What this document covers:the menstrual and reproductive disorders that don't get their own DiPiro chapter but show up constantly on rotations and on exams: PCOS, dysmenorrhea, endometriosis, PMS/PMDD,and a short module on medication abortion. Contraception, menopausal hormone therapy, and pregnancy/lactation each have their own dedicated document, so this one deliberately stays out of their lane except where a drug (like a combined oral contraceptive or a GnRH agonist) is being borrowed to treat one of these five conditions.
The core problem:almost everything here is a downstream consequence of the hypothalamic-pituitary-ovarian (HPO) axis running too hot, too erratically, or in a tissue that shouldn't have it. PCOS is too much androgen and too little regular ovulation. Dysmenorrhea is a normal cycle producing too much prostaglandin. Endometriosis is normal endometrial tissue growing in the wrong place and still responding to hormones. PMS/PMDD is a normal cycle to which the brain is abnormally sensitive.
What you do about it:almost every drug class you'll reach for either quiets the axis(combined hormonal contraceptives, GnRH agonists/antagonists), corrects the metabolic driver(metformin, GLP-1s), blocks a downstream effector(NSAIDs for prostaglandins, spironolactone for androgen receptors, SSRIs for serotonin sensitivity), or restarts ovulation on purpose(letrozole, clomiphene). Once you sort a patient into one of those four buckets, the drug choice stops being a memorization exercise.
Every condition in this document is either a problem of too much signal(PCOS's excess LH/androgen, endometriosis and dysmenorrhea's excess prostaglandin, PMDD's exaggerated response to normal hormone swings) or tissue in the wrong place(endometriosis). The fix for "too much signal" is almost always to flatten the cycle out, either chemically (continuous combined hormonal contraceptives, GnRH agonists) or by blocking the downstream messenger (NSAIDs, SSRIs, spironolactone). Keep asking "is this drug flattening the axis, or is it blocking one specific effector?" and the whole document organizes itself.
You don't need med-chem-level detail here, just enough physiology to know why timing dosing to "day 3-7" or "day 5" of a cycle actually matters, and why almost every drug in this document either mimics, suppresses, or times itself around this loop.
| Phase | What's happening | Dominant hormone |
|---|---|---|
| Follicular(cycle day 1 to ovulation) | A follicle matures in the ovary; the endometrium proliferates in response | Rising estrogen |
| Ovulation(~day 14 of a 28-day cycle) | LH surge triggers release of the ovum; the ruptured follicle becomes the corpus luteum | LH surge |
| Luteal(ovulation to menses) | Corpus luteum secretes progesterone to sustain the endometrium in case of implantation | Estrogen + progesterone |
| Menses | No implantation, corpus luteum degenerates, hormone support drops, endometrium sheds | Hormone withdrawal |
This is why cycle day numbering shows up everywhere in this document: letrozole and clomiphene are dosed starting cycle day 3-5because that's early follicular phase, before a dominant follicle has been selected, which is when you want to nudge follicle recruitment. PMDD symptoms cluster in the last week of the luteal phasebecause that's when progesterone is falling and estrogen is swinging. Dysmenorrhea starts within hours of mensesbecause that's exactly when the endometrium is releasing its prostaglandin payload.
Clinically, cycle day 1 is defined as the first day of full menstrual flow, not spotting. If a patient can't reliably identify day 1 (irregular cycles, anovulation), you can't time letrozole or clomiphene off it, which is exactly why a combined oral contraceptive is sometimes used first in anovulatory PCOS patients: it creates an artificial, predictable "day 1" via the withdrawal bleed so ovulation induction can actually be timed.
These five conditions share overlapping symptoms (pelvic pain, irregular periods, infertility), which is exactly why exam questions and real patients both get them confused. Pattern-match on the clues below before reaching for a drug.
| Condition | Pain timing | Fertility effect | Diagnostic approach |
|---|---|---|---|
| PCOS | Not primarily painful; hirsutism/acne instead | Anovulatory infertility (no egg released) | Clinical + labs: 2 of 3 Rotterdam criteria |
| Primary dysmenorrhea | Starts withmenses, peaks 24-48h, resolves | None | Clinical, diagnosis of exclusion for "primary" |
| Endometriosis (secondary dysmenorrhea) | Starts beforeor lingers aftermenses, or with intercourse | Mechanical: ectopic tissue on ovaries blocks ovulation | Surgical visualization (laparoscopy); no reliable imaging or lab test |
| PMS | Physical + mild mood symptoms, luteal phase, resolves with menses | None | 2-3 months of symptom diary |
| PMDD | Severe mood symptoms, last 6 days of luteal phase, impairs work/life | None | DSM-5 criteria + symptom diary; rule out thyroid disease, anemia, psychiatric illness |
If cramping pain shows up with no bleeding, starts beforemenses, appears suddenlyin someone with no prior history of cramps, or occurs during sex, think secondary (most often endometriosis). Primary dysmenorrhea is boringly predictable: it starts when the bleeding starts. A patient whose "cramps" show up a week early is not describing primary dysmenorrhea.
The symptom checklist overlaps almost completely. What separates them: PMDD needs ≥5 symptomsincluding at least one core mood symptom (affective lability, irritability/anger, depressed mood, or anxiety), a ≥30% increase in symptom severityin the 5 days before menses versus the 5 days after, and symptoms severe enough to impair work or relationships. PMS affects ~40% of menstruating people; PMDD affects ~5%. If a stem says "mild bloating and irritability that doesn't stop her from going to work," that's PMS. If it says "can't get out of bed and missed two days of work," that's PMDD.
The most common endocrinopathy in premenopausal patients and the leading cause of anovulatory infertility, affecting roughly 10%of the general population (the exact number moves depending on which diagnostic criteria you apply).
Insulin has its own receptors on the ovary. When insulin is chronically elevated (from insulin resistance, which is present in the large majority of PCOS patients regardless of body weight), it acts on those receptors alongside LH to push the ovary toward producing more androgensinstead of completing normal follicular maturation. The result is a self-reinforcing loop: high insulin drives high androgens, high androgens worsen insulin resistance, and normal ovulation gets crowded out.
| Hormone | Direction in PCOS |
|---|---|
| Androgens | ↑ |
| LH | ↑ |
| Insulin | ↑ |
| FSH | ↓ |
| Progesterone | ↓ (from anovulation, no corpus luteum forms) |
| SHBG (sex hormone-binding globulin) | ↓ (insulin suppresses hepatic SHBG production, which raises freeandrogen further) |
Insulin resistance is not part of any diagnostic criteria for PCOS, but it should still be screened for, because it's the lever that moves everything else. Improve insulin sensitivity (weight loss, metformin, a GLP-1) and androgen levels fall andovulation often returns on its own, without ever touching the ovary directly. This is why metformin, a diabetes drug, is a first-line PCOS drug.
PCOS carries a 5- to 10-fold increased risk of type 2 diabetesfrom chronic hyperinsulinemia, plus elevated cardiovascular risk, endometrial cancer risk (from unopposed estrogen when cycles are anovulatory for years at a time), and a real burden of depression and anxiety that needs its own screening, not just the reproductive symptoms.
There isn't one universal PCOS test. The diagnostic debate matters because which criteria you use changes who gets diagnosed.
| Criteria | Hyperandrogenism | Oligo/anovulation | Polycystic ovaries | Rule |
|---|---|---|---|---|
| NIH (1990) | Required | Required | Not required | Need both |
| Rotterdam (2003) | Not all required | Not all required | Not all required | Need 2 of 3(most widely used today) |
| Androgen Excess Society (2008) | Required | Either this or ovaries | Either this or anovulation | Hyperandrogenism plus 1 other |
Other causes of the same picture (thyroid disease, hyperprolactinemia, non-classic congenital adrenal hyperplasia) must be excluded first, since PCOS is ultimately a diagnosis of exclusion layered on top of a clinical pattern.
Before choosing a drug, ask the single most important question in PCOS management: does this patient want to become pregnant right now?The goals (restore cycles, reduce androgens, improve insulin sensitivity, protect the endometrium, address cardiovascular risk, screen for depression/anxiety) are the same either way, but the drug list splits almost completely.
Goal: regulate cycles, lower androgens, protect the endometrium
Goal: induce ovulation
Lifestyle modification and weight loss are first-line for everyone, regardless of track, and GLP-1/GLP-1-GIP agents are now guideline-endorsed for weight loss when appropriate. For hirsutism specifically, non-pharm options (shaving, bleaching, waxing, electrolysis, laser hair removal) are always reasonable to mention alongside drug therapy.
Combined oral contraceptivesare the workhorse: they suppress LH (turning down androgen production at the source), directly suppress ovarian androgen secretion, and raise hepatic SHBG production, which binds up more free testosterone. One drug, three separate mechanisms working the same direction.
Metforminis the insulin-sensitizer of choice: it reduces the risk of progressing to diabetes, lowers LH and androgen levels, and can restore ovulation on its own even when pregnancy isn't the goal, simply because the insulin-driven suppression of ovulation lifts.
Spironolactoneis added specifically for hirsutism, working as an antiandrogen. Dose 50-100 mg BID for 6-12 months, typically starting at 50 mg BID. It's more effective than other antiandrogens for this indication. Watch for polymenorrhea(more frequent periods), which is more common without a CHC on board, an argument for combining the two if hirsutism control alone isn't cutting it. Also watch for hyperkalemia (it's a potassium-sparing diuretic) and mastodynia (breast tenderness).
Letrozole (Femara)is first-line, even though it's an off-label, non-FDA-approveduse (letrozole is FDA-approved as an aromatase inhibitor for breast cancer, not for ovulation induction). Dose: 2.5 mg daily for 5 days, taken on cycle days 3-7, escalating to 5 mg and then a max of 7.5 mg in subsequent cycles if ovulation doesn't occur. A 2018 meta-analysis found letrozole produces higher live birth ratesthan clomiphene, especially in patients with obesity, even though the two drugs achieve similar ovulation rates. The gap between "ovulates" and "has a baby" comes down to endometrium and cervical mucus, see the pearl below.
Clomiphene citrate (Clomid)is second-line and is a SERM (selective estrogen receptor modulator). Dose: 50 mg daily for 5 days, starting cycle day 5. If ovulation doesn't occur, increase by 50 mg increments each cycle to a max of 150 mg/day; doses above 100 mg don't improve pregnancy rates further. It carries FDA approval for ovulation induction, unlike letrozole.
Metformincan be used as monotherapy or as an adjunct to either agent. As monotherapy it restores ovulation in about 46%of patients versus 24% on placebo; combined with clomiphene, ovulation rates climb from 42% to 76%, though this doesn't always translate to more live births. It has no known teratogenicity and does not need to be stopped in the first trimester if a patient conceives while on it.
Clomiphene is an estrogen receptor modulator, and because it sits on receptors throughout the reproductive tract (not just the ovary), it also thins the endometrium and thickens cervical mucus, the same anti-fertility trick progestin-only contraceptives use on purpose. That's counterproductive when the actual goal is conception. This is also why dexamethasoneis sometimes added to clomiphene (100 mg clomiphene days 3-7, dexamethasone 2 mg days 3-12): it thins the mucus back out. Letrozole, with its shorter half-life and different receptor profile, doesn't cause the same endometrial problem, so more of the ovulations it induces actually result in a pregnancy that implants.
Classic trap question. The doseof clomiphene or letrozole is titrated to achieve ovulation, full stop. If a given dose produces ovulation but that cycle doesn't result in pregnancy, repeat the same dosenext cycle rather than escalating. Escalating a dose that's already doing its job just adds side effect risk for no benefit. Clomiphene in particular should not be used for more than 5-6 cycles; many patients simply won't respond, and a plan for a next step should exist before you get there.
Vasomotor symptoms and sleep disturbances are common and expected. Ovarian hyperstimulation syndrome (OHSS)is rare but serious: the ovary overproduces follicles and hormones, causing fever, nausea, vomiting, and in severe cases has caused deaths, patients need to know to seek care if these develop. Both agents raise the rate of multiple gestations(twins/triplets) because more than one follicle can mature and ovulate in the same cycle. A possible small increased ovarian cancer risk has been raised with clomiphene specifically.
The most common gynecologic complaint there is: sharp, intermittent pelvic pain, sometimes radiating to the back or legs, sometimes dragging along fatigue, nausea, vomiting, or diarrhea. Split it into primary (the pain isthe disease) and secondary (the pain is a symptomof something else, most often endometriosis).
During a normal period, the endometrium secretes prostaglandins, which induce myometrial (uterine muscle) contractions, that's the cramp. Pain starts within hours of the onset of bleeding, peaks at 24-48 hours, and it typically shows up within the first three years after menarche. Younger age (especially very early menarche) and possibly genetics both track with more severe symptoms; a full-term pregnancy tends to make it substantially better or resolve it entirely, likely because labor desensitizes the uterus to prostaglandin-driven cramping.
This single mechanistic fact explains the entire first-line drug class. NSAIDs work because they block prostaglandin synthesis at the source. That's also why scheduled dosing beats PRN, and why starting the NSAID beforemenses begins (in a patient who can predict her cycle) works better than waiting for pain to start: you want the prostaglandin synthesis blocked before it ramps up, not chasing pain that's already underway.
A recurring theme across this whole document: taking combined hormonal contraceptives continuously(skipping the placebo week or hormone-free interval) is not just fine, it's often better, for dysmenorrhea, PMDD, and endometriosis alike. The old idea that patients "need" a monthly withdrawal bleed for health reasons has no real evidence behind it. If a withdrawal bleed does happen (extended-cycle regimens still typically break every ~3 months rather than going fully continuous), NSAIDs are still fair game during that window since the prostaglandin-producing endometrium is briefly back.
OTC combination products(Midol, Pamprin, Premasyn) are mostly acetaminophen-based, sometimes with pamabrom (a mild diuretic for bloating), caffeine, and pyrilamine, or built around ibuprofen/naproxen. They're not harmful, but a scheduled, adequately-dosed NSAID alone usually outperforms the multi-ingredient gimmick products, worth knowing when a patient asks which box to grab.
Consider a secondary cause (most commonly endometriosis) if pain occurs before or latein menses, appears suddenlywith no prior history of cramps, occurs during intercourse, or if the patient is infertile. Any of these should prompt looking past "it's just cramps" toward a structural or hormonal cause, covered next.
Endometrial tissue, the same tissue that's supposed to only live inside the uterus, growing outsideof it, most often binding to the ovaries, but also the bladder or the walls of the GI tract. It still responds to the same hormonal cycle as the uterine lining does, which is exactly the problem: it tries to slough and bleed every month just like normal endometrium, except it has nowhere to go.
| Complication | Why it happens |
|---|---|
| Infertility | Tissue binding to the ovaries creates a physical barrier that blocks ovulation |
| GI symptoms (usually constipation) | Tissue on the bowel wall causes local inflammation and impairs motility |
| Menorrhagia and anemia | Ectopic tissue bleeding adds to overall menstrual blood loss |
| Secondary dysmenorrhea | Ectopic tissue still responds to cyclic hormones and still tries to slough, with no outlet |
Ultrasound can't reliably see the ectopic tissue. Diagnosis is a diagnosis of exclusion clinically, confirmed only by surgical (laparoscopic) visualization, and surgeons generally only go looking when the clinical picture (dysmenorrhea pattern, infertility, GI symptoms) is already convincing. This means endometriosis is very plausibly underdiagnosed: nobody's counting the cases that were never confirmed. A patient with a "misdiagnosed ovarian cyst" that turns out to be endometrial implants during surgery is a real and common pattern.
Just like PCOS, the treatment goal splits the drug list. If the goal is pain control, you're suppressing the ectopic tissue's response to hormones. If the goal is fertility, suppressing hormones works againstyou, so different tools are needed.
| Goal | Approach |
|---|---|
| Pain | 1. Levonorgestrel IUD, progestin-only, thins any endometrial tissue regardless of location |
| 2. Continuous combined hormonal contraceptive | |
| 3. GnRH agonist + hormone replacement "add-back" therapy (e.g. leuprolide) | |
| Infertility | GnRH analogs (agonists or antagonists), surgery to excise/ablate implants, IVF |
Continuous GnRH agonist dosing (as opposed to the pulsatile dosing used to stimulatefertility) downregulates pituitary GnRH receptors and shuts off ovarian hormone production almost completely. That deliberately mimics menopause, hot flashes, sweats, headache, the whole picture, because without circulating estrogen, the ectopic tissue has nothing to respond to and pain improves. The problem: real menopause without estrogen support also means real bone loss. That's why a GnRH agonist for endometriosis is paired with low-dose hormone replacement ("add-back") therapy, enough estrogen to protect bone density without enough to reactivate the ectopic tissue. Reach for a GnRH agonist here as a last-lineoption, after IUD and continuous CHC have been tried, specifically because higher-dose contraceptive hormones are a gentler first move.
Don't assume "agonist" and "antagonist" point in opposite clinical directions here. Continuous dosing of eitherclass ultimately shuts down ovarian hormone output; agonists do it by receptor downregulation after an initial flare, antagonists do it by direct receptor blockade without a flare. For endometriosis, the end result you're counseling on, menopausal symptoms and the need for bone protection, is the same either way.
Premenstrual syndrome (PMS)is the cyclic appearance of one or more physical or mood symptoms in the days before menses, followed by a symptom-free stretch. Premenstrual dysphoric disorder (PMDD)is the same basic phenomenon turned up to a degree that actually disrupts work or relationships, beginning in the last week of the luteal phase and resolving once menses starts. PMS affects roughly 40%of menstruating people; PMDD is far less common at roughly 5%.
| Category | Symptoms |
|---|---|
| Physical | Breast tenderness, abdominal bloating, headache, swollen extremities, fatigue, acne, food cravings/increased appetite |
| Mood/cognitive | Oversensitivity, crying easily, poor concentration, forgetfulness, depression, angry outbursts, anxiety |
Requires at least 5 symptomsin the week before menses, including at least one of: affective lability (mood swings), marked anger/irritability/increased conflict, depressed mood or hopelessness, or anxiety/tension/feeling on edge. The remaining symptoms needed to reach five come from: decreased interest in usual activities, difficulty concentrating, low energy, appetite change, hypersomnia or insomnia, feeling out of control, or physical symptoms. Two more diagnostic anchors: symptom severity must increase by at least 30%in the 5 days before menses compared to the 5 days after, and the picture must not be an exacerbation of an existing psychiatric condition.
Diagnosis of either condition leans on a 2-3 month symptom diary, not a single-visit snapshot, precisely because the defining feature is the cyclic pattern itself. Symptoms tend to worsen with increasing age and parity, remit during pregnancy and after menopause (both hormonally stable states), and thyroid disorders, anemia, and psychiatric illness all need to be ruled out before landing on the diagnosis.
Not fully understood, but theories converge on hormonal shifts in the luteal phase: low progesterone, high or rapidly falling estrogen, changes in the estrogen-to-progesterone ratio, endogenous endorphin withdrawal, excess prolactin, prostaglandin effects, and increased aldosterone activity. Genetics may also play a role.
| Line | Options |
|---|---|
| 1st | Lifestyle changes: regular exercise, relaxation techniques, stress management, good support system |
| 2nd | SSRIs, combined hormonal contraceptives (continuous), alprazolam for prominent anxiety |
| Last | GnRH agonists |
Dietary changes and high-dose vitamin B6 are commonly tried but lack proven efficacy, worth knowing so you don't oversell them.
The best data is with sertraline and fluoxetine, though other SSRIs and some other antidepressants (moderate efficacy with venlafaxine and clomipramine, less with bupropion and amitriptyline) have been tried. The counterintuitive counseling point: unlike major depression, where patients are warned it takes 6 weeksto see benefit, SSRIs for PMDD start working almost immediately, sometimes within days. That's why luteal-phase-only dosinghas been studied and shown effective, taking the SSRI only during the roughly two weeks before menses. In practice, continuous daily dosing is often used anyway because dosing on-and-off invites adherence problems.
If a combined hormonal contraceptive is used for PMDD, it must be dosed continuously, since it's the swings and drops in hormone levels that drive symptoms, and a traditional placebo week reintroduces exactly that swing. Counsel patients that hormonal therapy can occasionally worsenmood symptoms rather than help, since hormones themselves may be part of the underlying trigger; if symptoms get worse after starting, that's a signal to reassess, not push through.
Most common example: leuprolide. Very effective for the behavioral and physical symptom cluster, notably less effective for the psychiatric symptoms specifically, so an SSRI is often continued alongside it. As with endometriosis, expect it to mimic menopause and to require bone density monitoring with long-term use.
| Symptom | Approach |
|---|---|
| Bloating/edema | Salt restriction; spironolactone 25 mg up to TID for 10 days prior to menses (~60% effective for bloating) |
| Hyperprolactinemia-related breast pain | Bromocriptine 0.5-2.5 mg daily, titrated every 2-7 days to a range of 2.5-15 mg daily |
| Insomnia | Sleep hygiene first; low-dose trazodone or intermittent diphenhydramine |
| Anxiety | Alprazolam, or buspirone dosed continuously or luteal-phase-only |
| Dysmenorrhea overlap | Treat as primary dysmenorrhea (NSAIDs, heat) |
Elevated prolactin suppresses the HPG axis and can independently cause menstrual disruption and infertility on its own, separate from PMDD, this is why hyperprolactinemia has to be ruled out during PMDD workup rather than assumed. Bromocriptine, a dopamine agonist, directly lowers prolactin and restores normal cycling in roughly 80%of hyperprolactinemic patients treated with it, which is why it shows up both as a PMDD symptom-control option and as a standalone fertility treatment when hyperprolactinemia is the actual root cause.
Increasingly a space where pharmacists are directly involved, both clinically and in navigating a fast-shifting legal landscape. This section covers the pharmacology; the legal landscape is state-specific and changes fast, treat any specific legal claim as needing current verification rather than something to memorize as fixed.
Mifepristoneis an antiprogestin. Pregnancy depends heavily on high progesterone output from the corpus luteum through about the 7th week of gestation; mifepristone blocks that support, causing endometrial changes and increasing the tissue's sensitivity to prostaglandins. Misoprostolis an exogenous prostaglandin that then drives the uterine contractions and cervical softening needed to complete the process. Used together, they target two different, complementary steps.
| Day | What happens |
|---|---|
| Day 1 | Mifepristone 200 mg PO x1 |
| 24-48 hours later | Misoprostol 800 mcg buccally (route also may be sublingual or intravaginal depending on guideline) |
| 7-14 days later | Follow-up to confirm completion |
Eligibility: pregnancy must be under 70 days' gestationper the package insert (some guidelines extend to 77 days / 11 weeks). Misoprostol-only regimens exist and are used when mifepristone access isn't available, though they're less effective than the combination. Methotrexate plus misoprostol was used before mifepristone's approval and is now essentially reserved for ectopic pregnancy management as a single agent.
Black box warning:heavy bleeding can signal an incomplete abortion or infection and needs prompt evaluation. Expected bleeding/spotting can last up to 30 days (average 9-13 days); uterine cramping is expected, especially after misoprostol, along with prostaglandin effects like nausea, dizziness, and diarrhea. Contraindications:an IUD currently in place, chronic steroid therapy or adrenal insufficiency, ectopic pregnancy, a hemorrhagic disorder or current anticoagulant therapy, and inherited porphyrias.
Mifepristone was FDA-approved in 2000 under a REMS (Risk Evaluation and Mitigation Strategy) program that originally required in-person dispensing by a specially certified prescriber. That requirement was lifted permanently in December 2021, and by 2023 the REMS was updated to allow qualified pharmaciesto dispense it directly (after completing a pharmacy agreement form) without an in-person visit, alongside continued use of a signed patient agreement form. Dispensing right now is opt-in, meaning relatively few pharmacies actually stock and dispense it, not that it's broadly unavailable by law.
Emergency contraception (levonorgestrel or ulipristal) is notthe same as medication abortion, and neither one causes birth defects or works by disrupting an existing pregnancy; EC works by delaying or preventing ovulation, before fertilization has even occurred. A 2012 survey of Florida pharmacists found 56%believed EC caused birth defects and 46%believed it caused abortion, both false. This misunderstanding has directly driven real-world pharmacist refusals to dispense EC, so it's worth being precise about the distinction when counseling colleagues, not just patients.
One more product-identity trap: Korlymis also mifepristone 300 mg tablets, but it's approved for hyperglycemia in Cushing syndrome, notfor medication abortion, and carries its own handling requirements and different interactions/contraindications. Don't assume "mifepristone" always means the same product or the same indication.
| PCOS - hirsutism / androgen control | ||
| Spironolactone | 50 mg BID | 100 mg BID, continue 6-12 months symptom control |
| PCOS - ovulation induction | ||
| Letrozole (1st line) | 2.5 mg daily x5 days, cycle days 3-7 | Increase to 5, then max 7.5 mg daily if no ovulation |
| Clomiphene (2nd line) | 50 mg daily x5 days, starting cycle day 5 | Increase by 50 mg increments to max 150 mg/day; >100 mg adds no benefit |
| Metformin (adjunct/monotherapy) | Titrate per standard diabetes dosing | No first-trimester teratogenicity; safe to continue if pregnancy occurs |
| Dysmenorrhea | ||
| Ibuprofen | 400 mg minimum, every 6-8 hours, scheduled not PRN 80-100% effective | |
| Combined hormonal contraceptive | Standard contraceptive dosing, can combine with NSAID ~90% effective | |
| Endometriosis | ||
| Levonorgestrel IUD | Standard placement, first-line for pain | |
| Leuprolide (GnRH agonist) + add-back HT | Last-line for pain; add-back protects bone density mimics menopause | |
| PMS / PMDD | ||
| Sertraline / fluoxetine (SSRI) | Continuous or luteal-phase-only dosing; effective almost immediately, not 6 weeks | |
| Spironolactone (bloating) | 25 mg up to TID x10 days prior to menses | |
| Bromocriptine (hyperprolactinemia) | 0.5-2.5 mg daily | Titrate q2-7 days, range 2.5-15 mg daily |
| Alprazolam (anxiety) | 2nd line, prominent anxiety symptoms | |
| Medication abortion | ||
| Mifepristone | 200 mg PO x1, Day 1 | <70 days gestation per label |
| Misoprostol | 800 mcg buccal, 24-48h after mifepristone | Follow-up 7-14 days later |
| Parameter | When | Watching for |
|---|---|---|
| Insulin sensitivity / A1C | At PCOS diagnosis and periodically | Progression toward diabetes (5-10x baseline risk) |
| Ovulation (basal temp, LH kits, or clinical response) | Each cycle on letrozole/clomiphene | Confirming the current dose is working before deciding whether to escalate |
| Potassium | Periodically on spironolactone (PCOS or PMDD dosing) | Hyperkalemia |
| Menstrual/symptom diary | 2-3 months, ongoing for PMS/PMDD | Confirming the cyclic pattern that defines the diagnosis, and treatment response |
| Mood symptoms on hormonal therapy | Each visit, PMDD patients specifically | Paradoxical worsening, a signal to reassess rather than push through |
| Bone mineral density | Baseline and periodically with long-term GnRH agonist use | Bone loss from the induced hypoestrogenic state |
| Bleeding pattern / signs of infection | 7-14 days post medication abortion | Incomplete abortion, ongoing pregnancy, infection (black box: heavy bleeding) |
| Depression/anxiety screening | PCOS diagnosis and ongoing | High comorbidity burden that's easy to overlook amid the reproductive symptoms |