria gonorrhoeae and Chlamydia trachomatis. Symptoms include frequency, urgency, and dysuria (most common).
Men who are 50 years or older, especially those with prostatic hyperplasia, will have signs and symptoms of incomplete bladder emptying, hesitancy, slow stream, difficulty initiating urination, and dribbling after urinating. Due to the enlargement of the prostate gland, there will be partial blockage of urine flow from the bladder, which in turn, creates a reservoir where bacteria can grow and cause an infection. The most common offending microorganism for this age group is Escherichia coli.
Interestingly, while UTIs are rare among men under 60, by the age of 80, both women and men have similar incidence rates. The bladder tends to have a higher residual volume in older males because the prostate grows no matter what, it´s just a part of aging for males. Some may end up with more or less lower urinary tract symptoms, but the prostate is enlarged in general.
Other risk factors for UTI in males are men who are not circumcised, urethral strictures, fistulas, hydronephrosis (or dilated ureters overfilled with urine due to failure of drainage to the bladder), and the use of urinary catheters.
DIFFERENT TYPES OF UTIs IN MALES:
EPIDIDYMITIS:
The infection starts from the retrograde ascending route from the prostatic urethra, backing up to the vas deferens, and eventually ending in the epididymis.
In men who are younger than 35 years of age, the usual pathogens are C. trachomatis and N. gonorrhoeae (sexually transmitted).In men who are older than 35 years of age, the usual offending agents are Enterobacteriaceae and gram-positive cocci (E. coli as mentioned previously).ORCHITIS:
This unique UTI is caused by viral pathogens, such as mumps, coxsackie B, Epstein-Barr (EBV), and varicella (VZV) viruses. Several studies have shown that patients having orchitis have a history of epididymitis. Fortunately, this infection is uncommon, and it was the main reason to develop the MMR vaccine. It is caused by viruses other than mumps, so you can still have orchitis even if you are vaccinated. Antibiotics are not prescribed for viral orchitis.
BACTERIAL CYSTITIS:
Having a similar pathophysiology of ascending infection mechanism, male patients in this category often present frequency, urgency, dysuria, nocturia, and suprapubic pain. On a side note, having hematuria is concerning, especially without symptoms, because it’s automatically a red flag that should prompt an immediate evaluation in search of other causes besides infection, such as underlying malignancy. Possible etiologies are calculi, glomerulonephritis, and even schistosomiasis infection that can ultimately result in squamous cell carcinoma of the bladder.
Arreaza: Let me share a little anecdote about hematuria. One Sunday when I was a resident I woke up with hematuria. Of course, I immediately went to urgent care, knowing hematuria means trouble in men. I had a urine dipstick test, which was normal. The first thing the nurse practitioner asked me was, “Did you eat any beets?”, and I never eat beets, but that day I had a full bag of beet chips. So, yes, that was the cause of my pseudo-hematuria. Lesson learned: Always ask about beets when you have a patient with painless hematuria with a normal dipstick.
PROSTATITIS:
This is an infection of the prostate gland. The most common offending agent is E. coli. Acute prostatitis will present with signs of “acute” infection, such as fever, chills, and suprapubic pain. On rectal exam, we will find a prostate that is warm, swollen, boggy, and very tender.
Make sure you perform a gentle prostate exam as you may spread bacteria to the blood and cause bacteremia and potentially sepsis. Patients are normally very sick and it is not your typical cystitis, but it is more severe.
Chronic Prostatitis can arise from different causes, ranging from retrograde ascending infection, “chronic” exposure to urinary pathogens, and even autoimmune etiologies. The majority of patients often are asymptomatic.
URETHRITIS:
This infection is further classified into two groups, gonococcal and non-gonococcal. For gonococcal urethritis, N. gonorrhoeae is the most common pathogen. Agents of non-gonococcal urethritis include C. trachomatis, Ureaplasma, trichomonas, and Herpes Simplex Virus (HSV). Patients often present symptoms of dysuria, pruritus, and purulent penile discharge.
PYELONEPHRITIS:
Following a retrograde ascending mechanism, an infection may travel from the bladder and make its way to the kidney, causing damage and inflammation to the renal parenchyma. According to Dr. John Brusch, E. coli is responsible for approximately 25% of cases in males.
Pyelonephritis presents with chills, fever, nausea/vomiting, flank pain/costovertebral angle tenderness, and dysuria. Other findings include pyuria and bacteriuria. Pyelonephritis is a common cause of sepsis.
Diagnosis of UTIs.
URINE STUDIES: Urine culture remains the gold standard for diagnosis of UTI.
Other studies include suprapubic aspiration, catheterization, midstream clean catch, and Gram stain. Imaging studies are not always needed, but you may order plain films, ultrasonography, CT scans, and MRIs. It will depend on the severity of your case and your clinical judgment.
UTIs in women: In males, we should perform urine culture and susceptibility studies. However, in women, urine studies are not needed all the time, they should be reserved for women with recurrent infection, treatment failure, history of resistant isolates, or atypical presentation. This is done to confirm the diagnosis and guide antibiotic selection.
Interestingly, in a recent evidence review, published in the American Family Physician journal, women can self-diagnose their uncomplicated cystitis. All that is needed is having typical symptoms (frequency, urgency, dysuria/burning sensation, nocturia, suprapubic pain), without vaginal discharge. If you have those elements, you have enough information to diagnose, or even the patient can self-diagnose, an uncomplicated UTI without further testing, but in males, you should ALWAYS perform urine studies.
TREATMENTS:
Men with UTI should ALWAYS receive antibiotics, with urine culture and susceptibility results guiding the antibiotic choice. Laboratory results will help us determine the best treatment plan. UTIs are often treated with a variety of antibiotics. Dr. Robert Shmerling, of Harvard Medical School, states that most uncomplicated lower tract infections can be eradicated with a week of treatment with antibiotics.
Common antibiotics for UTI are fluoroquinolones, trimethoprim-sulfamethoxazole (TMP-SMZ), minocycline, or nitrofurantoin.
On another hand, if it’s an upper tract infection or prostatitis, the course of treatment can be extended for longer periods. For those patients who are hemodynamically unstable or have severe upper UTI, hospital admission is required to monitor for complications and IV antibiotics.
UTIs in males are less frequent than UTIs in females, except when patients are 80 years and older when the incidence is similar in both sexes. UTIs in males must prompt further evaluation because if left untreated, they can have detrimental effects on your patients’ health.
As a take-home point, UTI in males is less common than in females, and it requires urine studies or other studies to identify the etiology and guide treatment. Antibiotics are always used, and you may guide your treatment depending on the results. Imaging is not always needed, but use your clinical judgment to make a more specific diagnosis and detect complications promptly.
__________
Conclusion: Now we conclude episode number 168, “UTI is Males.” Future Dr. Tran described the different anatomical areas that can be infected in males with UTI. She reminded us that UTIs in males always need to be treated with antibiotics and urine cultures are done to guide treatment. Dr. Arreaza mentioned a few differences in the diagnosis and treatment of UTIs in females. For example, women can self-diagnose an uncomplicated cystitis, and urine studies or antibiotics are not always needed in women.
This week we thank Hector Arreaza and Di Tran. Audio editing by Adrianne Silva.
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:
Shmerling, R. H. (2022, December 5). Urinary tract infection in men. Harvard Health Publishing. https://www.health.harvard.edu/a_to_z/urinary-tract-infection-in-men-a-to-z.Brusch, J. L. (2023a, March 27). Urinary tract infection (UTI) in males. emedicine.medscpae.com. https://emedicine.medscape.com/article/231574-overview.Kurotschka PK, Gágyor I, Ebell MH. Acute Uncomplicated UTIs in Adults: Rapid Evidence Review. Am Fam Physician. 2024;109(2):167-174. https://www.aafp.org/pubs/afp/issues/2024/0200/acute-uncomplicated-utis-adults.htmlRoyalty-free music used for this episode: Tropicality by Gushito, downloaded on July 20, 2023, from https://www.videvo.net/royalty-free-music/
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Episode 167: Aspirin in Pregnancy
19 avril· Rio Bravo qWeek
Episode 167: Aspirin in Pregnancy
Dr. Marquez explains the use of aspirin during pregnancy to prevent preeclampsia. Dr. Arreaza adds comments and questions and clarifies that aspirin is not used for the treatment of preeclampsia.
Written by Verna Marquez, 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 to the topic: Pregnancy is a special time in a woman’s life, and we want to make sure that both the mother and the baby are safe and healthy.
1. What is aspirin? Aspirin is one of the most ancient medications in history, it is known as acetyl-salicylic acid (ASA) and it belongs to the family of non-steroidal anti-inflammatory drugs (NSAID), and it is also an anti-platelet, among other properties that may be unknown.
It is widely used for pain, fever, and inflammation, but due to adverse effects during viral illness (i.e. Reye Syndrome), it is used less frequently during viral infections.
As we know, aspirin is widely used to treat myocardial infarction and ischemic stroke, and especially for secondary prevention. The use of aspirin for primary prevention of cardiovascular disease has become less popular, but we are going to leave that discussion for another episode because today we will talk about the use of aspirin in pregnancy!
2. Why should we use aspirin in pregnancy?
Low-dose aspirin in pregnancy is most commonly used to prevent or delay the onset of preeclampsia. Aspirin lowers the risk of preeclampsia by 10% and its consequences (such as growth restriction and preterm birth). Several organizations have agreed on the risk factors we will mention briefly. These organizations are ACOG (American College of Obstetricians and Gynecologists), USPSTF (US Preventive Services Task Force), and SMFM (Society for Maternal-Fetal Medicine).
3. Who should we start on aspirin in pregnancy?
Aspirin is not for every pregnant patient, for example, a healthy nulliparous or any patient who had an uneventful, full-term delivery previously, is considered low risk and should NOT be started on aspirin because there is no benefit in preventing any condition.
Low-dose aspirin is recommended for women who have at least a high-risk factor because the incidence of preeclampsia is about 8% in these patients. The risk factors are:
•Previous pregnancy with preeclampsia (especially early onset and with an adverse outcome)
•Type 1 or 2 diabetes mellitus.
•Chronic hypertension.
•Multifetal gestation.
•Kidney disease.
•Autoimmune disease with potential vascular complications (antiphospholipid syndrome, systemic lupus erythematosus).
Your patient only needs 1 high-risk factor to be put on aspirin in pregnancy.
4. What are the moderate risk factors?
A patient needs to have more than 1 moderate risk factor to meet the criteria for prenatal aspirin.
•Nulliparity.
•Obesity (BMI >30).
•Family history of preeclampsia in mother or sister.
•Age ≥35 years.
•Sociodemographic characteristics (Black persons, lower income level [recognizing that these are not biological factors]).
•Personal risk factors (for example, previous pregnancy with low birth weight or small for gestational age newborn, previous adverse pregnancy outcome [such as stillbirth], interval >10 years between pregnancies). However, low-dose ASA prophylaxis is not recommended solely for the indication of prior unexplained stillbirth in the absence of risk factor for preeclampsia.
•In vitro conception.
USPSTF/ACOG may also suggest aspirin in selected patients with only one moderate risk factor, but it would require consultation with a specialist in obstetrics.
5. When should we start aspirin?
After 12 weeks of gestation, ideally before 16-20 weeks of gestation. If a patient is more than 16 weeks pregnant, aspirin can be started but most of the benefit has been noted when initiated before 16 weeks because many of the abnormalities that cause preeclampsia are developed early in pregnancy. It is not recommended to start before 11 weeks.
It is important to mention also that low-dose aspirin appears to have little or no benefit in patients who already have developed preeclampsia. Starting aspirin in preeclampsia can even cause damage such as bleeding in cases of thrombocytopenia.
6. What is the dose?
The dose is between 75 to 162 mg daily. Conveniently, we have an 81 mg presentation in the United States, and it falls within the recommended range. It can be taken in the morning or at night, and adherence of >90% is associated with better prevention.
7. When do we stop aspirin?
Expert opinion recommends stopping aspirin at the time of delivery.
8. What are the contraindications to ASA use during pregnancy?
Absolute contraindications to aspirin:
-Patients with a history of ASA allergy (urticaria) or hypersensitivity to other salicylates are at risk of anaphylaxis and should not receive low-dose ASA.
-Because of significant cross-sensitivity between ASA and other NSAIDs, low-dose ASA is also contraindicated with known HPS to NSAIDs.
-Exposure to low-dose ASA in patients with nasal polyps may result in life-threatening bronchoconstriction and should be avoided.
Relative contraindications are history of GI bleed, active peptic ulcer disease, other sources of GI or GU bleeding, and severe hepatic dysfunction.
Aspirin is an excellent way to prevent preeclampsia in patients who are at high or moderate risk. Remember to think about the high-risk factors, and if your patient has only 1 positive, then aspirin needs to be started. Mainly, previous preeclampsia, diabetes, hypertension, multifetal gestation, and kidney or autoimmune disease. Look for moderate risk factors and start aspirin if the patient has 2 or more of those risk factors.
_________________
Conclusion: Now we conclude episode number 167, “Aspirin in Pregnancy.” Dr. Marquez explained that aspirin is started between 12-16 weeks of gestation to prevent preeclampsia in patients with at least 1 high-risk factor or patients with 2 or more moderate-risk factors. Dr. Arreaza also mentioned that aspirin is not for low-risk patients or for patients who already developed preeclampsia. As you know, preeclampsia can result in severe consequences for the fetus and the mother, but by preventing it, we can improve the chances of having a positive outcome in pregnancy.
This week we thank Hector Arreaza and Verna Marquez. Audio editing by Adrianne Silva.
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:
August, Phyllis and Arun Jeyabalan, Preeclampsia: Prevention. UpToDate, Last updated Feb 16, 2024. https://www.uptodate.com/contents/preeclampsia-prevention.Aspirin Use to Prevent Preeclampsia and Related Morbidity and Mortality: Preventive Medication, September 28, 2021, United States Preventive Services Taskforce https://www.uspreventiveservicestaskforce.org/uspstf/recommendation/low-dose-aspirin-use-for-the-prevention-of-morbidity-and-mortality-from-preeclampsia-preventive-medication.Royalty-free music used for this episode: Tropicality by Gushito, downloaded on July 29, 2023, from https://www.videvo.net/royalty-free-music/.
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Episode 166: Naturopathic Medicine Insights
5 avril· Rio Bravo qWeek
Episode 166: Naturopathic Medicine Insights
Future Dr. Luong talked about what she learned about naturopathic doctors (NDs). She discussed the principles of naturopathic medicine and mentioned some differences in regulations across states in the US. Dr. Arreaza shared his opinion about the pros and cons of naturopathic medicine.
Written by Teresa Luong, MSIV, American University of the Caribbean. 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.
Arreaza: This may be a controversial topic. The term “natural” in medicine triggers strong reactions among allopathic doctors like me. Today we have a medical student who took up the challenge to talk about Naturopathic Doctors.
Teresa:I am providing information based on research and living in Washington state, which is considered one of the birthplaces of modern naturopathic medicine, boasts the highest population of naturopathic doctors and a wide range of practice specialties. It's important to note that my responses are not personal opinions but rather informed insights.
There are about 8,500 licensed naturopathic doctors in North America. Naturopathic Doctors may not use the title of physicians in California.
What is a Naturopathic Doctor?
While it’s true that in California naturopathic doctors are not legally permitted to use the term ”physician” to describe themselves, some still choose to refer to themselves as “naturopathic physicians” colloquially or in their practice branding. So, confusion can arise because naturopathic doctors, while legally not recognized as physicians in California, can function as primary care providers, this overlap in roles can lead to the informal use of terms like ”naturopathic physician.“ However, it’s important to recognize that legally, they are not recognized as physicians in this state.
Naturopathic doctors (NDs) are healthcare professionals who embrace a holistic approach to healing, focusing on natural and non-invasive therapies to support the body's inherent ability to heal itself. Naturopathic medicine has its roots in traditional healing practices from around the world, blending ancient wisdom with modern scientific knowledge. The philosophy of naturopathy emphasizes the importance of treating the whole person—mind, body, and spirit—rather than just addressing isolated symptoms or diseases.
What is an allopathic approach vs a holistic approach?
Allopathic medicine: Allopathic medicine focuses on diagnosing and treating specific symptoms or diseases using pharmaceutical drugs, surgery, and other conventional interventions. Treatment is often targeted at managing symptoms or eradicating pathogens.
Holistic medicine: Holistic medicine takes a broader approach, considering the whole person and aiming to address the root causes of illnesses. Treatment may involve a combination of conventional therapies and alternative modalities such as nutrition, herbal medicine, acupuncture, and lifestyle modifications. The focus is on promoting overall health and well-being rather than just treating isolated symptoms.
Core Principles Naturopathic Practitioners:
The six core principles of naturopathic medicine serve as guiding tenets for both diagnosis and treatment. These principles include:
-first, do no harm.
-the healing power of nature
-identify and treat the root cause
-treat the whole person,
-the physician as a teacher;
-and prevention as the best cure.
Treatment modalities: Naturopathic doctors employ a wide range of therapeutic modalities to address the unique needs of each individual, such as:
-Clinical nutrition, which focuses on using “food as medicine” to promote healing and prevent disease.
-Herbal medicine utilizes the medicinal properties of plants to support various bodily systems and restore balance.
-Acupuncture, everybody is familiar with acupuncture.
-Other modalities may include hydrotherapy, homeopathy, physical medicine (such as massage and manipulation), and lifestyle counseling.
The role of allopathic medications (NSAIDs, antibiotics) and surgical procedures.
Naturopathic doctors typically prioritize natural therapies and lifestyle intervention, but may also integrate conventional medicine when necessary. Their views on traditional medications, such as NSAIDs, antibiotics, and surgical procedures vary depending on the individual practitioner and their approach to healthcare. Some may recommend them when appropriate, while others may prefer to explore alternative options first. Ultimately, their goal is often to promote holistic health and well-being.
Education and Training:
Pre-Medical Requirements: Aspiring naturopathic doctors typically complete undergraduate coursework in pre-medical sciences, including Biology, Chemistry, Physics, and Psychology.
Naturopathic Medical Program:Naturopathic doctors must graduate from a four-year accredited naturopathic medical school. The forst two years are basic sciences courses and the last 2 years are clinical courses.
After completing their naturopathic medical education, graduates must pass the Naturopathic Physicians Licensing Examinations (NPLEX) to become licensed practitioners. MDs need a residency, and NDs can start working immediately after school in some states, or they can do some additional training.
Scope of Practice: The scope of practice for naturopathic doctors varies depending on the regulations in each jurisdiction. In general, NDs are trained to:
- Prescribe natural therapies such as nutritional supplements, herbal remedies, and homeopathic medicines.
- Prescribe prescription medications, including some, but not limited to, controlled substances.
- Provide dietary counseling and lifestyle interventions tailored to individual health needs.
- Provide Primary Care, such as, performing physical exams, administering vaccinations, ordering laboratory tests,
- Offer acupuncture.
- They can use detoxification protocols and intravenous (IV) nutrient therapy into treatment plans.
- Utilize mind-body techniques like meditation, mindfulness, and relaxation exercises
In January 2022, the recognition of naturopathic doctors (NDs) and the extent of their scope of practice vary significantly from state to state within the United States. Here's an overview of states where NDs are recognized and their scope of practice:
Licensed States: In these states, naturopathic doctors are licensed to practice independently and have a broad scope of practice, including diagnosis, treatment, and prescription of medications and natural remedies within their scope. Some states may have specific restrictions or additional requirements.
-California: NDs are licensed and regulated by the California Naturopathic Medicine Committee. They have a comprehensive scope of practice, including the prescription of certain medications.
-Washington: NDs are licensed and regulated by the Washington State Department of Health. They have a limited formulary for prescription medications.
Unlicensed States (for example, Georgia and Virginia): In states where naturopathic medicine is not regulated, NDs have to work as healthcare consultants or working alongside other licensed healthcare providers, like MDs. The scope of practice in these states may be more limited, and NDs may not have the authority to diagnose, treat, or prescribe medications independently.
Pros:Naturopathic doctors utilize natural and holistic therapies, which may have fewer side effects compared to conventional medications. These therapies can complement conventional treatments, especially if they are collaborating with an MD.
If Naturopathic doctors work collaboratively, it can offer complementary care options to patients, which can provide patients with treatment modalities and perspectives beyond conventional medicine. This can be particularly beneficial for patients who are a bit apprehensive to traditional medicine for whatever reason.
Naturopathic medicine emphasizes preventive care and strategies to promote health and prevent disease. So they try to catch underlying imbalances and risk factors early, and see patients multiple times a week, which can help patients reduce their risk of developing chronic illnesses and improve their overall quality of life. By seeing a patient this frequently, it promotes stronger doctor-patient relationships and improves patient satisfaction.
Cons:
Lack of Regulation and Standardization: Naturopathic medicine is not regulated to the same extent as conventional medicine, and there may be variability in the education, training, and qualifications of naturopathic doctors. This lack of regulation and standardization can raise concerns about the quality and safety of naturopathic care.
Limited Scientific Evidence: Some naturopathic treatments lack rigorous scientific evidence supporting their efficacy and safety. Without robust clinical research, it can be challenging to assess the effectiveness of certain naturopathic interventions and differentiate between evidence-based practices and unproven therapies.
Potential for Harmful Practices: In some cases, naturopathic doctors may recommend treatments or interventions that have the potential to be harmful, particularly if they lack scientific support or are based on unfounded beliefs. Patients may be at risk of receiving ineffective or unsafe treatments without proper oversight and regulation.
Delayed Access to Conventional Care: So if a patient relies solely on naturopathic care, it may delay access to conventional medical treatments that are necessary for managing serious or life-threatening conditions
Cost and Insurance Coverage: Naturopathic services may not be covered by health insurance plans, or coverage may be limited compared to conventional medical services. This lack of insurance coverage can make naturopathic care inaccessible to some patients, particularly those with limited financial resources.
This information is provided to increase your knowledge on this topic, it is not intended to convince you to go against or support naturopathic medicine. Our goal is to inform you and you can draw your own conclusions about it. It is important to educate ourselves on this topic because naturopathic doctors are rising in California and we may encounter them in our future practices.
________________________________
Conclusion: Now we conclude episode number 166, “Naturopathic Medicine Insights.” Future Dr. Luong explained that naturopathic doctors receive training in naturopathic medical schools and receive a degree before they sit for a board exam. Many NDs may be working in outpatient primary care or even in hospital care. Dr. Arreaza shared his opinion about the pros and cons of having naturopathic medicine available for patients.
This week we thank Hector Arreaza and Teresa Luong. Audio editing by Adrianne Silva.
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!
Links:
American Association of Naturopathic Physicians:aanp.org. Complementary, Alternative, or Integrative Health: What’s In a Name? NIH National Center for Complementary and Integrative Health, https://www.nccih.nih.gov/health/complementary-alternative-or-integrative-health-whats-in-a-name. Accessed March 21, 2024. Bastyr University:bastyr.eduNational University of Natural Medicine (NUNM):nunm.eduFleming SA, Gutknecht NC. Naturopathy and the primary care practice. Prim Care. 2010;37(1):119-136. doi:10.1016/j.pop.2009.09.002. https://pubmed.ncbi.nlm.nih.gov/20189002/Atwood KC 4th. Naturopathy: a critical appraisal. MedGenMed. 2003;5(4):39. Published 2003 Dec 30. https://pubmed.ncbi.nlm.nih.gov/14745386/Public Notification: Artri King contains hidden drug ingredients, U.S. Food & Drug Administration (FDA), April 20, 2022. https://www.fda.gov/drugs/medication-health-fraud/public-notification-artri-king-contains-hidden-drug-ingredientsRoyalty-free music used for this episode: My Dinner with the Diablo by Tropicalia, downloaded on July 20, 2023 from https://www.videvo.net/.
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Episode 165: Early-Onset Sepsis Part 2
29 mars· Rio Bravo qWeek
Episode 165: Early-Onset Sepsis Part 2
Dr. Lovedip Kooner explains how to use the Kaiser Permanente early-onset sepsis calculator and explains other useful tools to assist in the diagnosis of EOS. Dr. Arreaza adds comments about the usefulness of this calculator
Written by Lovedip Kooner, MD. 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.
Introduction: As a recap, Early-onset sepsis is diagnosed within 72 hours (or within 7 days, according to some experts) after birth. We talked about GBS as the main culprit of EOS. 28% of EOS by GBS are babies born 4 hrsTwo or more physiologic abnormalities lasting for > 2 hrs
Note: abnormality can be intermittent.
An ill newborn, in general, is described as having abnormal vital signs, either hyper or hypothermia, tachycardia, bradycardia or arrhythmia, flaccid, doesn’t regard faces, no or muted reflexes and poor suck, mottled color, cyanosis or bruising, petechiae, retractions, nasal flair or poor nasal breathing (with choanal atresia, pinks up only when crying), gasping respirations, poor bowel sounds, possibly distended OR scaphoid (with atresias will have scaphoid abdomen and with anomalies like TEF depending on type, emesis or difficulty breathing when fed) obvious congenital anomalies, etc.
Clinical Illness in the Kaiser Permanentetool is defined as:
Persistent need for Nasal CPAP / High flow nasal cannula / mechanical ventilation (outside of the delivery room)Hemodynamic instability requiring vasoactive medicationsNeonatal encephalopathy/Perinatal depression: Seizure, Apgar Score @ 5 minutes < 5Need for supplemental O2 > 2 hours to maintain oxygen saturations > 90% (outside of the delivery room)
After all that information is entered into the Kaiser Permanente calculator, the options for management are clinical monitoring, laboratory evaluation, or antibiotic administration.
Example:
-Incidence: 0.5/1,000 live births
-Gestational age: 36 6/7 weeks
-Highest maternal antepartum temperature: 102 F
-ROM: 5 hours
-Maternal GBS: Positive
-Intrapartum antibiotics: Broad spectrum 3 hours prior to birth
-RESULT: EOS risk at birth 2.34.
Recommendations based on physical exam:
1. Well-appearing baby, risk 0.96, RECOMMENDATIONS: No culture, no antibiotics, vitals every 4 hours for 24 hours.
2. Equivocal, risk 11.61, RECOMMENDATIONS: Start empiric antibiotics and vitals per NICU.
3. Clinical Illness, risk 47.46, RECOMMENDATIONS: Start empiric antibiotics and vitals per NICU.
The Kaiser Permanente neonatal early-onset sepsis calculator was analyzed in a meta-analysis, as published in the American Family Physician in 2021. Six high-quality, non-randomized controlled trials were evaluated, including more than 170,000 neonates. The calculator was compared to the standard approach recommended by the CDC guidelines.
The analysis showed there was a statistically significant reduction in antibiotic use, a reduction in the number of laboratory tests, and a reduction in NICU admission in neonates who were managed following the sepsis calculator compared with the standard approach.
There was no difference in readmission rates to NICU and no difference in culture-positive sepsis between neonates treated using the sepsis calculator and those treated with the standard approach. In summary, I recommend using the Kaiser Permanente calculator as part of your evaluation. BTW, I received no money from KP. It is important to know that depending on resources and institutional policies, your management may change.
Use of CBC and CRP.
CBC interpretation in neonates: Remember that CBC in newborns needs to be evaluated following the normal parameters for neonates. For example, WBC up to 30,000 per mm3, and hemoglobin up to 19.9 gm/dL can be normal in neonates.
Serial white blood cell counts and immature–to–total neutrophil ratio (I/T ratio) generally greater than or equal to 0.2 by some experts is considered positive for sepsis. Complete blood cell counts taken 12-24 hours after birth are associated with increased sensitivity and negative predictive value compared to a sample taken 1-7 hours after birth.
C-reactive protein (CRP) is also often used and it rises within 6 hours of infection and peaks at 24 hours. Two normal CRP levels, one taken between 8-24 hours of age and the second 24 hours later, have an over 99% negative predictive value. Single values of CRP or procalcitonin obtained after birth to assess the risk of EOS are neither sensitive nor specific to guide EOS care decisions.
Procalcitonin: Procalcitonin may be difficult to interpret within the first 3 days after birth due to elevations caused by noninfectious etiologies and the physiologic rise after birth. It is important to note that neither single values of CRP nor procalcitonin after birth should be used to guide the management plan of infants undergoing evaluation for EOS>.
Extreme values in CBC: Extreme values (total WBC count 0.3; ANC
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Episode 164: More Than Just A Headache
22 mars· Rio Bravo qWeek
Episode 164: More Than Just A Headache
Dr. Song presents a case of a subacute headache that required an extensive workup and multiple visits to the hospital and clinic to get a diagnosis. Dr. Arreaza added comments about common causes of subacute headaches.
Written by Zheng (David) Song, MD. Editing and comments by Hector Arreaza, MD.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
Introduction to the episode: We are happy to announce the class of 2027 of the Rio Bravo / Clinica Sierra Vista Family Medicine Residency Program. Our new group will be (in alphabetical order): Ahamed El Azzih Mohamad, Basiru Omisore, Kenechukwu Nweke, Mariano Rubio, Nariman Almnini, Patrick De Luna, Sheila Toro, and Syed Hasan. We welcome all of you. We hope you can enjoy 3 enriching and fulfilling years. During this episode, you will hear a conversation between Dr. Arreaza and Dr. Song. Some elements of the case have been modified or omitted to protect the patient’s confidentiality.
1. Introduction to the case: Headache.
A 40-year-old male with no significant PMH presents to the ED in a local hospital due to over a month history of headaches. Per the patient, headaches usually start from the bilateral temporal side as a tingling sensation, and it goes to the frontal part of the head and then moves up to the top of the head. 8 out of 10 severities were the worst. Pt reports sometimes hypersensitivity to outdoor sunlight but not indoor light. OTC ibuprofen was helpful for the headache, but the headache always came back after a few hours.
The patient states that if he gets up too quickly, he feels slightly dizzy sometimes, but it is only for a short period of time. There was only one episode of double vision lasting a few seconds about 2 weeks ago but otherwise, the patient denies any other neurological symptom.
He does not know the cause of the headache and denies any similar history of headaches in the past. The patient denies any vomiting, chest pain, shortness of breath, cough, abdominal pain, or joint pain. The patient further denies any recent traveling or sick contact. He does not take any chronic medication. The patient denies any previous surgical history. He does not smoke, drink, or use illicit drugs.
What are your differential diagnoses at this moment?
Primary care: Tension headache, migraines, chronic sinusitis, and more.
2. Continuation of the case: Fever and immigrant.
Upon further inquiries, the patient endorses frequent “low-grade fever” but he did not check his temperature. He denies any significant fatigue, night sweats, or weight loss. He migrated from Bolivia to the U.S. 12 years ago and has been working as a farm worker in California for the past 10 years. He is married. His wife and daughter are at home in Bolivia. He is currently living with friends. He is not sexually active at this moment and denies having any sexual partners.
Differential diagnoses at this moment? Tension headache, migraine, infections, autoimmune disease, neurocysticercosis.
3. Continuation of the case: Antibiotics and eosinophilia.
As we kept asking for more information, the patient remembered he visited a clinic about four months ago for a dry cough and was told he had bronchitis and was given antibiotics and the cough got better after that. He went to another local hospital ED one month after that because the cough came back, now with occasional phlegm and at that time he also noticed two “bumps” on his face but nothing significant. After a CXR at the ED, the patient was diagnosed with community-acquired pneumonia and sent home with cough medication and another course of antibiotics. His cough improved after the second round of antibiotics. We later found on the medical record that the CXR showed “mild coarse perihilar interstitial infiltrates of unknown acuity”.
His blood works at the ED showed WBC 15.2, with lymphocyte 21.2%, monocyte 10.1%, neutrophil 61.7%, eosinophil 5.9% (normally 1-4%), normal kidney, liver functions, and electrolytes, and prescribed with benzonatate 100mg TID and doxycycline 100mg bid for 10 days.
He went to the same ED one month before he saw us for headache and fever (we reviewed his EMR, and temp was 99.8F at the ED). After normal CBC, CMP and chest x-ray. The patient was diagnosed with a viral illness and discharged home with ibuprofen 400mg q8h.
Due to the ongoing symptoms of headache and fever, the patient went back to the same clinic he went to four months ago for a dry cough and requested a complete physical and blood work. The patient was told he had a viral condition and was sent home with oseltamivir (Tamiflu®) for five days. However, the provider did order some blood work for him.
Differential diagnoses at this moment? Patients with subacute meningitis typically have an unrelenting headache, stiff neck, low-grade fever, and lethargy for days to several weeks before they present for evaluation. Cranial nerve abnormalities and night sweats may be present. Common causative organisms include M. tuberculosis, C. neoformans, H. capsulatum, C. immitis, and T. pallidum.
At his physical exam visit, the patient actually asked the provider specifically to check him for coccidiomycosis because of his job as a farm worker and he heard from his friends that the infection rate is pretty high in the Central Valley of California.
His serum cocci serology panel showed positive IGG and IGM with CF titer of 1:128. His HIV, syphilis, HCV, HBV are all negative.
The patient was told by that clinic to come to ED due to his history of headache, fever, and very high serum coccidiomycosis titer.
The senior and resident intern were on the night shift that night and we were contacted by the ED provider at around 9:30 pm for this patient. When reviewing his ED record, his vitals were totally normal at the ED, the preliminary ED non-contrast head CT showed no acute intracranial abnormality.
A lumbar puncture was performed by the ED provider, which showed WBCs (505 - 71%N, 20%L, 7%M), RBC (1), glucose (19), and protein (200). CSF: High Leukocytes, low glucose, and high protein.
On the physical exam, the patient was pleasant and cooperative, he was A&O x 4, he had a normal examination except for two brown healing small nodules on his forehead and left cheek and slight neck stiffness.
At that point, we knew the patient most likely had fungal meningitis by cocci except for the predominant WBC in his CSF fluid was neutrophil not the more typical picture of lymphocyte dominant. And because of his very benign presentation and subacute history, we were not 100% sure if we had a strong reason to admit this patient. We thought this patient could be managed as an outpatient with oral fluconazole and referred to infectious disease and neurology.
4. Continuation of case: Admission to the hospital.
Looking back, one thing that was overlooked while checking this patient in the ED was the LP opening pressure. Later, the open pressure was reported as 340mm H2O (very high). The good thing was, after speaking to the ED attending and our attending, the patient was admitted to the hospital and started on oral fluconazole.
Three hours after the admission, a rapid response was called on him. While the floor nurses were doing their check-in physical examination, the patient had a 5-minute episode of seizure-like activity which included bilateral tonic arm/hand movements, eye deviation to the left, LOC unresponsive to sternal rub, and the patient desaturated to 77%. He eventually regained consciousness after the seizure and pulse oximetry increased to 100% on room air.
The patient was started on Keppra and seen by a neurologist the following day. His 12-hour EEG was normal, but his head MRI showed “diffuse thickening and nodularity of the basal meninges are seen demonstrating enhancement, suggesting chronic meningitis, possibly related to cocci. Other etiologies including sarcoidosis and TB meningitis and/or infiltration by metastatic process/lymphoma are not excluded. The ventricles are slightly prominent in size”.
MRI of the cervical, thoracic, and lumbar spines also showed extensive diffuse leptomeningeal thickening, extensive meningitis, and nodular dural thickening.
Also, his chest x-ray showed “some heterogeneity and remodeling of the distal half of the left clavicle. Metabolic bone disease, infectious etiology and/old trauma considered”.
This could also be due to disseminated cocci infection.
The infectious disease doctor saw this patient and recommended continuing with fluconazole, serial LPs until opening pressure is less than 250 mmH2O and neurosurgery consultation for possible VP shunt placement. The neurologist recommended the patient continue with Keppra indefinitely in the context of structural brain damage secondary to cocci meningitis.
Take home points: Suspect cocci meningitis in patients with subacute headache associated with respiratory symptoms, new skin lesions, photophobia, neck stiffness, nausea, vomiting, eosinophilia, erythema nodosum (painful nodules on the anterior aspect of legs). Other symptoms to look for include arthralgias, particularly of the ankles, knees, and wrists.
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Brief summary of coccidiomycosis.
Etiology
Coccidioidomycosis, commonly known as Valley fever, is caused by dimorphic soil-dwelling fungi of the genus Coccidioides (C. immitis and C. posadasii). They are indistinguishable in clinical presentation and routine laboratory test results.1, 2, 3, 5
Epidemiology
In the United States, endemic areas include the southern portion of the San Joaquin Valley of California and the south-central region of Arizona. However, infection may be acquired in other areas of the southwestern United States, including the southern coastal counties in California, southern Nevada, southwestern Utah, southern New Mexico, and western Texas (including the Rio Grande Valley). There are also cases in eastern Washington state and in northeastern Utah. Outside the United States, coccidioidomycosis is endemic to northern Mexico as well as to localized regions of Central and South America.1, 2
Overall, the incidence within the United States increased substantially over the 1998-2019, most of that increase occurred in south-central Arizona and in the southern San Joaquin Valley of California. From 1998 to2019, reported cases in California increased from 719 to 9004.1, 6
The risk of infection is increased by direct exposure to soil harboring Coccidioides. Past outbreaks have occurred in military trainees, archaeologists, construction or agricultural workers, people exposed to earthquakes or dust storms. However, in endemic areas, many cases of Coccidioides infection occur without obvious soil or dust exposure and are not associated with outbreaks. Change in population, climate change, urbanization and construction activities, and increased awareness and reporting, are possible contributing factors.1, 2, 5
Pathology
In the soil, Coccidioides organisms exist as filamentous molds. Small structures called arthroconidia from the hyphae may become airborne for extended periods. Arthroconidia are usually 3-5 μm—small enough to evade bronchial tree mucosal mechanical defenses and reach deep into the lungs.1, 3
Once inhaled by a susceptible host into the lung, the arthroconidia develop into spherules (theparasitic existence in a host), which are unique to Coccidioides. Endospores from ruptured spherules can themselves develop into spherules, thus propagating infection locally.1, 3, 5
Although rare cases of solid organ donor-derived or fomite transmitted infections have been reported, coccidioidomycosis does not occur in person-to-person or zoonotic contagion, and transplacental infection in humans has never been documented.2, 5
Cellular immunity plays a crucial role in the host’s control of coccidioidomycosis. Among individuals with decreased cellular immunity, Coccidioides may spread locally or hematogenously after an initial symptomatic or asymptomatic pulmonary infection to extrathoracic organs.1, 3, 7
Clinical manifestation
The majority of infected individuals (about 60%) are completely asymptomatic. Symptomatic persons (40% of cases) have symptoms that are related principally to pulmonary infection, including cough, dyspnea, and pleuritic chest pain. Some patients may also experience fever, headache (common finding in early-stage infection and does not represent meningitis), fatigue, night sweats, rash, myalgia.1, 2, 3, 5
In most patients, primary pulmonary coccidioidomycosis usually resolves in weeks without sequelae and lifelong immunity to reinfection. However, some patients may develop chronic pulmonary complications, such as nodules or pulmonary cavities, or chronic fibrocavitary pneumonia. Some individuals with intense environmental exposure or profoundly suppressed cellular immunity (e.g., in patients with AIDS) may develop a primary pneumonia with diffuse reticulonodular pulmonary process in association with dyspnea and fever.1, 3, 5
Fewer than 1% of infected individuals develop extrathoracic disseminated coccidioidal infection. Common sites for dissemination include joints and bones, skin and soft tissues, and meninges. One site or multiple anatomic foci may be affected. 1, 2, 3, 7
It is estimated that coccidioidal meningitis, the most lethal complication of coccidioidomycosis, affects only 0.1% of all exposed individuals. Patients with coccidioidal meningitis usually present with a persistent headache (rather than a self-limited headache in some patients with primary pulmonary infection), with nausea and vomiting, and sometimes vision change. Some may also develop altered mental status and confusion. Meningismus such as nuchal rigidity, if present, is not severe.
Hydrocephalus and cerebral infarction may develop in some cases. Papilledema is more commonly observed in pediatric patients.1, 3, 4, 5, 7
When meningitis develops, most patients may not have any respiratory symptoms nor radiographic manifestation of pulmonary infection. However, a large number of these individuals also present with other extrathoracic lesions.7
Diagnosis
Although early diagnosis carries obvious benefits for patients and the health care systems as a whole (e.g., decreases patient anxiety, reduces the cost of expensive and invasive tests, removes the temptation for empirical antibacterial or antiviral treatments, and allows for early detection of complications), considerable diagnostic delays up to several weeks to months are common in both endemic areas and non-endemic areas.3, 7
Most symptomatic persons with coccidioidal infection present with primarily pulmonary symptoms and are often misdiagnosed as community-acquired bacterial pneumonia and treated with antibiotics. In endemic areas like south-central Arizona, previous studies found up to 29% of community-acquired pneumonia is caused by coccidioidomycosis. Healthcare providers thus should maintain a high clinical suspicion for coccidioidomycosis when evaluating persons with pneumonia who live in or have traveled to endemic areas recently. Elevated peripheral-blood eosinophilia of over 5%, hilar or mediastinal adenopathy on chest radiography, marked fatigue, and failure to improve with antibiotic therapy should prompt suspicion and testing for infection with coccidioidomycosis in endemic areas.1, 3, 5
Serological testing plays an important role in establishing a diagnosis of coccidioidomycosis. Enzyme immunoassay (EIA) to detect IgM and IgG antibodies is highly sensitive and therefore commonly used as the screening tool. Immunodiffusion is more specific but less sensitive than enzyme immunoassay. It is used to confirm the diagnosis of positive EIA test results. Complement fixing (CF) test, which indirectly detects the presence of coccidioidal antibodies by testing the consumption of serum complement, are expressed as titers. Serial measurements of titers are of not only diagnostic but also prognostic value.1, 2, 3, 5
Other methods, including culture, microscopic, or polymerase chain reaction (PCR) exam on tissue or respiratory specimens, are limited by their availability, sample obtaining and handling, or lack of sufficient evaluation.1, 2, 3, 5
Cerebrospinal fluid (CSF) examination in coccidioidal meningitis usually demonstrates lymphocyte dominated elevation of leukocytes, although polymorphonuclear leukocyte dominance can also be seen in the early stage of the infection. Profound hypoglycorrhachia and elevated protein levels in CSF examination are also very common in coccidioidal meningitis.1, 7
Although isolating Coccidioides from CSF or other CNS specimens are diagnostic for coccidioidal meningitis, in practice, diagnoses are often made based on the combination of clinical presentation, CSF examination that suggesting fungal infection, and positive Coccidioides antibodies found in CSF.7
Imaging, especially enhanced magnetic resonance imaging (MRI), can help in diagnosing coccidioidal meningitis. Basilar leptomeningeal enhancement is a more common finding even though hydrocephalus, cerebral infarction, and vertebral artery aneurysm can also be seen.7
Treatment
Most patients with focal primary pulmonary coccidioidomycosis do not require antifungal therapy. According to 2016 Infectious Diseases Society of America (IDSA) Clinical Practice Guideline, antifungal therapy should be considered in patients with concurrent immunosuppression that adversely affect cellular immunity (e.g., organ transplant patients, AIDS in HIV-infected patients, and patients receiving anti–tumor necrosis factor therapy) and those with significantly debilitating illness, extensive pulmonary involvement, with concurrent diabetes, pregnant women, or who are otherwise frail because of age or comorbidities. Some experts would also include African or Filipino ancestry as indications for treatment. Conversely, humoral immunity comprise splenectomy, hypocomplementemia, or neutrophil dysfunction syndromes are not major risk factors for this disease.1, 2, 3, 4, 5
Triazole antifungals (fluconazole or itraconazole) are currently considered as the first-line medications used to treat most cases of coccidioidomycosis. Amphotericin B is reserved for only the most severe cases of dissemination and patients with coccidioidal meningitis in whom triazole antifungal therapy has failed. It is also the choice of therapy for coccidioidomycosis in pregnant women during the first trimester because of the possible teratogenic effect of high-dose triazole therapy during this period of time.1, 3, 4, 5
Treating coccidioidal meningitis (CM) poses a special challenge because untreated meningitis is nearly always fatal. Lifelong therapy is recommended for CM because the majority 80% patients with CM experience relapse when therapy is stopped despite initial response to antifungal treatment. Shunting of CSF is required in cases of meningitis complicated by hydrocephalus.1, 3, 4, 5, 7
Prevention
Avoidance of direct contact with contaminated soil in endemic areas (e.g., respirator use by construction workers) may reduce disease risk, although clear evidence of its benefit is lacking.1, 5
Some special population groups may benefit from prophylactic use of antifungals, such as those about to undergo allogeneic solid-organ transplantation or patients with a history of active coccidioidomycosis or a positive coccidioidal serology in whom therapy with tumor necrosis factor α antagonists is being initiated. The administration of prophylactic antifungals is not recommended for HIV-1-infected patients even if they live in an endemic region.1, 5
Conclusion: Now we conclude episode number 164, “More than just a headache.” Dr. Song explained that a headache with an indolent course, accompanied by subacute respiratory symptoms, nausea, vomiting, photophobia, neck stiffness, and skin lesions can be secondary to Valley Fever. The Central Valley of California, as well as other areas with dry climate, are endemic and we need to keep this disease in our differential diagnosis.
This week we thank Hector Arreaza and Zheng (David) Song. Audio editing by Adrianne Silva.
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:
Roos KL, Tyler KL. Acute Meningitis. McGraw Hill Medical. Published 2023. Accessed August 18, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=2129§ionid=192020493Information for Healthcare Professionals. Published 2023. Accessed August 18, 2023. https://www.cdc.gov/fungal/diseases/coccidioidomycosis/health-professionals.html#printValley Fever (Coccidioidomycosis) a Training Manual for Primary Care Professionals. Accessed August 18, 2023. https://vfce.arizona.edu/sites/default/files/valleyfever_training_manual_2019_mar_final-references_different_colors.pdfAmpel NM. Coccidioidomycosis. Idsociety.org. Published July 27, 2016. Accessed August 18, 2023. https://www.idsociety.org/practice-guideline/coccidioidomycosis/Herrick KR, Trondle ME, Febles TT. Coccidioidomycosis (Valley Fever) in Primary Care. American Family Physician. 2020;101(4):221-228. Accessed August 18, 2023. https://www.aafp.org/pubs/afp/issues/2020/0215/p221.htmlValley Fever Statistics. Published 2023. Accessed August 18, 2023. https://www.cdc.gov/fungal/diseases/coccidioidomycosis/statistics.htmlUpToDate. Uptodate.com. Published 2023. Accessed August 18, 2023. https://www.uptodate.com/contents/coccidioidal-meningitis?search=7%20Coccidioidal%20meningitis&source=search_result&selectedTitle=1~10&usage_type=default&display_rank=1Royalty-free music used for this episode: Tropicality by Gushito, downloaded on July 20, 2023, from https://www.videvo.net/
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Episode 163: Vascular Dementia
15 mars· Rio Bravo qWeek
Episode 163: Vascular Dementia
Future Dr. Ruby explains gives a definition of vascular dementia and concisely explains the pathophysiology and presentation of this disease. Dr. Arreaza reminds us of the importance of treating diabetes to prevent dementia.
Written by Carmen Ruby, MSIV, Ross University School of Medicine. Editing and comments by Hector Arreaza, MD.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
What is vascular dementia?
Vascular dementia is a condition that arises due to damage to blood vessels that reduce or block blood flow to the brain. A stroke can block an artery and result in various symptoms, such as changes in memory, thinking, or movement. Other conditions like high blood pressure or diabetes can also damage blood vessels and lead to memory or thinking problems over time.
Vascular dementia (VaD) is a type of dementia that slowly worsens cognitive functions and is thought to be caused by vascular disease within the brain. Patients with VaD often exhibit symptoms similar to Alzheimer's disease (AD) patients. However, the changes in the brain are not due to Alzheimer’s disease pathology (amyloid plaques and neurofibrillary tangles) but due to a chronic reduction in blood flow to the brain, eventually leading to dementia.
Alzheimer’s disease pathophysiology is very complex, and studies have shown that patients with AD can experience simultaneously several vascular issues that can affect cognitive function. For example, patients with AD may experience mini-strokes and have a reduction of the flow of oxygen and nutrients to the brain tissue. So, AD can be worsened by vascular factors as well, but the vascular factors are not the main problem in AD.
Clinically, patients with VaD can appear very similar to those with AD, which makes it difficult to distinguish between the two diseases. Nevertheless, some clinical symptoms and brain imaging findings suggest that vascular disease is contributing to, if not entirely explaining, a patient's cognitive impairment.
Epidemiology.
In the US, VaD is the 2nd most common type of dementia (15-20% of cases). Prevalence increases with age (∼ 1–4% in patients ≥ 65 years.) People affected by vascular dementia typically start experiencing symptoms after age 65, although the risk is significantly higher for people in their 80s and 90s.
Etiology
VaD may occur as a result of prolonged and severe cerebral ischemia of any etiology, primarily:
Large artery occlusion (usually cortical ischemia) *Acute*Lacunar stroke (small vessel occlusion resulting in subcortical ischemia) *Acute/Subacute**Chronic* subcortical ischemia
Risk factors:
Advanced ageHistory of strokeUnderlying conditions associated with cardiovascular disease:Chronic hypertensionDiabetesDyslipidemiaObesitySmoking
Clinical Features:
Symptoms depend on the location of ischemic events and, therefore, vary widely amongst individuals, but a progressive impairment of daily life is common. Because of the diverse clinical picture, the term "vascular cognitive impairment" is gaining popularity over Vascular Dementia.
Dementia due to small vessel disease:
Symptoms tend to progress gradually or in a stepwise fashion and comparatively slower than in multi-infarct dementia.Generally associated with signs of subcortical pathology:
Dementia due to large vessel disease
Usually, sudden onsetMulti-infarct dementia: typically, stepwise deterioration Generally associated with signs of cortical pathology:Early symptomsReduced executive functioningLoss of visuospatial abilitiesConfusion ApathyMotor disorders (e.g., gait disturbance, urinary incontinence)Later symptomsImpaired memoryFurther cognitive decline: loss of judgment, disorientationMood disorders (e.g., euphoria, depression)Behavioral changes (e.g., aggressiveness)Advanced stages: further motor deterioration: dysphagia, dysarthriaDementia due to large vessel disease Usually, sudden onsetMulti-infarct dementia: typically, stepwise deterioration Generally associated with signs of cortical pathology:Cognitive impairment in combination with asymmetric or focal deficits (e.g., unilateral visual field defects, hemiparesis, Babinski reflex present)
Overall, the symptoms vary depending on which areas of the brain are affected.
Management and Treatment
There is hope when it comes to managing the symptoms of vascular dementia. Although there is no cure for the condition, there are medications available that can help make life easier for those living with it. Additionally, there are drugs commonly used to treat memory issues in Alzheimer's disease that may be effective for individuals with vascular dementia. Sometimes, people with vascular dementia may experience mood changes, such as depression or irritability. These changes can be managed with medications used for depression or anxiety.
Vascular risk modification: If your patient is experiencing cognitive impairment and has clinical or radiologic evidence of cerebrovascular pathology, getting screened for vascular risk factors, especially hypertension, is essential. Treatment can help prevent dementia, but it may not be as effective in reversing it. Statins are given after a stroke regardless of lipid levels.
Antithrombotic therapy: For patients with vascular dementia who have had a clinical ischemic stroke or transient ischemic attack, they must receive the appropriate antithrombotic therapy based on the specific stroke subtype to help prevent any future ischemic strokes.
When considering antiplatelet therapy for patients with vascular dementia who have not had a clinical ischemic stroke or TIA, it is important to make an individualized decision. For instance, we may prescribe aspirin at a dosage of 50-100 mg daily for patients with an infarction seen on brain imaging but not for those with only white matter lesions.
Cholinesterase inhibitor therapy: It is recommended to start cholinesterase inhibitor therapy, such as donepezil or galantamine, for patients with vascular dementia who have a gradual cognitive decline that is not a direct result of a stroke. The evidence suggests that this treatment may offer a small cognitive benefit, but the clinical significance is unclear. Experts do not recommend cholinesterase inhibitors for patients with dementia diagnosed after a stroke if there is no gradual cognitive decline.
Antipsychotics: We can briefly mention antipsychotics. They may be used but we have to remember they may increase mortality in the elderly, and the patient and family must be aware of this risk. Some examples are risperidone, quetiapine, and olanzapine, use them cautiously. Let’s talk beyond medications, what other treatments can we offer?
Non-pharmacologic options: In addition to medications, there are various ways to help a person with vascular dementia. Research has shown that physical exercise, sleep hygiene, and maintaining a healthy weight can not only enhance brain health but also reduce the risk of heart problems, stroke, and other diseases that affect blood vessels.
Patients must be encouraged to eat a balanced diet, get enough sleep,limit alcohol intake, and encouraged to quit smoking, as these are other crucial ways to promote good brain health and reduce the risk of heart disease. Additionally, comorbid conditions such as diabetes, high blood pressure, or high cholesterol, must be treated, because they affect brain function and quality of life overall.
It is essential to understand that emotional outbursts and personality changes can be caused by underlying brain disease and are not always intentional responses or reactions. When behavior problems overwhelm an individual, their family members, or friends, it is critical to seek support. Patient and caregiver support groups are helpful, offering a space to vent, grieve, and gain practical advice from others experiencing similar challenges. Exploring other sources of support, such as adult day programs, can also benefit caregivers and individuals affected by vascular dementia.
Conclusion: Now we conclude episode number 163, “Vascular dementia basics.” Future Dr. Ruby explained that vascular dementia is mainly caused by an impaired circulation of blood and oxygen to certain areas in the brain. This can be a result of large or small vessel disease. Dr. Arreaza reminded us of the importance of treating diabetes as a way to prevent dementia.
This week we thank Hector Arreaza and Carmen Ruby. Audio editing by Adrianne Silva.
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:
Smith, MD EE, Wright, MD, MS CB. Treatment of Vascular Cognitive Impairment and Dementia. Wilterdink, MD JL, ed. UpToDate. Published online May 24, 2022. Accessed February 27, 2024. https://www.uptodate.comVascular Dementia. Memory and Aging Center. Published 2020. https://memory.ucsf.edu/dementia/vascular-dementiaVascular dementia. AMBOSS. Published online June 29, 2023. Accessed February 28, 2024. https://www.amboss.com/usWhat Happens to the Brain in Alzheimer's Disease? National Institute on Aging, https://www.nia.nih.gov/health/alzheimers-causes-and-risk-factors/what-happens-brain-alzheimers-disease. Royalty-free music used for this episode: Space Orbit by Scott Holmes, downloaded on July 20, 2022 from https://freemusicarchive.org/music/Scott_Holmes/.
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Episode 162: Early-Onset Sepsis
28 févr.· Rio Bravo qWeek
Episode 162: Early-Onset Sepsis
Dr. Kooner explains how to diagnose early-onset sepsis by using clinical evaluation and clinical tools. Dr. Schlaerths describes the signs and symptoms of sepsis in neonates, and Dr. Arreaza adds comments about GBS bacteriuria.
Written by Lovedip Kooner, MD, editing Hector Arreaza, MD, and comments by Katherine Schlaerth, 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.
Introduction:
Neonatal sepsis is defined as pathogenic bacterial growth from blood or cerebral spinal fluid culture within the first 28 days of life. Neonatal sepsis can be divided into two categories: early-onset sepsis (EOS) and late-onset. EOS is neonatal sepsis within 72 hours or 7 days after birth, depending on the specialist.
How common is early-onset sepsis (EOS)?
According to the CDC, the infant mortality rate rose for the first time in 20 years in the USA. In the U.S., the incidence of EOS is 0.5 in 1,000 live births and carries a mortality rate of about 3%.
What causes EOS?
Most infections are due to ascending lower vaginal tract flora. Other causes include intra-amniotic infections and maternal hematogenous spread of systemic infections.
Group B streptococcus (S. agalactiae) accounts for about 1/3 of the infectious organisms, followed by E. coli which accounts for about 1/4, and Viridans streptococci account for about 1/5 of infections. Cases of E. coli are seen more often with prolonged rupture of membranes and intrapartum antibiotic exposure. Other notable infections are Listeria monocytogenes, coagulase-negative staphylococci (CoNS), herpes simplex virus, and enteroviruses.
The role of GBS.
Approximately 30% of women have vaginal and rectal GBS colonization and 50% will transmit it to the newborn. Without maternal antibiotic treatment, 1-2% of those infants will develop EOS. The American College of Obstetricians and Gynecologists (ACOG) recommends universal culture-based screening for GBS at 36-37 weeks and 6 days regardless of mode of delivery.
GBS bacteriuria: Treat it (symptomatic and asymptomatic) if >105 CFU/mL. Do not treat it in asymptomatic patients if GBS 18 hours, intrapartum fever, or GBS positive in previous pregnancy.
Nucleic acid amplification test: NAAT in pregnancy is not recommended to determine colonization status. However, if NAAT is obtained in the intrapartum period, give IAP if positive. But, you must also give IAP if negative + mentioned risk factors (18h, Maternal fever >100.4F)
What is considered adequate intrapartum antibiotic prophylaxis?
Penicillin and ampicillin are the recommended antibiotics for prophylaxis. Cefazolin can be given if there is a penicillin-allergy with a low risk for anaphylaxis. Clindamycin and vancomycin are reserved for cases of maternal penicillin allergy. Specifically, clindamycin can be used only if GBS is known to be sensitive to clindamycin. Vancomycin must be used if GBS is resistant to clindamycin. Do not use erythromycin. You will Administered at least 4 hours before delivery.
IAP is believed to reduce neonatal GBS disease by: (1) temporarily reducing maternal vaginal GBS colonization; (2) preventing colonization of the fetus or newborn's surfaces and mucous membranes; and (3) achieving antibiotic levels in the newborn's bloodstream sufficient to surpass the minimum inhibitory concentration (MIC) for eliminating group B streptococci.
Diagnosis of EOS:
Clinical presentation: Tachycardia, tachypnea, temperature instability, supplemental oxygen requirement, and lethargy. Hypoglycemia should not be considered a sign of EOS.
Diagnosing early-onset sepsis is achieved through blood or cerebrospinal fluid (CSF) cultures. Not effective methods for diagnosing EOS include laboratory tests, such as a complete blood cell count or C-reactive protein (CRP), as well as surface cultures, gastric aspirate analysis, or urine culture.
Most infants will generally show signs of EOS GBS infection within the initial 24 hours of birth, with approximately 85% exhibiting symptoms during this timeframe.
Waiting for cultures and/or signs can delay lifesaving treatment.
Management:
According to the American Academy of Pediatrics (AAP), the management of term and late-term infants is undertaken via the clinical condition assessment, the categorical risk factor assessment, and the multivariate risk assessment.
As a part of the 2015 AAP guidelines, the Categorical Risk Factor Assessment is more of an algorithmic approach based on the presence or absence of specific risk factor threshold values such as:
Ill-appearing infant. Mother diagnosed with chorioamnionitis.Mother GBS positive with inadequate intrapartum prophylaxis.ROM >18 hours.Birth before 37 weeks of gestation.
Antibiotics are not always needed, and they can even cause damage. Information taken from the American Academy of Pediatrics, “Management of Neonates Born at ≥35 0/7 Weeks’ Gestation With Suspected or Proven Early-Onset Bacterial Sepsis,” published on December 1, 2018:
(1) Any newborn infant who is ill-appearing or (2) when the mother has a clinical diagnosis of chorioamnionitis -> laboratory testing must be ordered, and empirical antibiotic therapy should be started.
(3) A mother who is colonized with GBS and who received inadequate intrapartum antibiotic prophylaxis, with a duration of ROM being >18 hours or birth before 37 weeks’ gestation -> laboratory testing should be ordered.
(4) A mother who is colonized with GBS who received inadequate IAP but with no additional risk factors -> observation in the hospital for ≥48 hours.
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Conclusion: Now we conclude episode number 162, “Early-onset Sepsis Introduction.” Dr Kooner explained the role of GBS in the pathophysiology of EOS, Dr. Schlaerth discussed the importance of clinical evaluation and Dr. Arreaza explained that GBS screening in the third trimester is not needed when there is a GBS positive urine culture early in pregnancy. Don’t miss part 2 of this discussion. By the way, we do not recommend using feces to prevent or treat sepsis, we just shared anecdotal information to end with a funny note.
This week we thank Hector Arreaza, Lovedip Kooner, and Katherine Schlaerth. Audio editing by Adrianne Silva.
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:
Neonatal Early-Onset Sepsis Calculator by Kaiser Permanente, available at: https://neonatalsepsiscalculator.kaiserpermanente.org/.Espinosa K, Brown SR. Neonatal Early-Onset Sepsis Calculator. Am Fam Physician. 2021;104(6):636-637.https://www.aafp.org/pubs/afp/issues/2021/1200/p636.html.Puopolo KM, Benitz WE, Zaoutis TE; COMMITTEE ON FETUS AND NEWBORN; COMMITTEE ON INFECTIOUS DISEASES. Management of Neonates Born at ≥35 0/7 Weeks' Gestation With Suspected or Proven Early-Onset Bacterial Sepsis. Pediatrics. 2018 Dec;142(6):e20182894. doi: 10.1542/peds.2018-2894. PMID: 30455342. https://pubmed.ncbi.nlm.nih.gov/30455342/.Briggs-Steinberg C, Roth P. Early-Onset Sepsis in Newborns. Pediatr Rev. 2023 Jan 1;44(1):14-22. doi: 10.1542/pir.2020-001164. PMID: 36587021. https://pubmed.ncbi.nlm.nih.gov/36587021/.Flannery DD, Puopolo KM. Neonatal Early-Onset Sepsis. Neoreviews. 2022 Nov 1;23(11):756-770. doi: 10.1542/neo.23-10-e756. PMID: 36316253. https://pubmed.ncbi.nlm.nih.gov/36316253/.Polin RA; Committee on Fetus and Newborn. Management of neonates with suspected or proven early-onset bacterial sepsis. Pediatrics. 2012 May;129(5):1006-15. doi: 10.1542/peds.2012-0541. Epub 2012 Apr 30. PMID: 22547779. https://pubmed.ncbi.nlm.nih.gov/22547779/.Royalty-free music used for this episode: Good Vibes_Adventure Time by Simon Pettersson, downloaded on July 20, 2023, from https://www.videvo.net/
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Episode 161: Depression Fundamentals
21 févr.· Rio Bravo qWeek
Episode 161: Depression Fundamentals
Future doctors Madeline Tena and Jane Park define depression and explain different methods to diagnose it. Non-pharmacologic and pharmacologic treatment is mentioned briefly at the end.
Written by Madeline Tena, MSIII, and Jane Park, MSIII. 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.
Per the language of Mental Health, depression can be defined as a mood, a symptom, a syndrome of associated disorders, or a specific mental disorder.
As a state of mood, depression is associated with feelings of sadness, despair, emptiness, discouragement, and hopelessness. The sense of having no feelings or appearing tearful can also be a form of depressed mood. A depressed mood also can be a part of a collection of symptoms that explain a syndrome.
Depression as a mental disorder can encompass depressive syndromes. Per the American Psychiatric Association DSM-5-TR, depressive disorders commonly include sad, empty, irritable mood, accompanied by changes in one’s functional capacity. They can be classified by severity and recurrence, and associated with hypomania, mania, or psychosis. Depressive disorders include major depressive disorder (including major depressive episodes), persistent depressive disorder, premenstrual dysphoric disorder, substance-induced depressive disorder, depressive disorder due to medical condition, other specified depressive disorder, and unspecified depressive disorder.
Today, we will cover unipolar depressive disorder, also known as major depressive disorder.
MDD.
Major depressive disorder is a mood disorder primarily characterized by at least one major depressive episode without manic or hypomanic episodes. Depressive episode is a period of at least 2 weeks of depressed mood or anhedonia in nearly all activities for most of the day nearly every day, with four or more associated symptoms in the same 2 weeks. We will discuss specific symptoms for diagnosis further on.
Epidemiology of depression.
Nationally or regionally representative surveys in 21 countries estimate that the 12-month prevalence of major depressive disorder across all countries is 5 percent. Furthermore, the prevalence of major depressive disorder plus persistent depressive disorder in developed countries (United States and Europe) is approximately 18 percent.
Multiple studies consistently indicate that in the general population of the United States, the average age of onset for unipolar major depression and for persistent depressive disorder (dysthymia) is approximately 30 years old.
During 2020, approximately ⅕ US adults have reported receiving a diagnosis by a healthcare provider, with the highest prevalence found among young adults age (18-24 year age… generation Z). Within the US there was considerable geographic variation in the prevalence of depression, with the highest state and county estimates of depression observed along the Appalachian and southern Mississippi Valley regions.
Why do we care about depression?
Because depression is associated with impaired life quality. It can impair a patient’s social, physical, and psychological functioning. Also, depression is associated with mortality. A study done by UPenn Family Practice and Community Medicine in 2005 showed that among older, primary-care patients over a 2-year follow-up interval, depression contributed as much to mortality as did myocardial infarction or diabetes.
A prospective study from 2005-2017 that followed 186 patients for up to 38 years further showed that patients with major depressive disorder had 27 times higher incidence rate of suicide than the general population. (1, 2). Also, patients dying by suicide visit primary care physicians more than twice as often as mental health clinicians. It is estimated that 45% of patients who died by suicide saw their primary care physician in the month before their death. Only 20% saw a mental health professional a month before their death. (3)
Suicidality in depression.
It seems that primary care physicians often do not ask about suicidal symptoms in depressive patients. A 2007 study by Mitchell Feldman at the University of California San Francisco showed that 152 family physicians and internists who participated in a standardized patient with antidepressants, suicide was explored in only 36% of the encounters. (4)
Physicians, including primary care physicians, should ask patients with depression about suicidality with questions such as: Do you wish you were dead? In the past few weeks, have you been thinking about killing yourself? Do you have a plan to kill yourself? Have you ever tried to kill yourself? (5)
Screening for depression.
The USPSTF recommends screening for depression in all adults: 18 years old and over regardless of risk factors. Some factors increase the risk of positive screening, such as temperament (negative affectivity/neuroticism), general medical illness, and family history. First-degree family members of people with MDD have a 2-4 times higher risk of MDD than the general population. Furthermore, social history can increase risk as well: sexual abuse, racism, and other forms of discrimination.
It is important to highlight the risk in women because they may also be at risk related to specific reproductive life stages (premenstrual period, postpartum, perimenopause). The USPSTF includes pregnant individuals and patients in the postpartum period to be screened for depression.
Screening tools.
The US Preventive Services Task Force recommends depression screening for major depressive disorder (MDD) in adolescents aged 12 to 18 years (grade B). Similarly, the Guidelines for Adolescent Depression in Primary Care (GLAD-PC) has also recommended annual screening for depression in children aged 12 and older. (6) Some tools used for screening in this age group are the Patient Health Questionnaire for Adolescents (PHQ-A) and the primary care version of the Beck Depression Inventory (BDI).
For the general adult population, it is recommended that all patients not currently receiving treatment for depression be screened using the Patient Health Questionnaire-2 (PHQ-2) (7)
PHQ 2 is a survey scored 0-6. The survey asks two questions: Over the last 2 weeks, how often have you been bothered by any of the following problems?
Little interest or pleasure in doing things.Feeling down, depressed, or hopeless.
Answers should be given in a numerical rating. 0=Not at all; 1=Several days; 2=More than half the days; 3=Nearly every day. A score ≥ 3 is considered positive, and a follow-up full clinical assessment is recommended.
The PHQ-2 has a sensitivity of 91% and a specificity of 67% when compared to a semi-structured interview. Keep in mind that the PHQ-2 may be slightly less sensitive to older individuals. Individuals who screen positive with PHQ-2 should have additional screening with the PHQ-9, which is a nine-item, self or clinician-administered, brief questionnaire that is specific to depression. (8) Its content maps directly to the DSM-5 criteria for major depression. (9)
The PHQ-9 is a set of 9 questions. The answers are scored similarly to PHQ-2, with a numerical scoring between 0 and 3. (0=Not at all; 1=Several days; 2=More than half the days; 3=Nearly every day). Dr. Arreaza, you will be my patient today, are you ready?
It’s important that you think about the last 2 weeks.
Over the last 2 weeks, how often have you been bothered by any of the following problems?
Little interest or pleasure in doing things. [Dr. Arreaza answers, “sometimes”. Jane asks, “is it several days or nearly every day?”. Dr. Arreaza answers, “nearly every day” 3]Feeling down, depressed or hopeless [Dr. Arreaza: every day 3]Trouble falling or staying asleep, or sleeping too much [Dr. Arreaza: not at all 0]Feeling tired or having little energy [Dr. Arreaza: not at all 0]Poor appetite or overeating [Dr. Arreaza: every day 3]Feeling bad about yourself- or that you are a failure or have let yourself or your family down [Dr. Arreaza: several days 1]Trouble concentrating on things, such as reading the newspaper or watching television [Dr. Arreaza: Several days 2]Moving or speaking so slowly that other people could have noticed. Or the opposite, being so fidgety or restless that you have been moving around a lot more than usual. [Dr. Arreaza: Not at all 0]Thoughts that you would be better off dead, or of hurting yourself [Not at all 0]
Jane: Your score is 12.
Maddy: Regarding severity, a total score of 1-4 suggests minimal depression. 5-9 suggests mild, 10-14 moderate, 15-19 moderately severe, and 20-27 severe depression. PHQ-9 with patients’ scores over 10 had a specificity of 88% and sensitivity of 88% for MDD. (10)
But if there are at least 4 non-zero items, including question #1 or #2, consider a depressive disorder and add up the scores. If there are at least 5 non-zero items including questions #1 or #2, consider major depressive disorder specifically. The questionnaire is the starting point for a conversation about depression.
A couple of things to note: 1. Physicians should make sure to verify patient responses given the questionnaire can be self-administered. Diagnosis also requires impairment in the patient’s job, social, or other important areas of functioning. 2. Diagnosis requires a ruling-out of normal bereavement, histories of manic episodes, depressive episodes better explained by schizoaffective disorder, any superimposed schizophrenia, a physical disorder, medication, or other biological cause of depressive symptoms.
Once a patient is newly diagnosed and/or started on treatment, a regular interval administration (e.g. 2 weeks or at every appointment) of PHQ-9 is recommended. The PHQ-9 has good reliability, validity, and high adaptability for MDD patients in psychiatric hospitals for screening and evaluation of depression severity. (12) Other than PHQ-9, there is also Geriatric Depression Scale-15 for older patients with mini mental status exam (MMSE) that scored over 10. (13)
For postpartum depression, the preferred screening tool is the Edinburgh postnatal depression scale[Click here (stanford.edu)].
Non-pharmacologic and pharmacologic treatment.
Now that we have diagnosed the patient, we have to start management. Patients can consider non-pharmacologic treatment such as lifestyle modifications. This can include sleep hygiene, reduction in drug use, increased social support, regular aerobic exercise, finding time for relaxation, and improved nutrition.
Furthermore, based on severity, patients can start psychotherapy alone or psychotherapy + pharmacotherapy. Admission is required for pts with complex/severe depression or suicidality. There should be an assessment of efficacy at 6 weeks.
There is a warning about patients aged 18-24 who are at increased risk of suicide when taking SSRI within the first couple weeks of treatment.
Mediations: SSRI, SNRI, tricyclic antidepressants, MAOIs, and Atypical antidepressants: including trazodone, mirtazapine (Remeron), bupropion (Wellbutrin SR). More research is being done on psychedelic drugs such as ketamine and psilocybin as possible treatments. There are therapies such as ECT available too.
Potential Harm of Tx:
Potential harms of pharmacotherapy:
-SNRI: initial increases in anxiety, insomnia, and restlessness, and possible sexual dysfunction and headaches as well. Compared with the SSRI class, the SNRI class tends to induce more nausea, insomnia, dry mouth, and in rare cases hypertension.
-Tricyclic: Cause of numerous side effects, very infrequently prescribed unless the patient is not responding to other forms of treatment. Side effects that are included are: dry mouth. slight blurring of vision, constipation, problems passing urine, drowsiness, dizziness, weight gain, excessive sweating (especially at night). Avoid TCAs in elderly patients.
-MAOIS: MAO-IS can cause side effects too, including dizziness or lightheadedness, dry mouth, nausea, diarrhea or constipation, drowsiness, and insomnia. Furthermore, other less common side effects can include involuntary muscle jerks, hypotension, reduced sexual desire/ ability to orgasm, weight gain, difficulty starting urine flow, muscle cramps, and paresthesia.
Remember to screen your patients. In case you establish a diagnosis, discuss treatments, including non-pharmacologic and pharmacologic options. Warn your patients about side effects and the timing to see the benefits of the medication, usually after 6 weeks.
__________________
Conclusion: Now we conclude episode number 161, “Depression Fundamentals.” Future doctors Park and Tena discussed depression and its risk factors, screening, and treatment. They went through the PHQ2 and PHQ9 as screening tools, as well as commonly used treatments and their side effects, such as SSRIs. Dr. Arreaza also highlighted the importance of asking about suicidality in your depressed patients, there is a lot of room for improvement in that aspect.
This week we thank Hector Arreaza, Madeline Tena, and Jane Park. Audio editing by Adrianne Silva.
Talk_Outro
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:
Angst F, Stassen HH, Clayton PJ, Angst J. Mortality of patients with mood disorders: follow-up over 34-38 years. J Affect Disord. 2002;68(2-3):167-181. doi:10.1016/s0165-0327(01)00377-9. https://pubmed.ncbi.nlm.nih.gov/12063145/Miron O, Yu KH, Wilf-Miron R, Kohane IS. Suicide Rates Among Adolescents and Young Adults in the United States, 2000-2017. JAMA. 2019;321(23):2362-2364. doi:10.1001/jama.2019.5054. https://pubmed.ncbi.nlm.nih.gov/31211337/ Feldman MD, Franks P, Duberstein PR, Vannoy S, Epstein R, Kravitz RL. Let's not talk about it: suicide inquiry in primary care. Ann Fam Med. 2007;5(5):412-418. doi:10.1370/afm.719. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2000302/.Brief Suicide Safety Assessment,National Institute of Mental Health (NIMH), July 11, 2020. https://www.nimh.nih.gov/sites/default/files/documents/research/research-conducted-at-nimh/asq-toolkit-materials/adult-outpatient/bssa_outpatient_adult_asq_nimh_toolkit.pdfBeck A, LeBlanc JC, Morissette K, et al. Screening for depression in children and adolescents: a protocol for a systematic review update. Syst Rev. 2021;10(1):24. Published 2021 Jan 12. doi:10.1186/s13643-020-01568-3. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7802305/Williams, John; Nieuwsma, Jason. Screening for depression in adults, UpToDate, updated on November 30, 2023. https://www.uptodate.com/contents/screening-for-depression-in-adults.Instrument: Patient Health Questionnaire-9 (PHQ-9), National Institute on Drug Abuse, https://cde.nida.nih.gov/instrument/f226b1a0-897c-de2a-e040-bb89ad4338b9.Lowe B, et al. Monitoring depression-treatment outcomes with the Patient Health Questionnaire-9 (PHQ-9). Med Care, 42, 1194-1201, 2004.Sun, Y., Fu, Z., Bo, Q. et al.The reliability and validity of PHQ-9 in patients with major depressive disorder in psychiatric hospital. BMC Psychiatry20, 474 (2020). https://doi.org/10.1186/s12888-020-02885-6. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3701937/Conradsson M, Rosendahl E, Littbrand H, Gustafson Y, Olofsson B, Lövheim H. Usefulness of the Geriatric Depression Scale 15-item version among very old people with and without cognitive impairment. Aging Ment Health. 2013;17(5):638-645. doi:10.1080/13607863.2012.758231. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3701937/.Royalty-free music used for this episode: Old Mexican Sunset by Videvo, downloaded on Nov 06, 2023 from https://www.videvo.net
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Episode 160: Artificial Intelligence in Primary Care
26 janv.· Rio Bravo qWeek
Episode 160: Artificial Intelligence in Primary Care.
Future Dr. Manophinives explains the present and future of AI in diagnosing and treating diseases.
Written by Rosalynn Manophinives, MS-IV, American University of the Caribbean. 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.
Today, we embark on an intriguing journey at the crossroads of technology and healthcare: The Future of Healthcare in Artificial Intelligence (AI) and Machine Learning (ML). Let’s start by establishing the groundwork for AI and ML. Artificial Intelligence involves machines mirroring cognitive functions like learning and problem-solving, while machine learning empowers machines to learn from data and refine their capabilities over time. In healthcare, these technologies aim to elevate diagnostic precision and treatment effectiveness which are pivotal aspects in primary care medicine.
Accurate diagnosis is the cornerstone of effective patient care in all forms of medicine because an accurate diagnosis guides treatment decisions and influences patient outcomes. This is why the integration of AI and ML holds immense promise in this field.
Section 1: AI in Diagnostic Assistance (4 mins)
Let’s explore how AI utilizes algorithms to analyze extensive datasets, enhancing diagnostic accuracy significantly.
AI serves as a revolutionary force in analyzing a large amount of data, particularly in medical imaging. Imagine AI algorithms as super brains, employing machine learning to decipher intricate details from X-rays, MRIs, and CT scans. Notably, studies have demonstrated their precision matching and even surpassing that of human experts. For instance, research published in the Journal of the American Medical Association revealed AI algorithms outperforming radiologists in detecting conditions like breast cancer.
AI's skills extend beyond images. It digs into genetic information, medical history, and treatment outcomes, acting as a detective to spot patterns, predict responses, and customize interventions. Studies support this, showcasing AI models outperforming dermatologists in diagnosing skin cancer from images.
Will AI replace doctors?
The beauty of AI is that it does not replace doctors but acts as a super investigator in your healthcare corner, expediting diagnoses, and refining treatments. So, AI isn’t merely accelerating processes; it’s enhancing healthcare outcomes, making diagnoses quicker, and treatments more precise, and minimizing errors. The future appears very promising with AI leading the way to more precise and tailored healthcare.
Section 2: Case Studies in Diagnosis (4 mins):
Help in research: Let’s delve into real-life examples of AI in action, further amplifying diagnostic accuracy. In a research study, Rajkomar and collaborators crafted an AI algorithm predicting patient deterioration within hours, leveraging electronic health record data. This tool allowed for proactive care, identifying potential issues before they escalated. Taking it up a notch, Aliper and collaborators compared AI to human researchers, resulting in AI outsmarting human brains in designing drugs targeting age-related diseases. These experiments underscore AI's potential in diagnostics, from catching issues early to designing groundbreaking drugs.
AI here enhances doctors' capabilities and acts as an additional set of eyes, boosting their superpowers, spotting nuances, and proposing game-changing solutions in medicine.
Section 3: AI in Risk Prediction (4 mins):
Let’s shift our focus to AI's role in predicting risks and prognosis, particularly in conditions like COPD.
AI employs sophisticated algorithms to analyze patient data comprehensively, including demographics, hospital visits, diagnoses, prescribed medications, and lab results. In COPD, AI not only predicts mortality but also anticipates hospital readmissions for respiratory issues or flare-ups. By scrutinizing various markers, AI resembles Sherlock Holmes, unraveling clues within data.
And AI doesn’t stop there, AI integrates risk predictions into medical practices, which fosters personalized care tailored to individual risk factors. A study led by Choi and their team analyzed retrospective patient data and they were able to identify individuals at risk of undiagnosed COPD, emphasizing the significance of catching potential issues early, finding those who might slip through the cracks otherwise, which is huge!
Section 4: AI in Treatment Planning (4 mins):
Let’s now explore how AI is revolutionizing treatment planning within medicine.
AI, equipped with machine learning algorithms, tailors treatments by analyzing patient-specific data and medical history. In cancer, for example, AI analyzes biopsy images and quantifies biomarkers, facilitating personalized treatments. Beyond cancer, AI extends its reach to cell therapies, predicting their effectiveness through genomic information and drug responses.
And here's the techie part: AI employs various smart algorithms like Convolutional Neural Networks (CNN) and Recurrent Neural Networks (RNN) to provide personalized treatment recommendations. It’s like having personalized treatment recommendations by experts that fit you like a glove, catering to individual needs.
Section 5: Fuzzy Cognitive Maps and Reduction of Medical Errors (4 mins):
Lastly, let me tell you about the impact of AI-driven treatment planning, specifically in reducing medical errors. Imagine this—medical decisions? They're tough. Sifting through tons of data, inaccessible medical records, physicians' lack of experience, and loads of conflicting info, makes the decision often not crystal clear. This is where a high percentage of medical errors occur, which is where Fuzzy Cognitive Maps (FCMs) come in. FCMs are like a super-smart tool that mimics human reasoning, tackling the messiness of medical data with grace.
FCMs are all about modeling complex systems, by combining fuzzy logic and neural networks, just like our brain does—connecting the dots between concepts and their cause-and-effect relationships. From patient records to test results, they make sense of it all.
And FCM is not just theory—FCMs are the real deal and they're not the newbies in town; they've been around for a while, evolving from their early days. They've proven their worth in various medical areas too – in radiotherapy planning, diagnosing language impairments, and even in grading tumors!
So, in a nutshell, FCMs are useful tools for medical decision support by taking on the complexities of diagnosing and treatment planning.
Closing:
In conclusion, the integration of Artificial Intelligence and Machine Learning in healthcare is a thrilling frontier, offering invaluable tools to enhance diagnostic accuracy and patient outcomes. As we evolve, responsible use of these advances is paramount, ensuring they optimize rather than replace the indispensable human touch in healthcare.
Thank you for joining me in exploring the future of healthcare in AI and Machine Learning. I trust this discussion has sparked curiosity and appreciation for the transformative potential of technology in healthcare.
-----------------------------------
Conclusion: Now we conclude episode number 160, “Artificial Intelligence in Primary Care.” This is a new and somewhat unknown field of medicine that is rapidly evolving these days. Future Dr. Manophinives explained that AI and ML can be a useful tool in the diagnosis of diseases by, for example, interpreting images accurately. AI also can help develop plans of care by interpreting large amounts of complex data and predicting trends, possible complications, and the effectiveness of multiple treatments. Keep your eyes and mind wide open to learn more about this advancing technology that will continue to support our efforts to bring health and well-being to our communities.
This week we thank Hector Arreaza and Rosalynn Manophinives. Audio editing by Adrianne Silva.
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:
Obermeyer Z, Emanuel EJ. Predicting the Future - Big Data, Machine Learning, and Clinical Medicine. N Engl J Med. 2016;375(13):1216-1219. doi:10.1056/NEJMp1606181. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5070532/.Rajkomar, Alvin, et al. "Scalable and accurate deep learning with electronic health records." npj Digital Medicine, 08 May 2018. https://www.nature.com/articles/s41746-018-0029-1Choi, Ellen, et al. "Retrospective analysis of real-world data to identify patients at risk for undiagnosed chronic obstructive pulmonary disease." PLoS ONE, 2020.Choi, Ellen, et al. "Machine Learning in Primary Care: Predicting Hospitalizations and Critical Events." AMIA Annual Symposium Proceedings, 2018.Beam AL, Kohane IS. Translating Artificial Intelligence Into Clinical Care. JAMA. 2016;316(22):2368-2369. doi:10.1001/jama.2016.17217. https://pubmed.ncbi.nlm.nih.gov/27898974/Johnson, Kipp W., et al. "Automated Fuzzy Cognitive Maps Generation for Supporting Clinical Decisions in Primary Care." IEEE Transactions on Fuzzy Systems, 2020.Royalty-free music used for this episode: Gushito, “Gista Mista”, downloaded on November 16th, 2023, from https://www.videvo.net/
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Episode 160: Artificial Intelligence in Primary Care