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Episode 141: Adrenal Insufficiency Basics
Future doctor Wilson explains how to recognize an acute adrenal insufficiency and explains how to treat it. Also, chronic adrenal insufficiency is explained. Dr. Arreaza adds comments about congenital adrenal hyperplasia.
Written by Candace Wilson, MSIV, American University of the Caribbean. Comments by Hector Arreaza, MD.
June 2, 2023.
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:
After having seen patients with adrenal insufficiency when I did a rotation in ICU, I saw how important it is to be able to recognize it quickly to ensure that patients receive appropriate treatment as quickly as possible.
Arreaza: AI is adrenal insufficiency but also AI stands for Artificial intelligence, so we had the idea to ask Chat GPT what are the adrenal glands and this is what we got: “The adrenal glands are small endocrine glands located on top of each kidney. They are small in size, but they play a vital role in producing and secreting essential hormones.” (end of quote)
Glucocorticoids play an important role in the mobilization of energy reserves by increasing gluconeogenesis, glycogen synthesis, protein catabolism, lipolysis, appetite, and insulin resistance.
Each adrenal gland is composed of two main parts: the outer region called the adrenal cortex and the inner region called the adrenal medulla. These two regions have distinct structures and functions.” The adrenal cortex has three zones, Zona glomerulosa (mineralocorticoids, mainly aldosterone), Zona fasciculata (cortisol), and Zona reticularis (androgens).
Mineralocorticoids are a class of steroid hormones produced by the Zona glomerulosa of the adrenal gland that influence electrolyte and water balance through modifying renal absorption of sodium and potassium.
Definition of AI: AI is “inadequate functioning of the adrenal glands”. Adrenal gland hormones: glucocorticoids, mineralocorticoids, and sex hormones.
Primary vs. secondary adrenal insufficiency.
Candace: Primary adrenal insufficiency is caused either by the abrupt destruction of the adrenal gland or by progressive destruction/atrophy, whereas secondary adrenal insufficiency is due to conditions that impair the hypothalamic-pituitary-adrenal axis leading to decreased ACTH production.
Causes of
primary
adrenal insufficiency includes autoimmune adrenalitis (which is the most common cause in the US); infectious adrenalitis (tuberculosis being the most common cause worldwide); adrenal hemorrhage; infiltration of the adrenal gland by tumors, amyloidosis, or hemochromatosis; adrenalectomy; cortisol synthesis inhibitors (such as rifampin, fluconazole, phenytoin, ketoconazole); 21B-hydroxylase deficiency; and vitamin B5 deficiency.
Fluconazole is commonly used to treat pulmonary cocci (Valley Fever in our community). What about secondary causes?
Causes of secondary adrenal insufficiency include sudden discontinuation of chronic glucocorticoid therapy; stress (such as infection, trauma, or surgery) during prolonged glucocorticoid therapy; and hypopituitarism.
Clinical presentation of adrenal crisis.
Adrenal insufficiency can present acutely or chronically with more insidious symptoms. We will first discuss the acutemanifestation of adrenal insufficiency, also known as adrenal crisis. In any patient who demonstrates vasodilatory shock, unexplained severe hypoglycemia, or unexplained hyponatremia whether or not the patient is known to have adrenal insufficiency, adrenal crisis should be considered a possibility. Adrenal crisis is a life-threatening emergency that requires immediate medical treatment and can occur in either primary or secondary adrenal insufficiency, though it is most common in patients with primary adrenal insufficiency. The main feature of adrenal crisis is shock, but patients may also have vague symptoms such as anorexia, nausea, vomiting, abdominal pain, weakness, fatigue, lethargy, fever, confusion, or coma. In patients with adrenal crisis from primary adrenal insufficiency, volume depletion and hypotension are the major clinical features, resulting from mineralocorticoid deficiency. In contrast, the patients with adrenal crisis from secondary adrenal insufficiency (which is an isolated glucocorticoid deficiency) will have hypotension secondary to decreased vascular tone without volume depletion.
Treatment of adrenal crisis.
Signs of an adrenal crisis should be recognized quickly, and management should be started as quickly as possible. When adrenal crisis is suspected, do not wait for laboratory results before initiating treatment as this is a life-threatening medical emergency. After all necessary laboratory tests have been collected (including serum electrolytes, glucose, routine measurement of plasma cortisol and ACTH) and IV access has been established, infuse 2-3L of isotonic saline or 5% dextrose in isotonic saline as quickly as possible and give bolus of hydrocortisone 100mg IV followed by 50mg IV every 6 hours or 200mg/24 hours as a continuous IV infusion for the first 24hrs.
The answer to many endocrine emergencies is IV fluids, in this case, you also add hydrocortisone and mineralocorticoids.
Alternative glucocorticoids if hydrocortisone is unavailable include methylprednisolone and dexamethasone. While patient is hemodynamically unstable, it is important to frequently monitor vital signs and serum electrolytes to avoid iatrogenic fluid overload. When the patient has stabilized, continue IV isotonic saline at a slower rate for 24-48 hours, and for patients with primary adrenal insufficiency, begin mineralocorticoid replacement with fludrocortisone 0.1mg orally daily when saline infusion is stopped. If there is concern for infectious precipitating cause of the adrenal crisis, perform an extensive infectious workup.
Addison’s disease.
Early symptoms of chronic adrenal insufficiency can be vague and nonspecific (such as fatigue, weight loss, and GI complaints), making the clinical diagnosis more difficult than acute adrenal insufficiency. Diagnosis must be confirmed with a thorough endocrine evaluation to determine the type and cause of the adrenal insufficiency, but treatment should be started before the diagnosis is established in acutely ill patients. Primary and secondary adrenal insufficiency shares some common clinical manifestations, such as fatigue, weight loss, anorexia, nausea, vomiting, abdominal pain, amenorrhea, diffuse myalgia, arthralgia, confusion, delirium, stupor, depression, psychosis, mania, anxiety, disorientation, and hallucinations.
Clinical manifestations of indicative of primary adrenal insufficiency include orthostatic hypotension, salt craving, hyperpigmentation especially of areas not typically exposed to sunlight (such as palmar creases, mucous membrane of the mouth), vitiligo (though hyperpigmentation is more common), hypotension, and auricular calcifications.
Lab findings.
Laboratory results will show electrolyte disturbances (such as hyponatremia, hyperkalemia, and hypercalcemia), azotemia, normocytic anemia, eosinophilia, increased renin, normal anion gap metabolic acidosis, hypoglycemia, increased ACTH, low cortisol, low aldosterone, increased cortisol releasing hormone, and decreased DHEA-S.
Clinical manifestations of secondary adrenal insufficiency is similar to those in primary adrenal insufficiency with the notable exceptions of: hypotension (which is less prominent than in primary AI), absence of dehydration, pale skin as opposed to hyperpigmentation. Laboratory results in secondary adrenal insufficiency will show normal aldosterone, sodium, potassium, and renin; decreased ACTH and cortisol; and increased cortisol-releasing hormone.
Treatment of chronic adrenal insufficiency.
Treatment of primary adrenal insufficiency focuses on replacing hypocortisolism with glucocorticoids and hypoaldosteronism with mineralocorticoids. In contrast, the treatment of secondary adrenal insufficiency focuses on the replacement of hypocortisolism with glucocorticoids without the need to supplement aldosterone.
Short-acting glucocorticoids (such as hydrocortisone) are the preferred medication for treatment since they roughly mimic the normal diurnal rhythm. Intermediate-acting (such as prednisone or prednisolone) and long-acting glucocorticoids (such as dexamethasone) are acceptable alternatives, especially in patients who are non-compliant with multiple-day dose schedules or those with severe late-evening or early-morning symptoms, but due to variable inter-individual metabolism of dexamethasone, be cautious of over-treating patients.
Whether the patient is receiving short-acting, intermediate-acting, or long-acting, ensure that patients receive the lowest glucocorticoid dose that relieves symptoms while avoiding signs and symptoms of glucocorticoid excess (such as weight gain, facial plethora, truncal obesity, osteoporosis, etc.).
Summary: Primary = Glucocorticoids and mineralocorticoids. Secondary = Glucocorticoids. Glucocorticoids can be short, intermediate, and long-acting. What about mineralocorticoids?
Fludrocortisone 0.1mg/day is the preferred agent for mineralocorticoid replacement in patients with primary adrenal insufficiency, though patients who are receiving hydrocortisone therapy in conjunction may require a lower dose of 0.05mg/day. Mineralocorticoid therapy may need to be increased during the summer due to salt loss in perspiration.
As a reminder, aldosterone works by controlling the reabsorption of sodium and excretion of potassium. It influences water reabsorption. It is part of the renin-angiotensin-aldosterone system (RAAS) to maintain blood pressure.
In addition, it is important that patients receive adequate education about their medical condition and causes, whether it is primary or secondary adrenal insufficiency, especially the maintenance of medication, adjustment during minor illnesses, and when to consult a clinician.
Bottom line: Adrenal insufficiency can be acute or chronic, primary or secondary. In primary adrenal insufficiency, laboratory results will show electrolyte abnormalities, such as hyponatremia and hyperkalemia, with increased ACTH. Whereas in secondary adrenal insufficiency, electrolytes will be normal, and ACTH will be decreased. Both primary and secondary adrenal insufficiency require treatment with glucocorticoid, but a mineralocorticoid should be added in the setting of primary adrenal insufficiency.
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Conclusion: Now we conclude episode number 141, “Adrenal Insufficiency Basics.” We encourage you to recognize acute adrenal insufficiency promptly and start IV fluids and glucocorticoid stat. Candace reminded us that chronic adrenal insufficiency presents with vague and insidious symptoms, including hypotension, fatigue, weight loss, anorexia, hyperpigmentation of the skin, and even vitiligo. Make sure to include our colleagues from endocrinology if you have concerns.
This week we thank Hector Arreaza and Candace Wilson. 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:
Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!
Episode 140: Bullous pemphigoid basics
Future Dr. Stetkevych explains the diagnosis and treatment of bullous pemphigoid. She explains how to differentiate BP from pemphigus vulgaris. Dr. Arreaza added some comments and summaries.
Written by Katherine Stetkévych, MSIV, Ross University School of Medicine.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
Definition. Bullous pemphigoid is an autoimmune condition in which the body produces antibodies against hemidesmosomes at the basement membrane of the skin. (Hemidesmosomes anchor the epidermis to the dermis.) As a result of this autoimmune reaction, inflammatory cells, and fluid fill under the epidermis, creating a blister.
As a reminder, a vesicle is a collection of free fluid <0.5 cm, and a bulla is the same but larger than 0.5 cm. Bullous pemphigoid is a member of the family of autoimmune subepidermal blistering diseases, which also includes herpes gestationis and cicatricial (sicatríshal) pemphigoid, but bullous pemphigoid is the most common out of that family and the one with the highest mortality. Let’s talk about the presentation.
Presentation.
Typically, bullous pemphigoid affects adults over the age of 60. We can say that it is a disease of elderly patients; the mean age of diagnosis is 80. There is no race or gender preference. The initial presentation is hives and pruritus. Patients may be itchy for ~10 months before the diagnosis. After patients have plaques, erythema, and itching, they have blisters.
What is notable about the blisters in bullous pemphigoid is that the blisters are taut. They bulge out from the skin; however, they do not spread when pressure is applied laterally to the blister, and pressing on an unaffected skin area will not cause a new blister to form. The spread or creation of a blister with pressure is called the Nikolsky sign, and the fact that bullous pemphigoid is negative for the Nikolsky sign helps differentiate this condition from pemphigus vulgaris. Another notable feature is that the blisters of bullous pemphigoid are painless.
If the blisters rupture, patients may experience short-term pain, but the erosion on the skin after the blisters rupture heal fast without scarring.
Bullous pemphigoid typically does not involve the oral mucosa; however, there is a subtype that does. Nonetheless, should a patient present with bullae that involve the oral mucosa, it is important to test for the Nikolsky skin, determine whether the blisters are painful, and work up the blisters to determine the correct diagnosis.
Diagnosis.
The differential diagnosis is extensive and includes dermatitis herpetiformis, bullous systemic lupus erythematous, bullous drug eruptions, bullous impetigo, even insect bites, burns, erythema multiforme, and contact dermatitis.
You can find non-specific findings such as peripheral eosinophilia in 50% of the patients. Serum tests include pemphigoid antibodies ELISA: BP 180 and 230 autoantibodies, desmoglein (desmoglain) 1 and 3. To get to a definitive diagnosis, you need a skin biopsy for histology and immunofluorescence. Histology will show subepidermal cleavage and the presence of inflammatory infiltrate with eosinophils or neutrophils.
The diagnosis will be confirmed by direct immunofluorescence (DIF). The biopsy should be taken from inflamed skin next to a blister with 2/3 of normal skin and 1/3 of inflamed skin. The sample can be transported in normal saline.
Management.
Bullous pemphigoid is treated with first-line topical high-potency corticosteroids, such as clobetasol. In cases of severe bullae, systemic corticosteroids or doxycycline may be prescribed. For patients with refractory bullous pemphigoid, the appropriate next step is to start biologic therapies.
With treatment, the prognosis is generally good for bullous pemphigoid. Some patients have spontaneous remission of the disease within a few years; however, for many, the disease is chronic, with recurrence and remission over months to years. If left untreated, bullous pemphigoid is usually a chronic, progressive disease that may cause functional limitation. Mucous membranous pemphigoid, the subtype of bullous pemphigoid which involves mucous membranes, may potentially be life-threatening if it involves the airway.
Pemphigus vulgaris.
Pemphigus vulgaris is an autoimmune condition similar to bullous pemphigoid. In pemphigus vulgaris, autoantibodies attack desmosomes in the epidermis, specifically desmoglein. Desmoglein is a cadherin protein that holds cells within the spinous layers of the epidermis together. Autoimmune destruction of desmoglein causes blisters to form superior to the basement membrane.
The average age of onset for pemphigus vulgaris is 40-60 years old. There is an increased prevalence of the disease in Ashkenazi Jewish, Indian, Southeast European, and Middle Eastern descent.
Presentation.
Because the basement membrane of the epidermis remains intact, and the protein responsible for cell-to-cell adhesion is destroyed by the immune system, bullae are easily formed. Thus, Nikolsky sign will be positive with pemphigus vulgaris—lateral friction on a blister will cause it to expand, and it may be possible to create new blisters by applying pressure to a normal-appearing area of skin. These blisters may rupture easily, leaving painful sores which may become infected. Additionally, the oral mucosa is frequently involved in pemphigus vulgaris, which helps distinguish it from bullous pemphigoid.
So, if you have a patient with skin blisters, and Nikolsyky sig is positive, and the oral mucosa is affected, then you can tell that this patient probably has pemphigus vulgaris. Tell us about the diagnosis.
Diagnosis involves taking a skin biopsy and examining it under immunofluorescence. Antibodies will be seen surrounding keratinocytes in a net-like pattern, which makes sense because desmoglein surrounds keratinocytes so that it can be attached to its neighboring keratinocytes. Histology of a skin biopsy may also be obtained, which will show a “row-of-tombstones” appearance along the inferior margin of the blister. This is because the so-called tombstones are the keratinocytes of the basement membrane, which remain anchored due to untouched hemidesmosomes.
Treatment.
Treatment is similar to that for bullous pemphigoid but more aggressive. Initial treatment includes a systemic glucocorticoid and rituximab; if rituximab treatment is not possible, mycophenolate or azathioprine may be substituted instead. For refractory cases, glucocorticoid, rituximab, and mycophenolate/azathioprine may be given at the same time. Once the disease has improved, the tapering of the glucocorticoid may be initiated.
Due to the risk of infection, loss of fluid from disseminated blisters, and potentially life-threatening involvement of the airway, the prognosis is poor with pemphigus vulgaris if left untreated.
In summary, bullous pemphigoid is a blistering, autoimmune disease that normally presents in elderly patients and does not involve the oral mucosa. The diagnosis may require a skin biopsy, and the treatment starts with topical steroids; for severe cases, you may need systemic steroids and antibiotics. Pemphigus vulgaris affects the oral mucosa, it presents in younger patients (40-60), and the treatment is more aggressive with systemic glucocorticoids and immunosuppressants.
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Conclusion: Now we conclude episode number 140, “Bullous Pemphigoid.” Katherine explained that bullous pemphigoid is an autoimmune disease that causes skin blisters more frequently in elderly patients. She then explained that pemphigus vulgaris is a similar disease but more serious, and it requires more aggressive treatment.
This week we thank Hector Arreaza and Katherine Stetkevych (pronounced as Stet-KE-vish). 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:
Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!
Episode 139: What is PCOS
Future Dr. Salimi explains the pathophysiology, signs, and symptoms of PCOS. Diagnostic criteria and the basics of treatment are also discussed. Dr. Arreaza adds some comments about the treatment of obesity.
Written by Elika Salimi, MS3, 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.
Hello there! My name is Elika and I am a third-year medical student at Western University of Health Sciences. Today I will be talking to you about polycystic ovary syndrome AKA PCOS.
If you answered YES to many of these questions, it is possible that your patient is suffering from polycystic ovary syndrome also known as PCOS, which is one of the most common endocrine disorders in women.
Pathophysiology:
The exact pathophysiology behind this syndrome is unknown; however, per the American College of Obstetricians and Gynecologists committee, some studies have shown a strong association between PCOS and obesity. In a woman with obesity disorder, the excess adipose tissue ends up increasing peripheral estrogen synthesis and as a result, there is a decrease in peripheral sensitivity to insulin which means many of these women tend to have hyperinsulinemia. To be more detailed, it is important to mention that during these anovulatory cycles, the increase in estrogen, which is also unopposed estrogen with a lack of progesterone, can lead to endometrial hyperplasia and consequently increase the risk of endometrial carcinoma.
Clinical Features:
Unless there is a clear history and physical or if perhaps there was an incidental ultrasound finding of polycystic ovaries, the diagnosis of PCOS is not exactly black-and-white. That is why it is important to increase awareness so that women can put the pieces of the puzzle together and come in to get evaluated. Multiple cysts in ovaries can present in patients without PCOS, and they are common in teenagers. To use the multiple cysts as part of the diagnosis, the patient has to be 2 years after menarche (AAFP).
Some of these clinical symptoms typically start during adolescence displaying menstrual irregularities such as she could’ve had her period and then stopped getting it or she has a very delayed onset of her menstrual cycle.
It is also possible to have spotty menstrual cycles also known as breakthrough bleeding or menorrhagia. And very important to many women, she could be infertile or have difficulties conceiving.
She could also have diabetes because of insulin resistance that comes with the metabolic syndrome that develops with PCOS, which is also increased if she has obesity. This obesity disorder going hand in hand with the metabolic syndrome, can also increase the risk of having sleep apnea, which could affect the quality of her sleep, finding herself more fatigued than she should be after adequate hours of rest.
Other symptoms include skin conditions such as hirsutism which is basically male pattern hair growth in women in areas such as the upper lip, chin, around the umbilicus, back, or even buttocks. She could also have male pattern hair loss on the head or too much acne or oily skin or acanthosis nigricans which are these brown/velvety hyperpigmented streaks on the neck or axilla, or groin. She could also find herself more depressed or anxious.
Diagnosis:
The diagnostic criteria and treatments are mainly addressed in the Journal of Clinical Endocrinology & Metabolism, an evidence-based guideline for the assessment and management of polycystic ovary syndrome, and the American Family Physician Journal:
The diagnosis of PCOS requires the presence of at least two criteria that are not due to any other endocrine disorder such as thyroid disease or hyperprolactinemia, or other.
1) Periods of oligo-ovulation and or anovulation which means she’s either having very low ovulatory cycles or she’s not ovulating at all.
2) hyperandrogenism and this could be based on her clinical features or laboratory studies showing elevated testosterone levels or LH to FSH ratio and
3) Seeing enlarged and/or polycystic ovaries on a pelvic ultrasound. This means that the pelvic ultrasound shows an ovarian volume of equal to or greater than 10 mL and/or there’s multiple cystic follicles that are about 2 to 9 mm in one or both of her ovaries which also usually tend to have a string of pearls appearance.
So, if you have 2 out of the 3, you have PCOS.
There are ways to confirm that there is in fact hyperandrogenism by doing lab studies and this could mean that her testosterone levels are elevated, or her androstenedione is elevated as well as elevated dehydro-epi-androsterone sulfate (DHEAS) and of course we need to rule out pregnancy and other endocrine disorders as I mentioned earlier. However, if the clinical picture of hyperandrogenism is there then that fulfills the diagnostic criteria for PCOS even if the serum antigen levels are normal.
This also applies to an elevated LH:FSH ratio of typically greater than 2 to 1 which is also a characteristic finding of most patients with PCOS but this is not exactly necessary for diagnosis. We also don’t need to find cystic follicles in order to diagnose PCOS.
Treatment:
In family medicine practices and even OB/GYN practice for PCOS the most common recommendation for all patients is to encourage them to increase their physical activity (exercise) and eat healthy and try to consider behavioral modifications to have a target BMI of ideally less than 25 kg/m² because this can reduce estrone production in adipose tissue.
Then we are thinking about ways to treat patients who are not planning to conceive versus those that are.
The first line treatment for hyperandrogenism to try to regulate menstrual cycle abnormalities is combined oral contraceptives also known as birth control pills. This also reduces endometrial hyperplasia which in turn can decrease the risk of endometrial carcinoma as mentioned earlier and it can reduce menstrual bleeding and you can reduce acne and try to assist with the hirsutism as well. As mentioned earlier, PCOS can also go hand-in-hand with insulin resistance or hyperinsulinemia and therefore we can also use metformin that can improve menstrual irregularities but also address the metabolic side of this as well. Summary: Diet, exercise, combined oral contraceptives, and metformin.
Some other more controversial medications to treat hyperandrogenism could be potassium-sparing diuretics such as spironolactone that also inhibits 17-a-hydroxylase or finasteride which is a 5-alpha-reductase inhibitor and flutamide which is an androgen receptor blocker. The mentioned examples are typically for those people that can’t really tolerate combined oral contraceptives.
Other things to consider for those that are suffering from obesity syndrome are to possibly consider bariatric surgery if of course the criteria are met, and this is on a case-by-case basis. Bariatric surgery may be an answer to many of our metabolic problems that’s why it is now called metabolic surgery.
Now the first-line therapy for inducing ovulation is a medication called letrozole which is an aromatase inhibitor that in turn reduces estrogen production stimulating FSH secretion and ultimately inducing ovulation, not to get too heavily into the weeds of how these medications work, but basically it improves pregnancy and live birth rate outcomes in patients who are infertile because of the fact that they have anovulatory cycles or a.k.a. they are not ovulating.
Then we also have clomiphene which is just an alternative to letrozole and has a different mechanism of action but it also stimulates ovulation by more particularly causing a pulsatile secretion of GnRH and in turn increasing FSH and LH as well, and this medication might be actually preferred over metformin monotherapy in women that are suffering from obesity syndrome who also have anovulatory infertility. However, apparently, clomiphene can cause more chance of multiple gestations versus letrozole.
Also, letrozole is preferred over clomiphene to induce ovulation because of a higher rate of live births, but we have the risk of multiple pregnancies with both these methods. Let’s talk about the second-line therapies.
As mentioned earlier we have this 2 to 1 ratio of FSH to LH in women with PCOS or at least a good amount of them. We said that that is not required to diagnose this disorder but we can also give women exogenous FSH plus human menopausal gonadotropin, but this is really a second-line treatment for ovulation induction and typically we go for second-line treatments if first-line therapies aren’t successful. But I will mention that using this exogenous gonadotropin is very expensive and it requires you to have access to specialized healthcare facilities and constant ultrasound monitoring so this may just not be feasible for many people but if you have the resources and it’s affordable for you then exogenous gonadotropins are actually preferred over clomiphene and metformin therapy.
Metformin can also use as a second-line monotherapy for fertility treatments and this in combination with clomiphene can increase pregnancy rates, especially in women who are suffering from obesity disorder, and of course, this is first-line therapy for insulin resistance.
Now if we’re talking about an invasive type of procedure for infertility it would be laparoscopic ovarian drilling which basically, we use a laser beam or surgical needle to reduce ovarian tissue to decrease its volume and try to reduce androgen production. Doing this can cause a hormone shift that can induce FSH secretion and ultimately improve ovarian function as well. This is also a second-line treatment for ovulation induction, but it can be performed as a first line if other indications for laparoscopy are present.
Third-line therapy would be in vitro fertilization which means that basically we take mature eggs from ovaries and then we fertilize them with sperm in a lab and then the fertilized egg or the embryo is transferred to a uterus to be implanted.
For the management of hirsutism, the first-line therapy is usually non-pharmacological and that’s electrolysis or light-based hair removal with laser or photo-epilation. For acne, we can consider benzoyl peroxide or topical antibiotics if necessary.
Final thoughts: Now I know that was a ton of information but ultimately, we are trying to make women more aware of PCOS and let them know that they are not alone, also we are trying to reduce complications such as cardiovascular problems, diabetes, endometrial cancer, infertility or even pregnancy loss. The best we can do is try to educate more women because many are suffering from this condition and they have no idea. Again, my name is Elika Salimi, and I am a third-year medical student. If you have any questions, you can reach me at [email protected].
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Conclusion: Now we conclude episode number 139, “What is PCOS.” Future Dr. Salimi explained that patients with Polycystic Ovary Syndrome present with: Hyperandrogenism, Oligo-ovulation or anovulation, and multiple cysts in ovaries. If your patient meets 2 out of the 3 criteria, then you can confidently give the diagnosis of PCOS. Dr. Arreaza reminded us that by treating obesity you are also treating PCOS.
This week we thank Hector Arreaza and Elika Salimi. 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:
Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!
Episode 138: SGLT-2 Inhibitors in heart failure
Future doctor Enuka explains the use of sodium-glucose-linked cotransporter-2 inhibitors (SGLT-2 inhibitors) in heart failure. Dr. Arreaza adds his experience with these medications and emphasizes their role as an effective treatment for type 2 diabetes.
Written by Princess Enuka, MSIV, Ross University School of Medicine. 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.
Intro:
Heart failure is a major medical condition that affects millions of people worldwide. It is one of the leading causes of hospitalization and death in developed countries. Recently, SGLT2 inhibitors have emerged as a promising treatment option for heart failure. Today, we will discuss their benefits, their effectiveness, and their adverse effects.
SGLT2 inhibitors, also known as sodium-glucose-linked cotransporter-2 inhibitors, are a relatively novel class of drugs that have shown promise in heart failure treatment. This transporter reabsorbs glucose from the glomerular filtrate back into the bloodstream. Under normal circumstances, SGLT-2 reabsorbs 100% of the filtered glucose unless it is saturated (as in hyperglycemia) or blocked by medications. SGLT2 inhibitors increase the amount of glucose excreted in the urine, which leads to blood glucose reduction. Examples include empagliflozin, dapagliflozin, and canagliflozin.
SGLT-2 inhibitors have become a first-line therapy for diabetes mellitus. I heard before that it was used in Europe for T1DM, but it seems like they are no longer used, according to my most recent review of articles. SGLT2 inhibitors are not approved by the FDA for use in type 1 diabetes due to the risk of DKA. Princess, besides the benefits in diabetes, what else did you find in your review?
Benefits/Efficacy:
SGLT2 inhibitors have additional benefits beyond their glucose-lowering effects. One of the benefits of SGLT2 inhibitors is their ability to increase myocardial energy production, alleviate systemic microvascular dysfunction, and improve systemic endothelial function.
Natriuresis and glucosuria mediated by SGLT2 inhibitors have been shown to lower cardiac pre-load and reduce pulmonary congestion and systemic edema, which is beneficial for heart failure management.
Studies have shown that these drugs can also improve cardiovascular outcomes in patients with heart failure with a reduced ejection fraction.
Some studies:
The EMPEROR-Reduced trial demonstrated that empagliflozin, brand name Jardiance®, reduced the risk of cardiovascular death and hospitalization for heart failure in patients with reduced ejection fraction by 25% compared to placebo. Several clinical trials have also shown that this result is significant whether patients have type 2 diabetes or not.
Also, in a multicenter, double-blind, randomized, placebo-controlled trial in patients with heart failure, treatment with dapagliflozin, brand name Farxiga®, improved heart failure-related symptoms and physical limitations after only 12 weeks of treatment. Patients treated with dapagliflozin had a significant, clinically meaningful improvement in the 6-minute walking test distance. The magnitude of these benefits was statistically and clinically significant, spanning all subgroups categorized. This included patients with and without type 2 diabetes and those with an ejection fraction above or below 60%.
Anecdote:
During a previous clinical rotation, I had a patient taking Jardiance for heart failure. He also had a history of chronic kidney disease and managed his condition well with medications and regular follow-ups. Interestingly, he was prescribed Jardiance®, which I initially believed was solely for diabetes management. When I asked him about it, he explained that his cardiologist prescribed Jardiance specifically for his heart.
At the time, I did not understand the rationale behind prescribing Jardiance®, especially since the patient did not have type 2 diabetes. But after researching the medication, I figured that his cardiologist had chosen Jardiance® due to its demonstrated benefits in reducing the risk of cardiovascular death and hospitalization for heart failure.
Although initially considered to be only glucose-lowering agents, the effects of SGLT2 inhibitors have expanded far beyond that. Their use has expanded to include heart failure and chronic kidney disease, even in patients without diabetes. It is, therefore, essential that cardiologists, diabetologists, nephrologists, and primary care physicians are familiar with this drug class.
Adverse effects:
It is worthwhile to note that SGLT2 inhibitors are not typically used as first-line treatment for heart failure, and not all patients with heart failure are appropriate candidates for these medications. SGLT2 inhibitors are generally well-tolerated, but they can cause adverse effects.
Genital and urinary tract infections and euglycemic diabetic ketoacidosis are the most common side effects experienced by patients. The incidence of these adverse effects is generally low and can be managed with appropriate monitoring and treatment. In addition, SGLT2 inhibitors can also cause dehydration, electrolyte imbalances, hypotension, and acute kidney injury (AKI). These imbalances are more common in elderly patients or those with renal impairment, like the patient I discussed earlier.
Genital yeast infections: Diabetes is also a risk factor for genital yeast infections because glucose in the urine is used as a substrate by microorganisms to grow in the GU tract. UTI and genital yeast infections are prevented by staying well hydrated while taking these meds. Increased intake of water will dilute the urine and decrease the concentration of glucose in urine. UTI/genital yeast infections are treated as usual, and the SGLT-2 can be resumed after infections are treated. In case of recurrence, the clinician may consider discontinuation of medication based on a case-by-case assessment. Patients using SGLT2 inhibitors for treatment should have regular follow-ups with their physicians for the early detection of adverse effects.
Bladder cancer: It is not clear if chronic glucosuria is tumorigenic since there are no long-term data. In clinical trials, 10 cases of bladder cancer were diagnosed among dapagliflozin users, five of which occurred only in the first six months of treatment. The FDA has recommended postmarketing surveillance studies. Dapagliflozin is not recommended in patients with active bladder cancer.
Bone fractures and limb amputation: One trial (CANVAS) demonstrated an increased incidence of bone fractures and limb amputations among users of canagliflozin, but another trial (CREDENCE) did not demonstrate such an increased incidence of bone fractures or limb amputations. This increased risk has not been proven with empagliflozin.
Summary: SGLT2 inhibitors have shown promise in heart failure treatment, particularly in patients with a reduced ejection fraction. Even though the specific mechanism of action through which they work on the cardiovascular system is currently unknown, they have been shown to reduce the risk of hospitalization for heart failure and cardiovascular death in several clinical trials. These medications lower blood glucose levels and have other beneficial effects on the cardiovascular system that make them good options for the management of heart failure.
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Conclusion: Now we conclude episode number 138, “SGLT-2 inhibitors in heart failure.” Princess explained that SGLT-2 inhibitors have many benefits that go beyond their glucose-lowering properties. Recently, the use of SGLT-2 inhibitors has been extended to include heart failure with reduced ejection fraction and chronic kidney disease, even in patients without diabetes. Dr. Arreaza also explained that FDA has not approved the use of SGLT-2 inhibitors for the treatment of type 1 diabetes because of the reported increased risk of diabetic ketoacidosis or DKA. There is ongoing research about additional uses of SGLT-2 inhibitors, and we are looking forward to hearing more about these medications in the future.
This week we thank Hector Arreaza and Princess Enuka. 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!
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Links:
Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!
Episode 137: Heart Transplant and LVAD
Future Doctor My explains two treatments for advanced heart failure, heart transplant and Left Ventricle Assist Device (LAVD). Dr. Arreaza adds historical information about the first artificial heart implant and the first LAVD.
Written by My Chau Nguyen, MSIV, American University of the Caribbean 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: Advanced heart failure is a major concern in the United States. Heart failure has a high 1-year mortality average of 33%. Although medical therapies have improved survival rates, some patients with progressive and advanced heart failure may still require heart transplantation or mechanical support such as left ventricular assist devices (LVADs) to prolong survival and improve quality of life.
It is estimated that 23 million people in the world have heart failure, and many of them are in end-stage heart failure. When it comes to treating severe heart failure, there are two main options: heart transplantation and left ventricular assist devices (LVADs).
Heart transplant: The operation to perform a heart transplant typically lasts between five to six hours but may take longer in patients who have undergone previous open-heart surgery or have an LVAD in place. However, because donors’ hearts are a scarce resource, not all patients are eligible for transplantation.
My experience with a heart transplant: I consider myself extremely fortunate for witnessing the whole complex procedure involved in lung and heart transplantation at Jackson Memorial Hospital in Miami, FL. It was an incredible experience to join the transplant team in retrieving a donor organ. Timing plays a critical role in heart transplants.
When a suitable donor becomes available, every second counts. We must quickly arrange transport and secure an operating room. It is essential that the distance between the donor and the hospital is within our designated region.
For example, we are in Region 5, including Arizona, California, Nevada, New Mexico, and Utah. Once everything is in order, we divide into two teams. One team sets off to retrieve the donor while the other prepares the patient in the operating room.
It is a race against time, as hearts and lungs must be transplanted within approximately four hours of removal from the donor. It was remarkable to see how everything was so precisely scheduled, from the arrival and departure of the teams to the transplantation of the organs. It is an inspiring experience to witness these life-saving procedures in action.
History of the artificial heart.
Arreaza: It is great to hear about your experience, but we know that not everyone can have a heart transplant. So, let us talk about other options. For example, an artificial heart. I lived in Utah for several years and I heard something about the first artificial heart being implanted there, so here is the information. William DeVries was the surgeon who led the implantation of the first artificial heart, the Jarvik-7, at the University of Utah on December 1, 1982. The patient was a retired dentist, Barney Bailey Clark, who survived 112 days connected to the device. Today, the modern version of the Jarvik-7 is known as the SynCardia temporary Total Artificial Heart. It has been implanted in more than 1,350 people as a bridge to transplantation.
Left Ventricular Assist Device (LVAD):
In recent years, LVADs have become increasingly popular as a viable alternative to transplantation, as they have demonstrated improved durability by using wear-free components, greatly improving mortality rates in heart failure patients.
Arreaza: The first left ventricular assist device (LVAD) system was created by Domingo Liotta at Baylor College of Medicine in Houston, Texas, in 1962. It is basically a pump that is used for patients who are on end-stage heart failure. The LVAD is surgically implanted, it is a battery-operated pump that helps the left ventricle pump blood to the rest of the body. LVADs can be used as a temporary treatment while patients are waiting for a transplant. It is called a “bridge-to-transplant therapy”. In some cases, an LVAD may restore a failing heart and eliminate the need for a transplant. An LAVD may also be used as a “destination therapy” in patients who are not candidates for heart transplants. LVAD can prolong and improve patients' quality of life.
My: The purpose of an LVAD is to support patients with heart failure by increasing perfusion and reducing filling pressures in the heart. It is important to note, however, that LVADs only partially assist the pumping action of the diseased ventricle and cannot fully replace the function of the heart. Therefore, the decision to have an LVAD or heart transplant must be taken after careful discussion between the patient and the cardiologist to determine which option is best to reach the patient’s goals of care.
Example of an LVAD:Recently, The Berlin Heart Ventricular Assist Device (VAD) has been a game-changer in saving children with severe heart conditions. As you may guess from the name, it is developed in Germany. It is recently approved by US FDA in 2011. This type of LVAD has been used in approximately 1,000 children worldwide, including 12 cases in the United States.
The Berlin Heart is a simple air-driven pump that takes over the work of one or both sides of a child's own heart. It pumps blood around the body to keep the brain and other organs healthy, allowing the child to grow and get stronger.
The use of this device is required until the child is transplanted, or for a small number of children until their own heart recovers. I once again had the privilege of witnessing the procedure performed by one of the inventors, my preceptor, Dr. Loebe in the NICU at Jackson Memorial Hospital.
Conclusion: Now we conclude episode number 137, “Heart Transplant and LVAD.” My explained two options for the treatment of advanced heart failure: Heart transplant and Left Ventricular Assist Device, or LVAD. She shared her recent experience in her surgery rotation at Jackson Memorial Hospital. Dr. Arreaza added the history of the first artificial heart implanted in Utah and the first LAVD. We hope you enjoyed it.
This week we thank Hector Arreaza, and future doctor My Chau 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!
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Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!
Episode 136: Street Med 2.
Future Dr. Bedi presents the history and purpose of street medicine and shares why she became interested in this topic. Dr. Saito tells his personal experience and shares the particular challenges of unhoused patients.
Written by Indudeep Bedi, OMS III, MSIII, Western University of Health Sciences. Comments by Steven Saito, 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.
Indu: I want to talk about street medicine in some general terms, as well as Tracy Kidder's article published in the NYT this year, called "You have to learn to listen," which is based on Kidder's book Rough Sleepers, on Dr. Jim O'Connell's work with the Boston homeless community.
Dr. Saito: Let's start by talking about street medicine in general. What exactly is street medicine?
Street medicine was a term coined by Dr. Jim Withers, from Pittsburgh, who has been practicing the art since the 90s. He founded the Street Medicine Institute (SMI) in 2009, which strives to connect providers worldwide to address homelessness. Providers practice healthcare, of course, but first and foremost, it is about building relationships and demonstrating you are one of them instead of the power differential that usually exists in our system. It requires a paradigm shift, and it's a shift in thinking. Dr. Jim Withers himself, for example, began to wear ragged clothes and put dirt in his hair to show these vulnerable individuals that he was accepting of who they were and respected them for it. In return, they respected him.
Dr. Saito: Do you know of other programs which exist?
There are a bunch of programs now that have spurred up, such as Doctors without Walls, San Francisco's community health center, of course, are very own CSV, and the Boston Pine Street shelter, which I will talk about more. The SMI publishes an annual report, and there are about 50 independent street medicine programs nationwide. Many global programs have sprung up, too. An international street medicine symposium was founded in 2005. In general, this is an excellent community of providers who can share best practices regarding this unique population. Even a student coalition at the SMI helps get student-run programs off the ground.
Dr. Saito: What is one of the homeless community's biggest problems?
That is a tricky question because of the complexity surrounding this issue. I will tackle this by answering that housing is one of the most considerable problems. The housing may be either transitional or permanent. Transitional operates to get the individual immediately off the street. In contrast, permanent housing takes longer to find, but many charities have bought real estate to create permanent housing. Permanent housing also includes the individual being vetted, in a lot of cases, to make sure that they will do okay if they have a place of their own. Are they able to be independent? Can they pay rent? Do they have a job? In 2009, however, a new program was implemented known as Housing First. This social program provided "a no-strings-attached" housing to the homeless population with substance use and mental health problems. What was great about this program is it was found that the relapse rate was much lower in this population when compared with other programs. In 2018, however, due to gentrification and rent increases, there was a very steep rise in homelessness in cities on the west coast, such as Seattle, San Francisco, and Los Angeles. To combat this, many state-wide programs were established that work with healthcare providers to provide these individuals with the help they need.
Dr. Saito: What is the article "You have to learn to listen" about?
I would first like to read a short excerpt from the article: "In American cities, visions of the miseries that accompany homelessness confront us every day — bodies lying in doorways, women standing on corners with their imploring cardboard signs dissolving in the rain. And yet, through a curious sleight of mind, we step over the bodies, drive past the mendicants, return to our own problems. O'Connell had spent decades returning, over and over, to the places that the rest of us rush by."
Dr. O'Connell completed his IM residency at Mass General in Boston and was about to move on to an oncology fellowship when he was approached by some colleagues with a request to take a position as a physician for one year in a grant-funded program from the city of Boston to address homelessness in the 1980s. The program operated outside of Pine Street Inn homeless shelter. One of the initial experiences that Kidder describes Dr. O'Connell having was his first day of being there, being surrounded by stern-faced nurses who obviously knew more than he did about this niche population. He really had to prove himself to them and the individuals who were homeless. Soon after he joined, Dr. O'Connell met a nurse by the name of Barbara McInnis, who told him, "I really think we want doctors, but you've been trained all wrong. If you come in with your doctor questions, you won't learn anything. You have to learn to listen to these patients." Nurse McInnis also taught Dr. O'Connell a common practice at their shelter, which was to soak patients' feet by filling a tub and pouring in betadine, as a lot of the population did not have footwear. This reflection of "placing the doctor at the feet of the people he was trying to serve" is beautiful. That is precisely what street medicine is about.
Dr. O'Connell has been managing the street medicine program at Pine Street since then, and that oncology fellowship remains forgotten. The program he is a part of now has 19 other shelters in order to tackle Boston's growing homelessness problem. However, it was apparent to Dr. O'Connell a few years in that these shelters were not really making a difference in terms of curbing the amount of homelessness. That problem was still continuing to grow. In addition, many other systemic issues were leading to the rise in homelessness, such as the AIDS epidemic around the time, lack of welfare programs, gentrifications, etc. But the difference was being made in the sense that these individuals who had been pushed to the margins, who were overlooked, and who were in essence burned by the healthcare system in one way or another and highly suspicious of providers for that reason, were now able to be coaxed into receiving and accepting the help they needed. This was done by, as said previously, placing the physician at the feet of the people he was trying to serve.
Over the years, the program continues to grow and even created a new clinic with beds, offering housing vouchers, but it also faces other problems, such as funding and efficiency. A significant focus for the homeless community is housing options. And most people will do really well after being housed, while for others, finding housing brings more troubles with it when they need to be continuously moved from home to home to avoid eviction. I think a lot of it has to do with the lack of resources that come with housing. Homelessness is so complex that finding a home is simply not enough, and these individuals can again fall through the cracks if those other issues are not addressed. While street medicine does a lot of good, it is a harsh reality that individuals have a low life expectancy and will die of this homelessness because of the other issues that remain a constant in their lives, such as substance use, HIV, AIDS, and mental health issues.
Dr. Saito: How did you come to be interested in this topic?
I have been interested in street medicine for a while now. I volunteered in some projects that exposed me to the perils facing the population, especially for addiction. For example, I had an excellent opportunity to work with an organization that would put up tents to test the communities for HIV and connect them with resources if needed. We would specifically go to the areas where people who were homeless or of low SES tended to congregate. I really started to think about it more recently when I encountered a patient on the Infectious Disease service who was incredibly complex in an immunocompromised state due to AIDS, with multiple hospitalizations and pretty much every infection under the sun. He was what we commonly refer to as non-compliant because of substance use, and whenever we found placement for him upon discharge, he would run away from that home. I think, as providers, we are very quick to judge and label patients as non-compliant without pausing to understand the nuances of their condition. He would later continually return to the hospital in an acute exacerbation of his illness. With each hospitalization, his baseline continues to worsen. And I was deeply saddened to come across such a patient and also recognized within myself this frustration with the system in which we operate. I am a bit despondent about his outlook, and the work of the CSV team is critical to these rough sleepers.
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Conclusion: Now we conclude episode number 136, “Street Med 2.” Future Dr. Bide recounted the experience of Dr. O’ Connell and some of the challenges faced by our unhoused patients. Dr. Saito added his personal experience and reminded us that compliance with medications may be difficult in unhoused patients. Here in Clinica Sierra Vista, we are proud of our street medicine program, and we hope many more volunteers would join us in our mission to bring “health for all.”
This week we thank Indudeep Bedi, Steven Saito, and Hector Arreaza. 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:
Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!
Episode 135: Exercise in Diabetes
Kishan and Princess explain how exercise lowers or raises blood glucose levels in diabetes. Dr. Arreaza adds some comments about insulin resistance.
Written by Kishan Ghadiya, MSIV, Ross University School of Medicine. Comments by Princess Enuka, MSIV, Ross University School of Medicine; 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.
Today is April 7, 2023. Ep. 135.
Intro:
It is widely known exercise is paramount for all individuals. The American Heart Association recommends at least 150 minutes of moderate-intensity exercise weekly for general health. Exercise is particularly important in patients with diabetes, who require extensive lifestyle modification to manage their sugar levels. However, it is not well known how glucose metabolism changes when patients with diabetes exercise.
My patient in the clinic.
I recently saw in the clinic a young patient newly diagnosed with type 2 diabetes who asked about how his exercise was helping his sugar levels. He was confused because he heard that exercising allows for better glucose control but complained that his sugar levels were higher after exercising.
To understand what is going on in this patient, it is important to understand the underlying pathophysiology of diabetes. First off, the two most common types of diabetes are type 1 and type 2. Type 1 occurs when the pancreas stops producing insulin altogether. Type 2 occurs when the insulin secreted by the pancreas is no longer effective in normalizing blood sugar levels; the body is not able to utilize glucose efficiently, the number of calories consumed exceeds the body’s demands, and thus increasing body weight, which leads to insulin resistance and eventually pancreatic beta-cell exhaustion. Diabetes is thus a disease state of prolonged hyperglycemia and confers many long-term complications such as accelerated cardiovascular disease, neuropathy, nephropathy, and retinopathy.
How does exercise lower blood glucose?
Once patients are diagnosed with diabetes, management is lifelong, and it takes considerable mental and physical effort to manage this change in health. Exercise is a key metric in diabetic management because lowering blood sugar is as simple as using excess glucose to create energy in our muscles. There are two main mechanisms in how exercise has a positive effect on diabetes.
What type of exercise would be the most effective in controlling blood sugar?
The data is very clear that there is no relationship between exercise technique and glucose level, but there is a relationship between exercise intensity and glucose levels. In other words, patients wanting better blood sugar outcomes may choose whatever exercise regimen as long as they are able to do high-intensity exercise (i.e., resistance training, strength training, High-intensity interval training, HIIT).
Anaerobic vs. aerobic
Blood sugar levels during exercise will be different based on the types of exercise patients choose. For example, high-intensity anaerobic exercise (such as weightlifting) causes large spikes of blood sugar because the liver creates large amounts of glucose for anaerobic glycolysis.
On the other hand, high-intensity aerobic exercise (such as running) confers lower blood glucose. Keep in mind both types of exercise confer excellent long-term patient outcomes, but the disparity in blood sugar is important to note as it can lead to confusion in patients that are very actively monitoring their sugar levels.
Hyperglycemia after anaerobic exercise.
So, returning to my patient mentioned above, further history revealed that he does weightlifting two or three times a week. Hyperglycemia would therefore be expected during and immediately after anaerobic exercise due to large amounts of glycolysis requiring the liver to create sugar. This patient’s increased blood sugar seen after exercising would not be a cause for concern as this is part of normal human body physiology.
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Conclusion: Now we conclude episode number 135, “Exercise in Diabetes.” Kishan explained that exercise improves insulin sensitivity and promotes muscle growth for improved glucose metabolism. Princess explained that anaerobic exercise may cause a transient rise in glucose while aerobic exercise causes glucose control over a longer period. Dr. Arreaza explained that insulin sensitivity is lost when we give frequent “high shots of sugar” to our body.
This week we thank Hector Arreaza, Kishan Ghadiya, and Princess Enuka. 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:
Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!
Episode 134: Martian Medicine 101.
Future doctor Collins and Dr. Arreaza talk about the health risks of going to space and to Mars, especially the effect of radiation.
Written by Wendy Collins, MSIII, Ross University School of Medicine. Comments by Hector Arreaza, MD.
You are listening to Rio Bravo qWeek Podcast, your weekly dose of knowledge brought to you by the Rio Bravo Family Medicine Residency Program from Bakersfield, California, a UCLA-affiliated program sponsored by Clinica Sierra Vista, Let Us Be Your Healthcare Home. This podcast was created for educational purposes only. Visit your primary care provider for additional medical advice.
Today is March 31, 2023.
Arreaza: Wendy, I confess I am excited for today’s topic. My love for space began with E.T. (I know, I am old). I was exposed to that famous movie when I was a little kid, and ever since, I have had a tremendous curiosity about space and Mars. Honestly, I did not think this could be a topic for our podcast until I met you.
Wendy: I got inspired to talk about space medicine because I want to go into this field. My college degree was in Physics, and I was fortunate to do Astrophysics and Particle Physics research as an undergraduate, as well as coral reef research. I am passionate about Medicine and treating patients, but I also love Aerospace Medicine because it’s so interdisciplinary. Flight surgeons get to scuba dive, work on oceanography, botany, engineering projects, and more, and collaborations like that sound exciting to me. Anyways let us talk about what is going on in the industry right now. Dr. Arreaza, do you know what humans are doing in space this year?
Arreaza: I do! I like to watch the launches online and in person. I have seen several SpaceX rockets from my backyard (something I never imagined I could do), and there has been some big news, we are going back to the moon!
Wendy: Yes! Artemis 1 was a successful unmanned mission to orbit the moon and it was launched in November and landed in December last year. Now we look to Artemis 2, which will be a manned lunar flyby. So, like Artemis 1, but with astronauts onboard. And the goal for future missions after that is to land on the moon, establish a lunar base, and eventually prepare us for a long-term space flight like that to Mars. And there is even a presidential order to land humans on Mars by 2033.
Arreaza: Yes, it is very exciting! BUT there are many, many human health risks to space flight.
Wendy: Even more for space flight outside of low earth orbit. Because of this, and because space flight is becoming commercialized, space medicine is a growing field, and growing in all medical specialties. Believe it or not, I was just in a talk by a NASA flight surgeon where it was mentioned that NASA is even looking for OB/GYN because 50% of their astronauts are women who need gynecological care, and they currently have to go off-site to receive it.
Arreaza: That’s so cool! I’ve read of a handful of civilian and military aerospace medicine training programs for physicians after residency. And since we’re in Bakersfield and only a stone’s throw away from this campus, why don’t we briefly mention the University of California Los Angeles?
Wendy: Yes, so UCLA established an aerospace fellowship very recently in 2021. That fellowship, unlike the rest of them, is actually for board-certified emergency medicine physicians only right now, I believe the only one that does not consider other specialties like internal medicine and family medicine, but the program is new so who knows that may change. The fellowship’s goal is to train the next generation of space flight surgeons. Part of the medical training includes working in arctic environments, Mars analog missions, which includes rotations at SpaceX and NASA’s jet propulsion laboratory. There are so many new avenues to pursue education and jobs in aerospace medicine but today we’re focusing on some research that’s near and dear, and revolves around how we get to Mars in one piece. You may ask, what are the health risks of going to Mars? Ultimately, I would like to chat about how we mitigate those risks, but first let’s define them.
Arreaza: So, we got some ideas from a paper published in 2020 by Patel et al. It is titled: Red risks for a journey to the red planet: The highest priority human health risks for a mission to Mars. Let’s begin.
Wendy: Spaceflight is dangerous with unique risks and challenges. As a space flight surgeon, your job revolves around ensuring the overall safety of the crew, as well as their physical and mental health and well-being. The major health hazards include radiation, altered gravity fields, and long periods of isolation and confinement. Each of these threats is associated with its own set of physiological and performance risks to the crew.
Arreaza: But crews do not experience stressors independently, so it is important to also consider their combined impact. NASA’s Human Research Program researches over 30 categories of health risks astronauts can face with space flight.
Wendy: Yes, but this article only discusses 4 of those categories, but don’t worry, they are the biggies, they are the “Red Risks.”
Arreaza: So, what are Red Risks?
Wendy: Red Risks are risks that are considered the highest priority due to their greatest likelihood of happening and because they are most detrimental to the crew’s health and performance, which impacts the success of the mission.
Arreaza: There also exists “yellow” and “green” risks too, which of course are important, but less severe or less likely to occur than the Red Risks.
Wendy: I just want to say I really like the title of this paper. Red risks for a journey to a red planet because Mars of course is red. Anyways as part of this paper, the “red risks” we are going to cover are space radiation health risks. This paper also covers spaceflight-Associated Neuro-ocular Syndrome, which is also known as SANS, behavioral health and performance, and inadequate food and nutrition. But today, we are only going to cover radiation health risks. But one thing this article did not discuss was the human health risk of infection, so let’s briefly mention it now.
Arreaza: Yes, I can imagine spacecrafts are not sterile environments. It would be important to mitigate infections and hygiene necessities and have antibiotics that are functional and not expired or altered by radiation. Alright let’s start with the first health risk on the list, radiation.
Wendy: Space radiation health risk is a large topic because it does not just predispose you to cancer, it also affects many organ systems. So, we are going to break down the health risks caused by space radiation exposure into of course radiation carcinogenesis, but also cardiovascular disease, degenerative tissue effects, and lastly acute in-flight as well as late central nervous system effects.
Arreaza:
Wendy: Yes the spacecraft does filter some radiation of course, but not Earth’s atmosphere. It’s actually a common misconception that astronauts on the International Space Station are protected by Earth’s atmosphere. But it’s not the atmosphere, it’s Earth’s magnetosphere, which is protective from radiation on some level because it absorbs many high-energy protons from space that, if not absorbed, would interact and cause damage to whatever is around.
Arreaza: But astronauts on the ISS are exposed to radiation, how much?
Wendy: So, about one weekon the ISS is approximately equivalent to one year’s exposure to radiation on the ground. But astronauts going to Mars are going to be in space a lot longer than one week. NASA’s 2020 Perseverance rover mission took 7 months to get to Mars.
Arreaza: And that’s without Earth’s magnetosphere, and not considering any travel back home. That’s a lot of radiation. How much radiation exposure would you get traveling to Mars?
Wendy: The crew to Mars would be exposed to pervasive, low dose-rate galactic cosmic rays, and to intermittent solar particle events.
Arreaza: Wow galactic cosmic rays?
Wendy: Yeah, they sound cool but they’re not the ones that give us superpowers like in the Fantastic Four. It means high charge and high energy protons will come into contact with the spacecraft and all the things inside. While the spacecraft will act as a shield, it will never be an entirely perfect shield and protons will penetrate and interact with human tissues, and you know what that means Dr. Arreaza…
Arreaza: DNA breaks which can cause diseases including cancer, cardiovascular and neurologic disorders.
Wendy: Exactly. It’s important to note there are so many variables including the spacecraft design, what’s happening with the sun, and the duration of the trip. And because of all these things, the risk assessment for radiation exposure is difficult to pinpoint because it's truly going somewhere we’ve never gone before. The types of radiation encountered in space are very different from the types of radiation exposure we are familiar with here on Earth. There have been radiobiology experiments working on simulating space radiation here on Earth, but we still lack reliable human data.
Arreaza:
Interestingly, the astronaut with the longest space flight, a Russian physician astronaut Dr. Valeri Polyakov, was on the ISS for 437 days. Dr. Polyakov recently passed away. His cause of death is not disclosed, but he lived a long life into his 80s, so at least we know he did not get terminal cancer after all that time in space.
Wendy: Yes, and that was just Dr. Polyakov’s longest flight. He was on five different Soyuz missions and 2 MIR missions. So, there will be radiation no matter what, what can be done about it?
Arreaza: There’s ongoing research focused on age, sex, and health of the astronaut. Not all people are affected by radiation the same way. Biomarkers are being investigated to determine who will be less sensitive to radiation.
Wendy: Exactly just like we have biomarkers to know if you are predisposed to developing cancers. But back to space.The major cancers of concern from space radiation are epithelial in origin, particularly lung, breast, stomach, colon, and bladder, and leukemias. Radiation is a “red risk” also because of the likelihood of developing cancer after the mission back on Earth. Dr. Polyakov was fortunate to live a long life, but what about our Mars astronauts with even greater radiation exposure?
Arreaza: This research paper even mentions cancer is a long-term health risk and although it is rated as “red”, most research in this area is currently delayed. This is because NASA’s Human Research Program is focusing on in-mission risks, not the risks after the mission. But research is still being done to establish radiation dose thresholds, specifically permissible exposure limits.
Wendy: So now let us talk about the effects of radiation that is not cancer.
Arreaza: So, we know radiation can cause many other health problems. This includes cardiovascular and cerebrovascular diseases, cataracts, digestive and endocrine disorders, immune deficiencies, and respiratory dysfunction.
Wendy: Specifically, we know cancer patients who have received high-dose radiation to the mediastinum, are at an increased risk for cardiovascular disease including heart attack and stroke. An astronaut who goes to Mars is more likely to die from a heart or vascular disease secondary to radiation than cancer.
Arreaza: NASA also is concerned about the effects of other inflight risks such as more blood flow to your head without the effect of gravity. Not to mention developing atherosclerosis, myocardial infarction, stroke, or arrhythmia just like anybody else on Earth.
Wendy: There is also chronic inflammation and increased oxidative stress from radiation, which contributes to cardiovascular disease. For example, the mechanism of increased endothelial dysfunction.
Arreaza: Health problems are not only a result of spaceflight but there can be pre-existing conditions. Astronauts are extensively screened medically, but diseases can also arise in astronauts who are “healthy” before leaving.
Wendy: Absolutely, which is why right now only extremely healthy individuals are candidates to become astronauts, although this will likely change as space becomes more accessible the more spaceflight commercializes.
Arreaza: Other diseases induced by radiation include CNS effects. Acute CNS problems that may arise during flight are impaired cognitive function, motor function, and behavioral changes. These would cause serious problems for astronauts.
Wendy: Besides acute, there are also chronic CNS problems. This includes Alzheimer’s disease, dementia, or accelerated aging. This has been shown with rodents exposed to radiation in which neurons and neural circuits change causing performance deficits.
Arreaza: It is important to note that no astronauts have suffered from life-changing radiation damage illnesses to date.
Wendy: Again, back to Dr. Polyakov is evidence of that. And again, more research needs to be done to understand the significance of radiation to human health and determine how much radiation is too much radiation.
Arreaza: That was Martian Medicine 101. Why are we talking about space medicine in this podcast?
Wendy: Space medicine might be an out-there topic for our Family Medicine podcast. But going into space has given us technologies that help us in our day-to-day in life for non-medical folks, but also for primary care staff. The aural thermometer that takes your temperature by being placed near your ear was developed by NASA. Also, ventricular assist devices LASIK, cochlear implants, and artificial limbs scratch-resistant lenses for glasses, are all works that have contributions from NASA. Anyways, radiation was a fun topic today, but stay tuned for Martian Medicine 102, coming soon when we will talk about the other health risks of going to Mars.
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Conclusion: Now we conclude episode number 134 “Martian Medicine 101.” As you can see, family medicine is unlimited, in the future you may be working on Mars as a family doctor. An inquisitive future doctor, Wendy Collins, explained that radiation is one of the major risks of long space flights because besides cancer, radiation may also cause cardiovascular diseases, immune deficiencies, and respiratory problems. Dr. Arreaza reminded us that radiation does not affect everyone the same way and even though astronauts are screened extensively, at this point it is difficult to determine with precision who will be a perfect fit for space flights. Stay tuned for Martian Medicine 102.
This week we thank Hector Arreaza and Wendy Collins. 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:
Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!
Episode 133: Neonatal Jaundice
Jennifer explained the pathophysiology of neonatal jaundice and how to treat it and described why screening for hyperbilirubinemia is important.
Written by Jennifer Lai, MS3, College of Osteopathic Medicine of the Pacific Western University of Health Sciences. 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 neonatal jaundice?
Jenni: Infant jaundice, also known as hyperbilirubinemia, is when there is a high level of serum bilirubin causing yellow discoloration of the newborn's skin and eyes. Bilirubin is a red-orange byproduct of hemoglobin catabolism that gives yellow pigment to skin and mucosa membranes.
Arreaza: When we see jaundice on the eyes, it is actually the conjunctiva color we are seeing. So, the term “scleral icterus” should be changed to “conjunctival icterus,” but you may get corrected by unaware clinicians. Bilirubin actually binds elastin.
What’s the pathophysiology/ big picture?
Jenni: The key problem is the accumulation of high levels of bilirubin in serum and if left untreated, it can bind to tissues and cause toxicity. There are multiple reasons why there might be too much bilirubin in the serum. Excess bilirubin can be due to a benign normal condition, but it can also be due to a pathologic reason. It is important to differentiate between these two because the management and treatment can differ significantly.
Arreaza: Highly bilirubin means that it is being either overproduced or under-eliminated.
Physiologic jaundice
Most of the time, hyperbilirubinemia is benign and physiologic, with yellowing typically occurring between 2-4 days.
Normally, there is a period of transition caused by the turnover of the fetal red blood cells and the immaturity of the newborn’s liver to efficiently metabolize bilirubin and increased enterohepatic circulation. The most common reason is that the liver isn't mature enough to get rid of the bilirubin in the bloodstream or because the baby’s gut is sterile, so it does not have the bacteria to convert the bilirubin to get it out of the body. In general, newborns have a higher level of total serum or plasma bilirubin levels compared to adults for the following reasons:
Pathologic Jaundice
Pathologic jaundice includes severe neonatal hyperbilirubinemia, extreme neonatal hyperbilirubinemia, and bilirubin-induced neurologic disorders. We determine the severity of the jaundice using the total serum bilirubin (TSB). It is defined as a TSB >25 (severe) and TSB >30 (extreme). Other concerning signs include a TSB over the 95% percentile, a greater than 5mg/dL/day or 0.2mg/dL/hour, or jaundice that lasts for more than 2-3 weeks.
Potential pathologic causes include but are not limited to:
Arreaza: Indirect bilirubin is the one elevated in newborns, but if you see direct hyperbilirubinemia, then you have to think of an obstruction.
Jenni: Severe hyperbilirubinemia can cause brain damage. The amount of bilirubin and the duration of bilirubin ultimately determine the severity of the brain damage. This is because the bilirubin blocks some mitochondrial enzymes from being able to function properly, also it inhibits DNA synthesis/protein synthesis, and can cause DNA damage. This can ultimately lead to acute bilirubin encephalopathy which is described as 3 different phases: Phase 1 with poor feeding, lethargy, hypotonia, and seizures, Phase 2 with increased tone in extensor muscles causing neck contractions (retrocollis and opisthotonos), and Phase 3 with generalized increased tone. If the bilirubin encephalopathy persists it can also ultimately cause cerebral palsy, sensorineural hearing loss, and gaze abnormalities.
How and when do we treat?
No phototherapy:
The goal of treating jaundice is to safely decrease the amount of bilirubin in the body. Oftentimes babies with mild hyperbilirubinemia don't get any treatment and we just watch and wait. In premature babies, there is an increased risk for brain toxicity because a lower amount of bilirubin can result in brain toxicity. For these babies, it is important to ensure there is adequate breast milk to both prevent and treat jaundice because it helps the baby get rid of bilirubin through the stool and urine.
Arreaza: Indirect sunlight exposure of the baby.
Phototherapy:
Other babies get phototherapy or more commonly known as light therapy. Phototherapy light treatment is when the baby’s skin is exposed to a special blue light which will help break down bilirubin and help with the excretion in stool and urine. The phototherapy should be continuous and placed on as much skin as possible and the treatment should be administered until bilirubin levels drop to a safe level based on the baby’s hour-specific thresholds.
Arreaza: Home phototherapy is an option (UV blanket) available for rent or purchase.
Phototherapy is very safe, however, with any treatment, there are risks and potential side effects. Some of these include skin rashes, loose stools, overheating, and dehydration. Occasionally, babies turn a dark gray-brown color in their skin and urine, but this is temporary and usually resolves on its own. While the baby is receiving phototherapy, it is important to continue breastfeeding to ensure appropriate fluid hydration, but in babies that cannot get enough breast milk, they may need to supplement with formula or even potentially start IV fluids.
Benefits of screening
It is therefore essential for universal bilirubin screening for all newborns prior to discharge to identify newborns who are at risk for developing severe hyperbilirubinemia. Hyperbilirubinemia is extremely common in newborns, with nearly all neonates having a higher total serum bilirubin than adults. The reason we screen is that this reduces the risk of developing severe hyperbilirubinemia and ultimately brain damage. This universal screening also then decreases hospital readmissions for neonatal hyperbilirubinemia.
Arreaza: So, we check at 12-24 hours in a typical pediatric unit. We use a bilimeter (transcutaneous) and if we suspect it is not accurate, we do a serum bili. Be aware of the accuracy of bilimeters.
How do we screen?
We do this prior to newborn discharge through a transcutaneous bilirubin device (TcB) or lab total serum bilirubin (TSB). The bilirubin level is used with the assessment of risk for the development of severe hyperbilirubinemia. Newborn bilirubin screening guidelines include TSB or TcB within 24-48 hours after birth or before discharge. TcB is the noninvasive test, but TSB is the gold standard for assessing neonatal bilirubin. Newborns with visible jaundice in the first 24 hours should be concerned for severe hyperbilirubinemia. These babies should be screened earlier because of the risk of pathologic causes of jaundice.
In addition to the bilirubin test, physicians will clinically assess by examining the skin under ambient or daylight to assess whether there is a yellow discoloration of the buccal, gingival, or conjunctival mucosa. Additionally, if a baby presents with scleral icterus, pallor, bruising, hepatosplenomegaly, or cephalohematoma (enclosed hemorrhage), these can be clinical presentations of neonatal jaundice.
Follow up:
After screening, we recommend that babies be closely monitored if jaundice does occur as it can be well managed with early treatment. A quick way to assess this at home is to press gently on the baby’s forehead and if the skin looks yellow where you press, it’s probably jaundice. If your baby doesn’t have jaundice, then the place where you pressed it should look lighter than normal.
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Conclusion: Now we conclude episode number 133, “Neonatal Jaundice.” Jennifer explained the pathophysiology behind the increased levels of bilirubin in babies. She reminded us that it is a physiologic process, but when the level of bilirubin is too high, then we need to start treatment. Treatments include indirect sunlight exposure of the baby, breastfeeding, and in some cases phototherapy, IV fluids, and even antibiotics and exchange transfusion in some cases. Dr. Arreaza reminded us of the importance of screening and monitoring “bili babies” in the clinic.
This week we thank Hector Arreaza and Jennifer Lai. 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:
Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!
Episode 132: Harm Reduction and Reproductive Health
Meghana explains how to implement harm reduction strategies in at-risk populations such as unhoused patients and injected drug users. Dr. Arreaza adds comments about PrEP for HIV and Expedited Partner Therapy (EPT)
Written by Meghana Munnangi, MPH, third-year osteopathic medical student, College of Osteopathic Medicine of the Pacific Western University of Health Sciences. 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: It can be frustrating for physicians trying to change “risky” behaviors in their patients and turn those behaviors into “healthy” behaviors. Doctors deal with this issue every day, but after reading more about the principle of harm reduction, I’m feeling more prepared to help our patients reduce their risks.
What is harm reduction?
Meghana: Harm reduction is a set of evidence-based interventions that arose within the public health community to reduce the harms associated with risky health behaviors. Most commonly, harm reduction refers to the policies and programs that aim to minimize the negative impacts associated with substance use disorder. The goal is to “meet people where they are” and to provide compassionate, judgment-free interventions and resources to at-risk populations.
Examples of people who are part of the “at-risk population.”
Some examples are injection-drug users and sex workers. With America experiencing the largest substance use and overdose epidemic we have ever faced, it is exceedingly important we provide services such as clean needle exchange, overdose reversal training, safer sex kits, and more to prevent unnecessary injury, disease, and death.
Arreaza: In some countries where prostitution is legal, women are required to have regular check-ups to continue work. I see that as a harm-reduction strategy. I disagree with having sexual workers, but if we are unable to eliminate them, then harm reduction may be the way to go.
Why is harm reduction important in medicine?
Meghana: Healthcare providers have a unique opportunity to improve the quality of life and limit the negative outcomes associated with risky health behaviors by incorporating harm reduction strategies into their practice. Harm reduction interventions not only decrease health risks in an individual but also in the community.
Examples of harm reduction strategies.
Meghana: Studies have shown that areas that have introduced clean needle exchange interventions have lower HIV seroprevalence compared to areas that do not have similar interventions [1]. It is critical as health care providers to respect our patient’s choices and provide supportive care that will not deter patients from accessing care in the future. Patients who engage in risky activities often face stigma and are treated poorly by the medical system making behavioral changes even more difficult [2]. Understanding that many patients may not be willing to change their behaviors and using a practical approach to medical counseling can strengthen physician-patient relationships.
Arreaza: I can think of another example. Pre-exposure prophylaxis for HIV in patients who have multiple sex partners. You wish those patients would have more insight into the risks associated with having multiple sexual partners, but if you cannot change them, you can still reduce the risk.
What is harm reduction in the context of the reproductive health field?
Meghana: Within Harm Reduction programs, there are many important strategies targeted toward improving sexual and reproductive health. Individuals who inject drugs and sex workers have limited access to family planning services and HIV testing. Studies have shown that individuals with substance use disorder have higher rates of unintended pregnancies, pregnancy-related mortality and morbidity, and lower rates of contraceptive use compared to the general population [3,4].
Harm reduction within the reproductive health field must include expanding access to condoms, contraceptive methods, STI and HIV testing, and prenatal care. Reproductive health harm reduction strategies can reduce rates of STIs, HIV, and unintended pregnancies. In addition to expanding access to condoms, STI screening, treatment, and partner therapy must be offered and encouraged to all patients.
Arreaza: As a reminder to our listeners, Expedited Partner Therapy (EPT) consists in treating the partner(s) of a patient with chlamydia or gonorrhea. You, as a physician, treat a patient with STI, but you also give a prescription or medication to that patient, and he/she takes the prescription or medication to his/her partner(s) without me (the doctor) seeing the partner in the clinic or hospital. This is a harm-reduction strategy. It is permissible in 46 states in the US and potentially allowable in Alabama, Kansas, Oklahoma, and South Dakota. It is prohibited in 0 states.
Meghana: Regarding birth control, a recent study by Dr. Frank and Dr. Morrison from the University of Michigan suggests that long-acting reversible contraceptives (LARCs) such as the Intrauterine Device (IUD) or the “Implant” should be offered and easily accessible to women with substance use disorder [5]. In America, around 45% of all pregnancies are unintended, and among women with substance use disorders, this number is doubled [6,7]. More so, women with substance use disorders are 25% less likely to use any form of contraception and are more likely to use less effective methods [5].
Patient autonomy is important.
Meghana: Autonomy is one of the fundamental principles of ethics in medicine, so it is important that all contraceptive decisions are made without any form of coercion. Also, all discussions must take into consideration previous trauma, such as intimate partner violence. Contraceptive counseling should be comprehensive, and patients should be educated on all methods, including emergency contraception and barrier methods. Patients should not be coerced into choosing a LARC simply because they engage in risky health behaviors and should be offered the same methods as the general population [8].
Arreaza: Let’s remember to offer Nexplanon to unhoused patients. On the topic of emergency contraception, you can listen to episode 129. Now, please give us a conclusion.
“If you can't fly then run, if you can't run then walk, if you can't walk then crawl, but whatever you do you have to keep moving forward.”― Martin Luther King Jr.
Meghana: Overall, family physicians are in a unique position to incorporate harm reduction strategies into their practice to improve the quality of life of their patients and to improve health outcomes in their community. Reproductive health harm reduction strategies should be considered and offered to all patients who engage in risky health behaviors. Individuals with substance use disorder and sex workers should be routinely tested for STIs, including HIV and Hepatitis C, as well as offered pregnancy testing and prenatal care if needed. Comprehensive contraceptive counseling, including condom use and emergency contraception, should be discussed with all patients, and conversations should be stigma-free and collaborative. Incorporating reproductive health interventions into already existing harm reduction programs is key to improving the overall health and well-being of our most vulnerable communities.
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Conclusion: Now we conclude episode number 132, “Harm Reduction and Reproductive Health.” Meghana gave us an excellent introduction to the principles of harm reduction in medicine. Applied to reproductive health, we can reduce risk by improving access to condoms, HIV and STI tests, and birth control methods, especially IUD and subdermal implants. Dr. Arreaza also reminded us of strategies such as pre-exposure prophylaxis for HIV (PrEP) and Expedited Partner Therapy for STIs.
This week we thank Hector Arreaza and Meghana Munnangi. 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:
Even without trying, every night you go to bed a little wiser. Thanks for listening to Rio Bravo qWeek Podcast. We want to hear from you, send us an email at [email protected], or visit our website riobravofmrp.org/qweek. See you next week!
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