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Summary Table

Feature	Detail
Risk Factors	Age over 35, obesity, underweight/excessive exercise, PCOS, endometriosis, pelvic inflammatory disease history, prior pelvic or tubal surgery, smoking, thyroid disorders, hyperprolactinemia
Etiology	Ovulatory dysfunction (most common, approximately 40%), tubal and peritoneal factors (approximately 30%), uterine abnormalities, unexplained (approximately 10 to 15%), cervical factors (rare)
Patient Presentation	Inability to conceive after 12 months of regular unprotected intercourse (or 6 months if age 35 or older). May report irregular or absent menses, dysmenorrhea, dyspareunia, or galactorrhea depending on the underlying cause
Classic Physical Exam	Findings depend on etiology: hirsutism and acanthosis nigricans (PCOS), galactorrhea (hyperprolactinemia), thyroid enlargement, BMI extremes, fixed retroverted uterus or adnexal tenderness (endometriosis), visual field defects (pituitary lesion)
Key Diagnostic Results	Day 21 progesterone to confirm ovulation, FSH and estradiol on cycle day 3 for ovarian reserve, hysterosalpingography (HSG) for tubal patency, semen analysis for male factor (should be obtained early), TSH and prolactin as baseline hormonal screen
Management	Ovulatory dysfunction: letrozole or clomiphene citrate for ovulation induction. Tubal factor: IVF. Endometriosis-related: surgical ablation followed by ovulation induction or IVF. Hyperprolactinemia: cabergoline. Unexplained: empiric clomiphene plus intrauterine insemination (IUI), then IVF
Keywords	"Irregular periods and inability to conceive," "day 21 progesterone," "cycle day 3 FSH," "HSG showing tubal occlusion," "oligo-ovulation," "anovulatory cycles"

1. Pathophysiology

Female infertility results from disruption at any point along the reproductive axis: the hypothalamus, pituitary, ovary, fallopian tube, uterus, or cervix. The key to understanding the pathophysiology is recognizing which level of the axis is affected, because the diagnostic workup and treatment differ accordingly.

Ovulatory dysfunction is the single most commonly tested category. Normal ovulation requires pulsatile GnRH secretion from the hypothalamus, which drives FSH and LH release from the anterior pituitary. FSH stimulates follicular development, and the mid-cycle LH surge triggers ovulation. Any process that disrupts this cascade leads to anovulation or oligo-ovulation. The WHO classifies ovulatory disorders into three groups:

WHO Group I (hypogonadotropic hypogonadism) results from inadequate hypothalamic or pituitary stimulation. Both FSH and estradiol are low. The classic scenario is functional hypothalamic amenorrhea, seen in women with excessive exercise, low body weight, or chronic stress. The hypothalamus reduces GnRH pulsatility, and the entire downstream axis shuts down. These patients present with amenorrhea and estrogen deficiency (no withdrawal bleed after progesterone challenge).

WHO Group II (normogonadotropic, eugonadal anovulation) is the most common group and is overwhelmingly represented by polycystic ovary syndrome (PCOS). In PCOS, excess ovarian androgen production and insulin resistance disrupt follicular maturation. Multiple small follicles accumulate but none reach dominance, resulting in chronic anovulation. FSH is normal to low, LH is often disproportionately elevated (LH:FSH ratio greater than 2:1), and androgens are elevated. These patients typically have irregular menses, hirsutism, and acne.

WHO Group III (hypergonadotropic hypogonadism) indicates ovarian failure. The ovaries no longer respond to gonadotropin stimulation, so FSH rises markedly via loss of negative feedback. This is seen in premature ovarian insufficiency (previously called premature ovarian failure) in women under 40. Causes include Turner syndrome mosaicism (45,X), autoimmune oophoritis, prior chemotherapy or radiation, and FMR1 premutations (fragile X carrier status). Estradiol is low and FSH is elevated above 40 mIU/mL on two occasions at least one month apart.

Tubal and peritoneal factors account for approximately 30% of cases. The most common cause is pelvic inflammatory disease (PID), particularly from Chlamydia trachomatis, which causes tubal scarring and adhesion formation. Each episode of PID roughly doubles the risk of tubal infertility. Endometriosis can also cause peritoneal adhesions and distort tubal anatomy. The fallopian tube is not merely a conduit; it provides the microenvironment for fertilization and early embryo transport. Damage to the tubal epithelium or obstruction prevents sperm-oocyte interaction.

Uterine factors are less common but important. Submucosal leiomyomas distort the endometrial cavity and impair implantation. Asherman syndrome (intrauterine adhesions), typically following aggressive curettage, destroys the endometrium and causes amenorrhea with cyclic pelvic pain. Mullerian anomalies such as a uterine septum increase the risk of recurrent pregnancy loss rather than primary infertility, but a septate uterus is the most common anomaly associated with adverse reproductive outcomes.

Cervical factors are rarely the sole cause but can contribute. Inadequate or hostile cervical mucus, prior cervical procedures (cone biopsy, LEEP), or cervical stenosis can impair sperm transit.

A point that exam questions emphasize: male factor contributes to approximately 40% of infertile couples, so a semen analysis must be obtained early in the evaluation, not after an exhaustive female workup.

2. Classification and Clinical Manifestation

WHO Classification of Ovulatory Disorders

Group	Mechanism	FSH	Estradiol	LH	Clinical Features	Classic Example
I	Hypogonadotropic hypogonadism	Low	Low	Low	Amenorrhea, no withdrawal bleed to progesterone, estrogen-deficient symptoms	Hypothalamic amenorrhea (athlete triad), Kallmann syndrome, Sheehan syndrome
II	Normogonadotropic anovulation	Normal to low	Normal	Normal to high (LH:FSH ratio often elevated)	Oligomenorrhea, hirsutism, acne, obesity, acanthosis nigricans	PCOS (most common cause of anovulatory infertility)
III	Hypergonadotropic hypogonadism	High (>40)	Low	High	Amenorrhea, vasomotor symptoms, vaginal dryness	Premature ovarian insufficiency, Turner syndrome

Classification by Anatomic and Functional Etiology

Category	Proportion	Key Presentations	Distinguishing Feature
Ovulatory dysfunction	~40%	Irregular or absent menses, anovulatory bleeding pattern	Abnormal menstrual history is the hallmark
Tubal/peritoneal	~30%	Often asymptomatic; history of PID, ectopic pregnancy, pelvic surgery, or endometriosis	Regular menses with confirmed ovulation but failure to conceive
Uterine	~10%	Abnormal uterine bleeding, cyclic pain with amenorrhea (Asherman), palpable fibroids	Abnormal cavity on imaging
Unexplained	~10 to 15%	All standard testing normal in both partners	Diagnosis of exclusion
Cervical	Rare	History of cervical surgery, absent or scant postcoital mucus	Diagnosis largely historical (postcoital test no longer recommended)
Male factor	~40% (overlap)	Normal female evaluation	Abnormal semen analysis

Endometriosis-Related Infertility (Revised ASRM Staging)

Stage	Description	Fertility Implication
I (Minimal)	Isolated implants, no adhesions	Mild reduction in fecundity; mechanism debated (inflammatory peritoneal environment)
II (Mild)	Superficial implants less than 5 cm total, no adhesions	Similar to stage I
III (Moderate)	Deep implants, small endometriomas, filmy adhesions	Tubal and ovarian distortion begins to impair oocyte pickup
IV (Severe)	Large endometriomas, dense adhesions, cul-de-sac obliteration	Anatomic distortion; IVF often required

3. Diagnostic Workup

Test	Purpose	Timing	Key Findings
Semen analysis	Rule out male factor	Early in evaluation (first or second visit)	Volume greater than 1.5 mL, concentration greater than 15 million/mL, motility greater than 40%, normal morphology greater than 4% (WHO 2010 criteria)
Mid-luteal progesterone (day 21)	Confirm ovulation	Day 21 of a 28-day cycle (7 days before expected menses)	Greater than 3 ng/mL confirms ovulation
Cycle day 3 FSH and estradiol	Assess ovarian reserve	Day 2 to 4 of menstrual cycle	FSH greater than 10 mIU/mL or estradiol greater than 80 pg/mL suggests diminished ovarian reserve
Anti-Mullerian hormone (AMH)	Assess ovarian reserve (cycle-independent)	Any day of cycle	Low AMH (less than 1.0 ng/mL) suggests diminished reserve
TSH	Screen for thyroid dysfunction	Baseline	Both hypo- and hyperthyroidism cause anovulation
Prolactin	Screen for hyperprolactinemia	Baseline	Elevated prolactin suppresses GnRH pulsatility
Hysterosalpingography (HSG)	Assess tubal patency and uterine cavity	Follicular phase (day 6 to 12), after menses stop	Contrast fills and spills bilaterally (normal); filling defect or obstruction (abnormal)
Transvaginal ultrasound	Evaluate ovarian morphology and uterine anatomy	Baseline and serial for follicular monitoring	Polycystic ovarian morphology, endometriomas, fibroids, antral follicle count
Sonohysterography (SIS)	Evaluate intrauterine pathology	Follicular phase	Superior to HSG for detecting submucosal fibroids, polyps, and adhesions
Laparoscopy	Evaluate peritoneal disease (endometriosis, adhesions)	When indicated	Gold standard for diagnosing endometriosis; allows concurrent treatment
Hysteroscopy	Evaluate and treat intrauterine pathology	When indicated	Gold standard for intrauterine adhesions, polyps, submucosal fibroids

The evaluation of an infertile couple should begin simultaneously in both partners. Exam questions commonly test whether you obtain a semen analysis early rather than putting the male partner through testing only after the female workup is complete. A semen analysis is inexpensive, noninvasive, and rules out a contributing factor in nearly half of cases. This is a frequently tested "next best step."

Confirming ovulation is the first priority in the female workup. The best initial test is a mid-luteal serum progesterone, drawn approximately 7 days before expected menses (day 21 in a 28-day cycle, day 28 in a 35-day cycle). A level greater than 3 ng/mL confirms that ovulation occurred. This is the single most tested lab value in infertility vignettes. An alternative is serial transvaginal ultrasound showing follicular development and collapse, but this is more resource-intensive and typically reserved for monitored cycles. Urinary LH kits (ovulation predictor kits) detect the LH surge but do not confirm that ovulation actually followed, making them less reliable for clinical confirmation.

Ovarian reserve testing determines how the ovaries will respond to stimulation and helps guide prognosis. The two most commonly tested markers are cycle day 3 FSH (with concurrent estradiol) and AMH. An FSH above 10 mIU/mL on day 3 indicates diminished reserve. However, a normal FSH does not guarantee adequate reserve if estradiol is simultaneously elevated above 80 pg/mL, because high estradiol can suppress FSH through negative feedback, masking true ovarian depletion. This is a classic exam trap. AMH is increasingly favored because it can be drawn on any cycle day and correlates well with antral follicle count. Antral follicle count on ultrasound (counting follicles 2 to 10 mm on days 2 to 4) is another reliable reserve marker.

Hormonal screening with TSH and prolactin should be performed at baseline. Hypothyroidism causes anovulation through elevated TRH, which stimulates prolactin release. Hyperprolactinemia from any cause (prolactinoma, medications, hypothyroidism) suppresses GnRH pulsatility and causes anovulation, often with galactorrhea and amenorrhea. If prolactin is elevated, obtain a pituitary MRI to rule out a prolactinoma.

Tubal patency assessment is performed via hysterosalpingography (HSG), which is the best initial test for tubal evaluation. HSG involves injecting radiopaque contrast through the cervix and obtaining fluoroscopic images. Normal findings show contrast filling the uterine cavity and bilateral free spillage from the fimbriated ends. HSG also has a mild therapeutic benefit: the flushing of oil-based contrast through the tubes modestly increases pregnancy rates in the 6 months following the procedure. Limitations of HSG include a false-positive rate for proximal tubal occlusion (tubal spasm can mimic obstruction) and inability to diagnose peritoneal disease. If HSG is abnormal or if there is strong clinical suspicion for endometriosis or adhesions, laparoscopy with chromopertubation is the gold standard for definitive tubal and peritoneal assessment.

Uterine cavity evaluation is best performed with sonohysterography (saline infusion sonography) or hysteroscopy. HSG provides some uterine cavity information but is inferior to these modalities for detecting submucosal fibroids, polyps, and adhesions. Hysteroscopy is the gold standard because it allows direct visualization and simultaneous treatment.

The workup sequence a test-writer expects you to follow:

History and physical in both partners
Semen analysis (male factor)
Confirm ovulation (day 21 progesterone)
Ovarian reserve (day 3 FSH/estradiol, AMH)
Tubal patency (HSG)
Uterine cavity evaluation if indicated
Laparoscopy only when noninvasive testing is inconclusive and clinical suspicion for peritoneal disease is high

4. Management and Treatment

Etiology	First-Line Treatment	Second-Line / Escalation	Key Details
Anovulation (PCOS / WHO Group II)	Letrozole 2.5 to 7.5 mg daily on cycle days 3 to 7	Clomiphene citrate 50 to 150 mg on cycle days 5 to 9; gonadotropins (FSH injections) if oral agents fail	Letrozole now preferred over clomiphene for PCOS per current guidelines; add metformin if insulin resistant
Hypothalamic amenorrhea (WHO Group I)	Address underlying cause (weight gain, reduce exercise); pulsatile GnRH or gonadotropin therapy (FSH/LH injections)	IVF if unresponsive	Clomiphene is ineffective here because it requires intact hypothalamic-pituitary axis with endogenous estrogen
Premature ovarian insufficiency (WHO Group III)	Donor oocyte IVF	No ovulation induction will work with depleted follicle pool	Hormone replacement therapy for bone and cardiovascular protection; spontaneous pregnancy rare (5 to 10%)
Hyperprolactinemia	Cabergoline 0.25 to 1 mg twice weekly	Bromocriptine 2.5 mg two to three times daily (if cabergoline unavailable)	Cabergoline preferred due to better efficacy and fewer side effects; surgery for macroadenomas unresponsive to medical therapy
Tubal factor	IVF (bypasses the tubes entirely)	Tubal microsurgery if mild disease and patient prefers; salpingectomy before IVF if hydrosalpinx present	Hydrosalpinx must be removed or occluded before IVF (embryotoxic fluid reduces implantation rates)
Endometriosis	Laparoscopic ablation/excision of implants, then ovulation induction or timed intercourse	IVF for moderate to severe disease or failed surgical management	Medical suppression (GnRH agonists, OCPs) does NOT improve fertility and delays conception
Uterine factors	Hysteroscopic resection (submucosal fibroids, polyps, septum, adhesions)	IVF with gestational carrier if uncorrectable uterine factor	Intramural fibroids greater than 4 cm distorting the cavity should be resected
Unexplained infertility	Clomiphene or letrozole plus IUI for 3 to 4 cycles	IVF	Empiric treatment attempts to increase the number of oocytes (ovulation induction) and bring sperm closer to the egg (IUI)

Ovulation induction is the cornerstone of treating anovulatory infertility. For PCOS (WHO Group II), letrozole has replaced clomiphene as the preferred first-line agent based on the landmark NICHD trial, which demonstrated higher live birth rates and lower multiple pregnancy rates with letrozole compared to clomiphene. Letrozole is an aromatase inhibitor that reduces peripheral estrogen conversion, thereby releasing the hypothalamus from negative feedback and increasing endogenous FSH secretion. It is dosed at 2.5 mg daily starting on cycle day 3 through day 7, with dose escalation up to 7.5 mg if no ovulatory response. Clomiphene citrate, a selective estrogen receptor modulator, remains an acceptable alternative. It is dosed at 50 mg daily on cycle days 5 to 9, increasing by 50 mg increments per cycle up to a maximum of 150 mg. Clomiphene works by blocking estrogen receptors at the hypothalamus, which reduces negative feedback and increases FSH release. A critical point: clomiphene has antiestrogenic effects on the endometrium and cervical mucus, which is why it can paradoxically decrease implantation rates despite successful ovulation. This is one reason letrozole is now favored.

For patients with PCOS and insulin resistance, metformin (1500 to 2000 mg daily) can be added as an adjunct to improve ovulatory response, though it is not effective as monotherapy for fertility.

If oral agents fail after 3 to 6 cycles, the next step is gonadotropin therapy with injectable FSH (e.g., recombinant FSH at 75 to 150 IU daily with dose titration based on ultrasound follicular monitoring). Gonadotropin therapy carries a higher risk of ovarian hyperstimulation syndrome (OHSS) and multiple gestations, requiring close monitoring with serial ultrasound and estradiol levels. OHSS is characterized by ovarian enlargement, ascites, pleural effusion, hemoconcentration, and in severe cases, thromboembolic events.

For WHO Group I (hypothalamic amenorrhea), addressing the underlying cause is paramount: weight restoration in underweight patients, reducing excessive exercise, and managing stress. Pharmacologically, pulsatile GnRH therapy is the physiologically ideal treatment because it restores the normal hypothalamic signal. When pulsatile GnRH is unavailable, exogenous gonadotropins (combined FSH and LH) are used. Clomiphene does not work in these patients because it requires an intact hypothalamic-pituitary-ovarian axis with baseline estrogen activity, which is absent in Group I.

For WHO Group III (premature ovarian insufficiency), the follicle pool is depleted or nonfunctional. No amount of gonadotropin stimulation will produce viable oocytes. The only realistic path to pregnancy is donor oocyte IVF. These patients should also receive hormone replacement therapy (estrogen plus progesterone) for long-term bone, cardiovascular, and vasomotor symptom management.

For hyperprolactinemia, cabergoline is the treatment of choice. It is a dopamine agonist that directly suppresses prolactin secretion from the anterior pituitary. Dosing begins at 0.25 mg twice weekly and is titrated based on prolactin levels. Cabergoline is preferred over bromocriptine because of superior efficacy, longer half-life, and fewer gastrointestinal side effects. Prolactin normalization restores GnRH pulsatility and ovulatory function in most patients. For macroadenomas (greater than 10 mm), MRI monitoring is needed, and surgical resection (transsphenoidal approach) is reserved for tumors unresponsive to medical therapy or causing compressive symptoms.

For tubal factor infertility, IVF is the treatment of choice because it bypasses the tubes entirely. A critical exam point: if a hydrosalpinx is present, it must be removed (salpingectomy) or proximally occluded before IVF. Hydrosalpinx fluid is embryotoxic and leaks into the uterine cavity, reducing IVF implantation rates by approximately 50%. This "salpingectomy before IVF" principle is heavily tested.

For endometriosis-related infertility, laparoscopic ablation or excision of endometriotic implants improves natural fecundity in mild to moderate disease. After surgery, patients proceed with ovulation induction and timed intercourse or IUI. For severe disease (stage III to IV), IVF is typically necessary. An important point: medical suppression of endometriosis (with GnRH agonists, progestins, or combined oral contraceptives) does not improve fertility and actually delays conception by preventing ovulation during treatment. This is a frequent distractor on exams.

For uterine factors, hysteroscopic surgery is both diagnostic and therapeutic. Submucosal fibroids, endometrial polyps, uterine septa, and intrauterine adhesions (Asherman syndrome) are all amenable to hysteroscopic resection. For Asherman syndrome, lysis of adhesions is followed by placement of an intrauterine balloon or IUD and estrogen supplementation to promote endometrial regrowth.

For unexplained infertility, the empiric approach is superovulation plus IUI for 3 to 4 cycles, using either clomiphene or letrozole to produce 2 to 3 mature follicles while IUI places washed sperm directly into the uterine cavity. If this fails, IVF is the next step.

5. Differential Diagnosis and Distractors

Differential Diagnosis	Why It Is Similar	Key Discriminator
PCOS vs. hypothyroidism	Both cause oligomenorrhea and anovulation	PCOS: hyperandrogenism (hirsutism, acne, elevated testosterone), normal TSH. Hypothyroidism: fatigue, cold intolerance, weight gain, elevated TSH without hyperandrogenic features
PCOS vs. congenital adrenal hyperplasia (late-onset)	Both cause hyperandrogenism and irregular menses	Late-onset CAH: elevated 17-hydroxyprogesterone (greater than 200 ng/dL baseline, exaggerated response to ACTH stimulation). PCOS: normal 17-OHP
PCOS vs. Cushing syndrome	Both cause obesity, hirsutism, menstrual irregularity	Cushing: central obesity with striae, proximal muscle weakness, hypertension, elevated 24-hour urinary free cortisol or failed dexamethasone suppression
Premature ovarian insufficiency vs. menopause	Both show elevated FSH and low estradiol	Age is the discriminator: POI occurs before age 40. Menopausal symptoms in a woman under 40 should prompt karyotype (Turner mosaicism) and FMR1 premutation testing
Hypothalamic amenorrhea vs. premature ovarian insufficiency	Both present with amenorrhea and estrogen deficiency	FSH is the key: low in hypothalamic amenorrhea (WHO Group I) vs. elevated above 40 in POI (WHO Group III). This is one of the most commonly tested distinctions
Tubal factor vs. unexplained infertility	Both present with regular ovulatory cycles and failure to conceive	HSG showing bilateral tubal occlusion or hydrosalpinx confirms tubal factor. Normal HSG with normal semen analysis and confirmed ovulation points to unexplained infertility
Asherman syndrome vs. cervical stenosis	Both can cause amenorrhea after uterine instrumentation	Asherman: amenorrhea with cyclic pelvic pain (functional endometrium trapped behind adhesions), failed withdrawal bleed to estrogen-progesterone. Cervical stenosis: hematometra on ultrasound, relieved by cervical dilation
Endometriosis vs. PID	Both cause pelvic pain and may lead to tubal infertility	PID: acute onset, fever, cervical motion tenderness, mucopurulent discharge, elevated WBC/ESR. Endometriosis: chronic cyclic pain, dysmenorrhea, dyspareunia, no infectious signs
Hyperprolactinemia (prolactinoma) vs. medication-induced hyperprolactinemia	Both show elevated prolactin with amenorrhea and galactorrhea	Medication history is the key: antipsychotics, metoclopramide, and SSRIs all raise prolactin. If prolactin is greater than 200 ng/mL, a prolactinoma is overwhelmingly likely regardless of medication use

6. Traps and High-Yield Pearls

The most common way students lose points on infertility questions is by failing to order a semen analysis early. When presented with a couple unable to conceive, many test-takers default to an extensive female-only workup. The exam consistently rewards the answer that includes male evaluation in the initial assessment, because male factor is present in nearly 40% of cases and a semen analysis is low-cost and noninvasive.

A second major trap involves ovarian reserve interpretation. Students correctly identify an elevated day 3 FSH as a marker of diminished reserve but fail to check the concurrent estradiol. If estradiol is elevated above 80 pg/mL on the same day 3 draw, the "normal" FSH is being artificially suppressed and should not be trusted. The exam tests whether you recognize this false reassurance.

Another frequently tested concept is the distinction between WHO Group I and Group III anovulation based on the FSH level. Both present with amenorrhea and low estrogen, but the FSH tells you whether the problem is central (low FSH, the brain is not sending the signal) or peripheral (high FSH, the ovary is not responding). This single lab value determines the entire treatment strategy: gonadotropins or pulsatile GnRH for Group I versus donor oocyte IVF for Group III. Students who memorize treatments without understanding this physiologic framework will select the wrong therapy.

Clomiphene in hypothalamic amenorrhea is a deliberate distractor. Because clomiphene is a "first-line ovulation induction agent," students reflexively choose it for any anovulatory patient. However, clomiphene requires intact hypothalamic-pituitary signaling and baseline estrogen activity to work. In WHO Group I, both are absent, and clomiphene will fail.

For tubal factor, the trap is proceeding directly to IVF when a hydrosalpinx is present. The correct next step is salpingectomy first, then IVF. Hydrosalpinx fluid is embryotoxic and dramatically reduces implantation. Skipping this step is a commonly tested error.

Finally, students often incorrectly select medical suppression (GnRH agonists, oral contraceptives) as treatment for endometriosis-related infertility. While these medications reduce endometriotic implants and relieve pain, they suppress ovulation and therefore directly prevent conception during treatment. They have no role in the management of infertility due to endometriosis. The correct approach is surgical ablation followed by ovulation induction or IVF.

The core competencies being tested in infertility questions are: systematic evaluation of both partners, correct interpretation of hormonal levels to localize the defect, appropriate test sequencing (noninvasive before invasive), and matching the treatment to the underlying etiology rather than applying a one-size-fits-all approach.

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