The Menstrual Cycle

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On today’s episode we welcome Dr. Jay Huber. Jay is a 3rd year fellow in reproductive endocrinology and infertility at the Warren Alpert Brown School of Medicine, and today he demystifies the HPO axis, the menstrual cycle, and all of the hormonal interplay.

It’s always helpful to follow along to one of the “menstrual cycle” diagrams, one of which we include here for reference:

Wikipedia

As Dr. Huber reminds us, the ovary really runs the show due to its negative feedback effect on the hypothalamus. However, thinking top down:

  • GnRH is release from the hypothalamus in a pulsatile fashion, triggering release of FSH and/or LH, depending on the timing of the cycle.

  • In the follicular phase of the ovary, FSH stimulates development of a dominant follicle. Once the dominant follicle is large enough, it produces a high enough level of estrogen to give positive feedback to the hypothalamus. Further GnRH is released, promoting preferential LH release downstream, until an LH surge is triggered, giving us the ovulation event on day 14.

  • After this, the levels of LH and FSH decline in response to negative estrogen feedback, in the luteal phase of the ovary.

  • Simultaneously, the estrogen produced by the dominant follicle in the ovarian follicular phase above causes downstream effects on the endometrium, marking the proliferative phase here of endometrial growth in preparation for implantation.

  • Once the follicle releases the oocyte, the follicular cells become the corpus luteum, which then produces progesterone. Progesterone matures the endometrium to be ‘pro-gestational’ for implantation and the secretory phase of endometrial maturation occurs.

  • If no fertilization event occurs, the corpus luteum degenerates, and by day 23-25, progesterone withdrawal results in shedding of the endometrial lining. If a fertilization event occurs, beta-hCG prompts the corpus luteum to continue to make progesterone.

Further reading from the OBG Project:
Get updates on this and more content, as well as other awesome features for FREE if you’re a PGY-4 — sign up for OBG First!
Managing AUB-O
PCOS: Making the Diagnosis

Vision Changes in Pregnancy

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Today we are joined by Dr. Ben Young. Ben is an ophthalmology resident at Yale New Haven Hospital in Connecticut, and is sharing with us a common complaint that we know very little about - the eye in pregnancy!

Ben also hosts Eyes For Ears, an educational podcast and flashcard reference for ophthalmology residents. If you happen to know any vision sciences students or residents, let them know about it!

We start out talking about the “ocular vital signs,” which are:
- Visual Acuity
- Pupils (“swinging light test”)
- Intraocular pressure
- Visual Fields
- Extra-ocular movements

Image copyright of FOAMCast

The most common reasons for ophthalmology issues in pregnancy relate to either 1) vision changes requiring a new prescription, or 2) dry eye. However, don’t forget some key pearls:

- Monocular (single eye) double vision — dry eye. Binocular (both eye) double vision — badness!
- A Snellen chart and a flashlight are the best tools you have to help out a consultant.
- Check out this video on how to perform a swinging flashlight test.

Further reading from the OBG Project:
Get updates on this and more content, as well as other awesome features for FREE if you’re a PGY-4 — sign up for OBG First!
Is Cataract Surgery in Women Associated with Decreased Mortality?

Herpes Simplex

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Today we get back on track in our STI saga with herpes simplex!

Clinically speaking, the most important thing to remember is the treatment of HSV, which is summed up nicely in the CDC guidelines. That said, we’ve tried to put together a little table for ease of reference here.

In pregnancy, suppressive therapy should be initiated at 36 weeks with one of two regimens: acyclovir 400mg TID or valacyclovir 500mg BID.

We also don’t discuss much about disseminated HSV infection or neonatal HSV infection in today’s podcast. These can be devastating to adults and neonates alike, but we will touch on the neonatal aspect in a future episode on TORCH infections.

Find additional resources at The OBGProject!
- STD Screening in Pregnancy
- Ulcerative Genital Conditions in HIV-positive Patients

Breastfeeding Part I

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Today we start a two part series on breastfeeding with Dr. Erin Cleary, Assistant Professor of Obstetrics and Gynecology and Clinician Educator at the Warren Alpert Brown School of Medicine. She’s also the incoming MFM fellow at the Ohio State University — so look out for her in July, Buckeye listeners!

Also, thank you Dr. Daniel Ginn, our first Patreon sponsor — and apologies for the dad joke with your name!

We start today with a discussion of the anatomy of the breast, and in particular with lactation. At the bottom of this post is a corresponding Netter image to guide your listening.

The physiology of lactation is somewhat confusing, but in bulleted summary:
Lactogenesis I Early in pregnancy, human placental lactogen, prolactin, and chorionic gonadotropin contribute to maturation of the breast tissue to prepare for lactogenesis.

  • In the second trimester, secretory material which resembles colostrum appears in the glands.  A woman who delivers after 16 weeks gestation can be expected to produce colostrum.

  • Differentiated secretory alveolar cells develop at the ends of the mammary ducts under the influence of prolactin.  Progesterone acts to inhibit milk production during pregnancy. This makes sense from a viewpoint of energy expenditure- grow your baby first in utero, then switch to focus on growing it with milk.

Lactogenesis II is the onset of copious milk production at delivery.  In all mammals, it is associated with a drop in progesterone levels; in humans, this occurs during the 1st 4 days postpartum, with “milk coming in” by day 5

  • During the next 10 days, the milk composition changes to mature milk.  Establishing this supply is Lactogenesis III, and is NOT a hormonally-driven process like Lactogenesis I or II. Rather, this is supply/demand-driven with expression of milk

  • When the milk is not removed, the increased pressure lessens capillary blood flow and inhibits the lactation process.  Lack of sucking stimulation means lack of prolactin release from the pituitary.

Next week, we’ll be back again with Dr. Cleary discussing breastfeeding myths and contraindications, so stay tuned!

Netter’s Anatomy. Copyright Elsevier texts.

Menopause Part II: Hormone-Replacement Therapy

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Today we’re talking on menopause once more with Dr. Renee Eger, assistant professor and clinician educator at the Warren Alpert Medical School of Brown University. We spend the second half of our menopause series reviewing HRT and the Women’s Health Initiative (WHI).

You can read more about the WHI here. The study really is two study methodologies in one: there were up to three randomized-controlled trial arms, and an observational arm. The components concerning HRT are dealt with through one of the RCTs.

The RCT dealing with HRT enrolled women into one of three arms: a placebo, an estrogen-only arm in patients without a uterus, or and estrogen-progesterone combination in patients with a uterus. The study was halted at 5.2 years in the E-P arm due to an increase in coronary heart disease, breast cancer, VTE, and stroke, which outweighed a benefit noted in colorectal cancer and fracture risk. The E-alone arm was stopped at 6.8 years average follow up, when the risk of heart disease was found not to be different than placebo.

Subsequent studies, including the Heart and Estrogen/progestin Replacement Study (HERS) have demonstrated at least that E-P and E should not be used for primary or secondary prevention of coronary disease, and thus HRT should not be prescribed for these indications. However, many benefits are particularly pronounced in younger patients using HRT. Thus, the position of the North American Menopause Society (NAMS) reads (emphasis ours):

“For women aged younger than 60 years or who are within 10 years of menopause onset and have no contraindications, the benefit-risk ratio is most favorable for treatment of bothersome VMS and for those at elevated risk for bone loss or fracture.

”For women who initiate HT more than 10 or 20 years from menopause onset or are aged 60 years or older, the benefit-risk ratio appears less favorable because of the greater absolute risks of coronary heart disease, stroke, venous thromboembolism, and dementia.

”Longer durations of therapy should be for documented indications such as persistent VMS or bone loss, with shared decision making and periodic reevaluation. For bothersome GSM symptoms not relieved with over-the-counter therapies and without indications for use of systemic HT, low-dose vaginal estrogen therapy or other therapies are recommended.”

How should you prescribe HRT or other medications to relieve VMS? Below is a summary from ACOG PB 141. Check out CO 565 and CO 556 as well if you are really interested in the topic!