POI is loss of normal ovarian function before age 40.

Characterized by amenorrhea/oligomenorrhea (abnormal menses, either absence of period or less period), elevated gonadotropins (FSH, LH), and low estrogen levels.

Unlike menopause, ovarian activity may be intermittent, some women still ovulate occasionally.

Causes / Risk Factors

Genetic

• Turner syndrome (45, XO).

• Fragile X premutation (FMR1 gene).

• Other chromosomal abnormalities.

Autoimmune

• Autoimmune oophoritis (immune system attacks ovaries).

• Associated with thyroiditis, Addison’s disease.

Iatrogenic

• Chemotherapy, radiotherapy.

• Surgical removal of ovaries.

Infections (rare)

• Mumps oophoritis, pelvic Tuberculosis.

Idiopathic

• In up to 60–70% of cases, no cause is known.

  Clinical Features / Symptoms

Menstrual disturbances: nil to low menstrual flow (<40 years).

Infertility due to ovulation problem.

Symptoms of low estrogen hormone:

• Hot flushes, night sweats.

• Vaginal dryness, painful sex.

• Sleep disturbances, mood changes.

Long-term risks:

• Osteoporosis (low bone density).

• Cardiovascular disease (due to estrogen deficiency).

  Diagnostic Criteria

Age less than 40 years.

≥4 months of no menstrual flow or menstrual irregularity.

FSH in menopausal range (>40 IU/L) on two occasions, at least 4 weeks apart.

Low estradiol.

Exclude pregnancy, thyroid disorders, high prolactin levels

Complications

Infertility (main challenge).

Reduced bone mineral density → fractures, osteoporosis.

Early onset cardiovascular disease (rarely).

Emotional/psychological impact: anxiety, depression, grief over infertility.

Management

Hormone Replacement Therapy (HRT)

• Estrogen + progestin (if uterus is present,the uterus might be small in size but could grow larger while on HRT).

• Relieves menopausal symptoms, protects bone and heart health.

Bone & Heart Health

• Calcium, vitamin D, weight-bearing exercise.

• Regular bone density monitoring.

Fertility Options

• Natural conception is rare but possible (~5–10%).

• Donor egg IVF is the most effective treatment.

• Fertility preservation (egg/embryo freezing) may be considered if ovarian function is declining but not lost.Outcome not too favourable.

Psychological Support

• Counseling, support groups for coping with infertility and early menopause.

  Key Difference from Menopause

Menopause = natural cessation of ovarian function around age 50.

POI = pathologic, occurs before 40, and ovarian activity may still fluctuate (some spontaneous ovulation/pregnancy possible).

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Prolactin is a hormone secreted by the anterior pituitary gland.

Its main role is breast development and milk production, but excess levels disrupt the hypothalamic–pituitary–ovarian (HPO) axis, leading to lack of ovulation and then results to infertility.

Causes

Physiological (normal situations)

• Pregnancy, breastfeeding (lactation).

• Stress, sleep, sexual intercourse.

Pathological

• Pituitary tumors (prolactinomas) – most common cause.

• Other pituitary or hypothalamic lesions (craniopharyngioma, empty sella).

Systemic diseases

• Low thyroid hormones (High level of Thyrotropin-Releasing Hormone (TRH) stimulates prolactin).

• Chronic renal failure.

• Liver cirrhosis.

Medications which remove inhibition of prolactin)

• Antipsychotics (risperidone, haloperidol).

• Antidepressants (SSRIs, tricyclics).

• Anti-emetics (metoclopramide, domperidone).

• Antihypertensives (verapamil, methyldopa).

Idiopathic hyperprolactinemia meaning no identifiable cause.

Clinical Features

Reproductive:

• Women: scanty periods, amenorrhea (absent menstrual flow), ovulation problems, infertility.

• Men: Reduced libido, erectile dysfunction, infertility.

Galactorrhea: Milk secretion not related to pregnancy or breastfeeding.

Hypogonadism:

• Hot flushes, vaginal dryness (women).

• Gynecomastia, decreased body hair (men).

Mass effects (if prolactinoma is large):

• Headaches.

• Visual problems

  Diagnosis

Do a Serum prolactin test: Elevated (>25 ng/mL in women, >20 ng/mL in men).

Rule out physiologic causes, pregnancy, low thyroid hormones, and medications.

Thyroid function test: To exclude thyroid hormones.

MRI of pituitary: If persistent elevation of prolactin levels

Complications

Infertility

Osteoporosis (weak bones).

Visual loss

Management

Treat underlying cause

• Stop or switch medications that increase prolactin.

• Stop or reduce intake of milk. Increase intake of potatoes and yam.

• Treat low thyroid hormones (thyroxine normalizes prolactin).

Medical therapy (first-line for prolactinomas):

• Dopamine agonists: Bromocriptine, Cabergoline (preferred: more effective, better tolerated).Combined with intake of vitamin B6 supplements.

Surgery (transsphenoidal resection):

• For patients intolerant to medical therapy or with tumor resistant to drugs.

Radiotherapy: Rare, for aggressive tumors not controlled by other means.

Fertility Aspect

Hyperprolactinemia is a reversible cause of infertility.

Normalizing prolactin often restores ovulation and spontaneous conception.

If fertility is the main concern, treatment usually involves dopamine agonists, like

Accounts for 25 - 35% of female infertility cases.

Causes

Pelvic Infections (PID - Pelvic Inflammatory Disease)

• Commonly from Chlamydia trachomatis or Neisseria gonorrhoeae.

• Leads to scarring and adhesions.

Tuberculosis (genital TB)

• Especially common in developing countries.

Endometriosis

• Endometrial tissue outside the uterus.

Previous Pelvic or Abdominal Surgery

• Appendectomy, cesarean section, ovarian cyst removal → scar tissue formation.

Hydrosalpinx

• Tube blocked and filled with fluid, which can also reduce embryo implantation success in IVF.

Congenital anomalies (rare).

Types of Blockage

Proximal block: Near the uterus.(tubal flushing can be helpful)

Distal block: Near the fimbria end (commonest, often after infection and tubal flushing not recommended).

Unilateral or bilateral blockage.

Clinical Features

Often asymptomatic (discovered during infertility workup).

Sometimes:

• History of PID, TB, or surgery.

• Chronic pelvic pain.

• Dyspareunia (painful sex).

• Dysmenorrhea (painful periods).

Infertility is usually the main complaint.

Diagnosis

Hysterosalpingography (HSG):

• X-ray with dye injected into uterus/tubes.

• Shows blockages but may cause discomfort.

Sonohysterography with contrast (Saline Infusion Sonography / Sonohysterogram):

• Ultrasound with saline and contrast (HyCoSy).

Laparoscopy with Chromopertubation (gold standard but HSG is preferable):

• Direct visualization + methylene blue dye test.

• Can treat adhesions at the same time.

  Complications

Infertility (egg and sperm cannot meet).

Ectopic pregnancy (if tube partially blocked).

Chronic pelvic pain (from adhesions, hydrosalpinx).

Management

Medical Treatment:

• Antibiotics for active infection (but cannot reverse scarring).

Surgical Treatment:

• Tuboplasty: Surgery to open or repair blocked tubes (limited success)

• Tubal flushing or hydrotubation: application of normal saline with pressure to clear out any blockages, effective by 70 percent if blockage is near the uterus.

• Salpingectomy or salpingostomy: Removal/opening of damaged tubes (especially if hydrosalpinx before IVF).

Assisted Reproductive Technology (ART):

• IVF (In Vitro Fertilization): Best option for women with both tubes blocked.

• Success rates higher if hydrosalpinx is removed before IVF.

  Key Fertility Insight

One open tube: Natural conception possible (if ovulation occurs from the ovary on that side).

Both tubes blocked: Natural conception impossible → IVF is needed.

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"Hydro" = fluid, "salpinx" = tube.

Often affects both tubes but can be unilateral.

The fluid is typically inflammatory, toxic to embryos, and interferes with implantation.

Causes

Pelvic Inflammatory Disease (PID): Chronic infection from Chlamydia or Gonorrhea.

Tuberculosis (genital TB): Common cause in developing countries.

Endometriosis: Scarring around tubes.

Previous pelvic/abdominal surgery: Adhesions block fimbrial ends.

Congenital malformations (rare).

Pathophysiology

The fimbria end of the tube is blocked.

Tube fills with serous or watery inflammatory fluid.

Fluid:

• Washes embryos out of the uterus.

• Has toxic/inflammatory substances that damage embryos.

• Alters endometrial receptivity (reduces chance of implantation).

  Clinical Features

Many women are asymptomatic - hydrosalpinx is discovered during infertility workup.

Possible symptoms:

• Infertility (most common presentation).

• Chronic pelvic pain.

• Pelvic mass (rare, if large).

• Watery vaginal discharge (sometimes, if fluid leaks into the uterus).

  Diagnosis

Transvaginal Ultrasound (TVUS):

• Shows thin-walled, elongated, fluid-filled tubular structure.

Hysterosalpingography (HSG):

• Contrast X-ray showing blocked, distended tubes.

Sonohysterography with contrast (HyCoSy).

Laparoscopy with Chromopertubation (Gold Standard):

• Direct visualization.

• Confirms blockage + extent of adhesions.

  Complications

Infertility (due to blockage + toxic effect of fluid).

Reduced IVF success rates (implantation failure, early miscarriage).

Ectopic pregnancy risk (if partial block).

Chronic pelvic pain (from adhesions).

Management

Surgical Treatment

• Salpingectomy (removal of tube): Best option before IVF; improves IVF success significantly.

• Salpingostomy (opening blocked fimbrial end): Sometimes used, but high recurrence risk.

• Tubal clipping/occlusion: Blocks hydrosalpinx fluid from reaching the uterus before IVF.

Assisted Reproduction

• IVF (In Vitro Fertilization): Best treatment especially after hydrosalpinx resolves, naturally or surgically.

• Natural conception is rare unless tube is repaired successfully.

Medical Treatment

• Antibiotics only if active infection, but do not reverse damage.

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Prevents normal egg pickup, sperm transport, and fertilization.

Responsible for 25 - 35% of female infertility cases (often overlapping with blocked tubes or hydrosalpinx).

Causes

Pelvic Infections (PID – Pelvic Inflammatory Disease)

• Chlamydia and Gonorrhea most common.

Salpingitis (inflammation of the fallopian tubes) can cause scarring and adhesions, leading to tubal blockage and increased risk of infertility or ectopic pregnancy.

Tuberculosis (genital TB)

• Major cause in developing countries.

Endometriosis

• Inflammatory lesions → pelvic adhesions around tubes/ovaries.

Previous Pelvic/Abdominal Surgery

• Cesarean section, appendectomy, ovarian cystectomy → adhesions involving tubes.

Ectopic Pregnancy surgery

• Tubal repair may leave scarring.

  Pathophysiology

Scarring inside the tube (intraluminal adhesions): Narrowing or complete obstruction such that sperm/egg can’t pass.

Scarring outside the tube (peritubal adhesions): Tube may be open but trapped/immobile, so fimbriae can’t capture the egg.

Distortion of tubo-ovarian relationship: Even if tube is patent, adhesions prevent normal egg pick-up.

Clinical Features

Often silent until infertility is investigated.

History clues:

• Past PID, endometriosis, abdominal/pelvic surgery, or TB.

May present with:

• Chronic pelvic pain.

• Dyspareunia (painful intercourse).

• Menstrual pain (if associated with endometriosis).

Infertility is usually the main symptom.

Diagnosis

Hysterosalpingography (HSG): Shows tubal blockages or irregularities.

Sonohysterography / HyCoSy: Ultrasound-based tubal patency test.

Laparoscopy with Chromopertubation (Gold Standard):

• Direct visualization of adhesions and scarring.

• Can classify severity (mild, moderate, and severe).

  Complications

Infertility (most common).

Ectopic pregnancy risk (if tube partially damaged).

Chronic pelvic pain (if adhesions extensive).

Management

Prevention (most important):

• Early treatment of pelvic infections.

• Safe surgical techniques to minimize adhesion formation.

Surgical Options (Tuboplasty / Adhesiolysis):

• Salpingostomy / Fimbrioplasty: For distal occlusion with fimbrial adhesions.

• Adhesiolysis: Cutting peritubal adhesions during laparoscopy.

• Success rates depend on severity (good in mild adhesions, poor in severe).

Assisted Reproductive Technology (ART):

• IVF is treatment of choice in severe tubal damage/adhesions.

• IVF bypasses tubes completely.

  Key Fertility Insight

Mild adhesions: Surgery may restore natural conception.

Severe scarring: IVF is usually more effective than surgery.

Tubal damage causes high ectopic pregnancy risk (even after surgery).

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Benign smooth muscle tumors of the uterus.

Commonest pelvic tumor in women of reproductive age.

Up to 40–50% of women may develop fibroids by age 40.

Although many women are asymptomatic, fibroids can contribute to infertility and pregnancy complications, depending on their size and location.

Types (by Location)

Submucosal fibroids

• Grow into uterine cavity.

• Strongest link with infertility (interfere with implantation).

Intramural fibroids

• Within uterine body muscle

• Large ones can distort cavity, affecting implantation.

Subserosal fibroids

• On outer surface of uterus.

• Usually do not affect fertility unless very large.

  Causes / Risk Factors

Exact cause unknown, but linked to:

• Genetics (family history).

• Hormones: Estrogen & progesterone promote growth.

• Race: More common and severe in African women.

• Nulliparity (not having children).

• Obesity.

  Clinical Features

Many women asymptomatic.

Menstrual symptoms: Heavy/prolonged periods (menorrhagia), clots, anemia.

Pressure symptoms: Pelvic fullness, frequent urination, constipation (if large).

Reproductive issues:

• Infertility.

• Recurrent miscarriages.

• Preterm labor.

• Malpresentation of fetus.

  How Fibroids Cause Infertility

Cavity distortion (submucosal/intramural) which prevents implantation.

Endometrial changes causes poor receptivity for embryos.

Tubal blockage if large fibroid compresses fallopian tubes.

Altered blood supply reduced implantation success.

Hormonal effects within endometrium.

Diagnosis

Transvaginal ultrasound: First-line.

Saline infusion sonography (SIS): Highlights submucosal fibroids.

MRI pelvis: Defines number, size, and location (helpful before surgery).

Hysteroscopy: Direct visualization of cavity fibroids with specialized cameras.

Complications

Infertility.

Pregnancy risks: Miscarriage, preterm labor, placental abruption, cesarean delivery.

Severe anemia from heavy bleeding.

Rare: Sarcomatous transformation (<1%).it is important to do biopsy on removed fibroids.

Management

Medical

Used mainly for symptom relief (not definitive for infertility).

• GnRH analogues → shrink fibroids temporarily.

• Tranexamic acid, NSAIDs for heavy bleeding.o

• Hormonal therapy (progesterone IUD, OCPs).

  Surgical

Myomectomy (removal of fibroids):

• Indicated in women desiring fertility.

• Hysteroscopic myomectomy: for submucosal fibroids.

• Laparoscopic/open myomectomy: for intramural/subserosal fibroids.

Hysterectomy (removal of uterus): For women not desiring fertility.

It is important to weigh the fertility potential of the womb against the outcome of a fibroid surgery. If surgery will cause damage to the womb, avoiding surgery might be

advisable and proceeding with fertility treatment may be beneficial.

Minimally Invasive

Uterine artery embolization (UAE): Shrinks fibroids, but not recommended for women who want pregnancy.

MRI-guided focused ultrasound: Limited availability.

Fertility Insight

Submucosal fibroids: Strongest evidence of causing infertility, removal improves conception,but in some cases severe scaring of the lining of the womb could occur.

Large intramural fibroids (>4–5 cm): May reduce IVF success

Subserosal fibroids: Usually no impact, surgery may not needed.

Fibroids (leiomyomas) are common uterine tumors. Only certain types (mainly submucosal and large intramural) impair fertility by distorting the uterine cavity or blocking tubes.

Treatment for infertility = myomectomy (preferably hysteroscopic if submucosal).

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Local overgrowths of endometrial tissue (glands, stroma, and blood vessels) that form projections inside the uterine cavity.

Usually benign, but they can interfere with fertility and sometimes cause abnormal bleeding.

Causes / Risk Factors

Exact cause not fully known, but linked to:

• Hormonal imbalance (estrogen stimulation without enough progesterone).

• Tamoxifen use (breast cancer medication).

• Obesity (higher estrogen levels).

• Chronic endometritis (low-grade uterine inflammation).

More common in women aged 30–50 years.

Clinical Features

Asymptomatic in many women (discovered during infertility workup).

Abnormal uterine bleeding:

• Intermenstrual spotting.

• Heavy or prolonged periods.

• Postcoital bleeding.

Infertility:

• Polyps can prevent implantation.

• Can act as a “foreign body” in the uterus.

Rarely: pelvic pain (if large).

How Endometrial Polyps Cause Infertility

Mechanical interference: Occupy space in uterine cavity → prevent embryo implantation.

Endometrial environment alteration: Affect blood flow and local receptivity.

Inflammatory response: May produce cytokines that reduce implantation.

Sperm/embryo interference: Large polyps may obstruct sperm transport or embryo movement.

Diagnosis

Transvaginal Ultrasound (TVUS):

• Can detect polyps, especially if done in the proliferative phase.

Saline Infusion Sonohysterography (SIS):

• Saline distends the cavity, polyps become clearly visible.

Hysteroscopy (Gold Standard):

• Direct visualization inside uterus.

• Allows simultaneous removal (polypectomy).

  Complications

Infertility.

Recurrent miscarriage.

Abnormal uterine bleeding → anemia.

Rare malignant transformation (endometrial carcinoma risk <1%).

Management

Small, asymptomatic polyps (<1 cm):

• Sometimes monitored (may regress spontaneously).

Symptomatic or infertility-associated polyps:

• Hysteroscopic polypectomy (gold standard):

  • Removes polyp and restores uterine cavity.

  • Improves natural conception and IVF success rates.

Medical therapy:

• Limited role. Hormonal therapy (progestins) may control bleeding but does not eliminate polyps.In very rare cases,taking progesterone drugs may forcefully flush out the polyps.

  Fertility Insight

Removing endometrial polyps increases pregnancy rates.

Studies show:

• Natural conception often improves after polypectomy.

• IVF implantation and pregnancy outcomes are better after removal.

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Structural malformations of the uterus that arise from abnormal development during embryonic life.

Affect about 3–5% of women in the general population, and up to 15% in women with

recurrent miscarriage or infertility.

Causes

Embryologic defect in womb development

Types of Congenital Uterine Anomalies

(According to American Society for Reproductive Medicine [ASRM] classification)

Agenesis/Hypoplasia (Mayer-Rokitansky-Küster-Hauser syndrome)

• Uterus absent or very small.

• Primary amenorrhea, infertility, but normal ovaries.

Unicornuate Uterus

• Small, single uterus.

• Often associated with a rudimentary horn (sometimes with endometrium → risk of ectopic pregnancy).

Didelphys Uterus

• Complete failure of fusion → two separate womb, each with its own cavity and often two cervices.

• May be asymptomatic or cause infertility/recurrent pregnancy loss.

Bicornuate Uterus

• Heart-shaped uterus with two cavities. That is abnormal and lead to infertility and miscarriage.

• Associated with miscarriage, preterm birth, and fetal malpresentation.

Septate Uterus (Most clinically significant for infertility)

• Failure of resorption → normal external contour but a fibrous or fibromuscular septum inside uterine cavity.

• Strongest link to infertility and recurrent miscarriage.

Arcuate Uterus

• Mild indentation at fundus.

• Usually benign, minimal impact on fertility.

  Clinical Features

Some women asymptomatic.

Common presentations:

• Infertility.

• Recurrent miscarriage.

• Preterm labor.

• Malpresentation (breech, transverse).

• Dysmenorrhea (if obstructive anomaly like non-communicating horn).

  Diagnosis

Ultrasound (2D or 3D transvaginal): Initial evaluation.

Hysterosalpingography (HSG): Outlines cavity shape but limited in differentiating septate vs bicornuate.

MRI pelvis: Best for defining uterine morphology.

Hysteroscopy + Laparoscopy (Gold Standard):

• Direct evaluation of cavity and external contour.

  Complications

Infertility.

Repeated pregnancy loss.

Preterm delivery.

Abnormal fetal position.

Dysmenorrhea or hematometra (in obstructive anomalies).

Management

Depends on anomaly type & fertility goals:

Septate Uterus (most treatable):

• Hysteroscopic septum resection (metroplasty):

  • Greatly improves fertility and reduces miscarriage.

Bicornuate / Didelphys Uterus:

Usually no treatment unless recurrent pregnancy loss.

Metroplasty (Strassman procedure) in selected cases.

A condition characterized by the formation of scar tissue (adhesions/synechiae) inside the uterine cavity, due to injury to the lining of the womb.

Leads to partial or complete obliteration of the endometrial cavity.

Can cause infertility, menstrual abnormalities, and recurrent pregnancy loss.

Causes

Most often due to trauma to the endometrium, especially when the uterus is inflamed or infected.

Iatrogenic (most common):

• After dilation and curettage (D&C) following miscarriage, abortion, or postpartum hemorrhage.

• Risk increases if performed on an already infected uterus.

Uterine surgery:

• Myomectomy, hysteroscopic polypectomy, cesarean section.

Infections:

• Genital tuberculosis (important in developing countries).

• Severe endometritis (e.g., after unsafe abortion).

  Pathophysiology

Endometrial basal layer gets destroyed → replaced with scar tissue → adhesions form between anterior and posterior walls.

Severity:

• Mild: Thin, filmy adhesions, cavity partly involved.

• Moderate: Denser adhesions, partial cavity obliteration.

• Severe: Thick, fibrous adhesions, cavity almost completely obliterated.

  Clinical Features

Menstrual abnormalities:

• Hypomenorrhea (scanty flow).brown or dark menstrual flow

• Amenorrhea (if severe adhesions block cavity).

• Cyclic pelvic pain (if blood trapped = cryptomenorrhea).

Infertility / Recurrent miscarriage.

History clues:

Previous D&C, uterine surgery, postpartum infection, TB.

A chronic gynecological condition in which endometrial tissue (glands + stroma) grows outside the uterine cavity, that is, tissues normally found in the womb are abnormally found in other parts of the body, most commonly on:

• Ovaries

• Fallopian tubes

• Pelvic peritoneum

• Uterosacral ligaments

These implants respond to hormonal changes → cyclic bleeding, inflammation, and scarring.

Affects 10–15% of reproductive-age women, but 30–50% of women with infertility.

Causes / Risk Factors

Exact cause not fully understood. Theories include:

• Retrograde menstruation (Sampson’s theory): Menstrual blood flows backward into pelvis.

• Genetic/immune factors: Family history, impaired immune clearance.

Risk factors:

• Early menarche, short cycles, heavy menstrual bleeding.

• Nulliparity (no childbirth).

• Family history.

  Clinical Features

Pain symptoms (classic):

• Dysmenorrhea (severe period pain).

• Dyspareunia (painful intercourse).

• Chronic pelvic pain.

• Dyschezia (pain on defecation) if bowel involved.

Infertility (major complaint).

Other: Fatigue, heavy bleeding, ovarian cysts (endometriomas = “chocolate cysts”).

How Endometriosis Causes Infertility

Tubal factor: Adhesions distort pelvic anatomy → egg cannot be picked up.

Ovarian factor: Endometriomas damage ovarian tissue → reduce egg quality/quantity.

Endometrial factor: Inflammatory environment → reduces implantation.

Hormonal/immune changes: Altered follicular development and embryo receptivity.

Diagnosis

Clinical suspicion (history of pelvic pain + infertility).

Imaging:

• Transvaginal ultrasound: detects ovarian endometriomas.

• MRI: maps deep lesions.

Laparoscopy (Gold Standard):

• Direct visualization and biopsy.

• Also allows treatment (adhesiolysis, ablation).

  Complications

Infertility (30–50%).

Chronic pelvic pain.

Recurrent ovarian cysts.

Adhesions → bowel/bladder involvement.

Rare malignant transformation in endometriomas.

Management

Medical Treatment (for pain, not infertility alone):

Pain killers ,NSAIDs not advised.Fertility supplement like NAC(N acetyl cysteine) supplement

Hormonal suppression:

• Combined OCPs.

• Progestins (oral, depot, IUD).

• GnRH agonists/antagonists.

• Aromatase inhibitors.

  Surgical Treatment:

Laparoscopic excision/ablation of endometriotic lesions + adhesiolysis.

Ovarian endometrioma cystectomy (Surgical removal of ovarian cyst) if large (>3–4 cm).

Improves fertility in some cases, especially mild/moderate disease.

Assisted Reproductive Technology (ART):

IVF is best option when:

• Severe endometriosis.

• Tubal damage.

• Poor ovarian reserve.

• Surgery has failed.

  Fertility Insight

Mild/moderate endometriosis: Surgery may restore fertility.

Severe endometriosis: IVF gives better success than repeated surgery.

Endometriomas: Surgery only if symptomatic or large (>4 cm), as over-surgery may reduce ovarian reserve

Endometriosis is when endometrial tissue outside uterus, causing pain and infertility. Infertility results from adhesions, ovarian damage, and poor implantation environment. Diagnosis is laparoscopy, and management for fertility is surgery in mild cases, IVF in severe

cases.

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Narrowing or complete obstruction of the cervical canal that prevents passage of menstrual blood, sperm, or surgical instruments.

Can occur at the internal os, external os, or along the canal.

More common in women with prior cervical surgery, vaginal insertion of herbs or postmenopausal women, but can also affect younger women of reproductive age.

Causes

Iatrogenic (most common):

• After cervical surgery (cone biopsy, LEEP, cauterization, dilation & curettage).

• Post-radiation therapy.

Congenital:

• Developmental defect present from birth.

Infections:

• Chronic cervicitis, genital tuberculosis.

Menopause / Hypoestrogenism:

• Atrophy of cervical tissue causing narrowing.

Trauma or scarring:

• Following difficult childbirth or repeated instrumentation,vaginal insertion of insertion,

  Clinical Features

Asymptomatic (mild cases, detected during infertility workup).

Menstrual problems:

Hypomenorrhea (scanty flow).

Amenorrhea (if completely blocked).

Dysmenorrhea (trapped blood).

A condition in which the cervical mucus environment is unfavorable to sperm survival, movement, or entry into the uterus.

Leads to reduced chances of natural conception despite normal ovulation, tubes, and sperm.

Accounts for about 5–10% of female infertility cases.

Normal Cervical Mucus Function

During ovulation, under estrogen influence, cervical mucus becomes:

Thin, watery, and stretchy ("spinnbarkeit").

High water content and alkaline pH.

Facilitates sperm passage, protects sperm from vaginal acidity, and supports capacitation.

Pelvic Infections

• Pelvic Inflammatory Disease (PID): Especially from Chlamydia trachomatis and

  Neisseria gonorrhoeae.

• Genital tuberculosis (important in developing countries).

Endometriosis

• Bleeding lesions causes inflammation which can cause fibrosis and also adhesions.

Pelvic/Abdominal Surgery

• Cesarean section, myomectomy, appendectomy, ovarian cystectomy.

• Adhesions form as part of healing.

Peritonitis

• Generalized infection or ruptured appendix.

  How Pelvic Adhesions Cause Infertility

Tubal factor: Distort or block fallopian tubes, preventing egg pickup.

Ovarian factor: Tether ovaries, preventing release or pickup of oocytes.

Uterine factor: Adhesions may distort uterine position or impair blood flow.

Pain factor: Dyspareunia and chronic pelvic pain may reduce sexual activity frequency.

Clinical Features

Often silent (detected only during infertility evaluation).

Chronic pelvic pain.

Dyspareunia (painful intercourse).

Infertility.

Bowel/bladder symptoms if adhesions involve these organs (constipation, painful urination).

Diagnosis

Ultrasound / MRI: Limited for adhesions but may show distorted anatomy.

HSG (hysterosalpingography): May suggest tubal occlusion.

Sonohysterography / HyCoSy: Alternative tubal test.

Laparoscopy (Gold Standard):

• Direct visualization of adhesions.

• Can classify severity (mild, moderate, severe).

• Allows simultaneous treatment (adhesiolysis).

  Complications

Infertility.

Chronic pelvic pain.

Ectopic pregnancy (if tubes partially damaged).

Bowel obstruction (rare but possible with severe adhesions).

Management

Prevention (key):

• Prompt treatment of pelvic infections.

• Gentle surgical techniques (minimal tissue trauma, use of adhesion barriers like hyaluronic acid gels).

Surgical Treatment:

• Laparoscopic adhesiolysis (cutting adhesions to restore anatomy).

• Effectiveness depends on severity:

  • Mild adhesions: Fertility often restored.

  • Severe adhesions: Low natural conception rate; high recurrence.

Assisted Reproductive Technology (ART):

• IVF bypasses tubes and ovaries, effective in severe adhesions.

• Preferred if adhesiolysis fails or adhesions recur.

  Fertility Insight

Mild pelvic adhesions: Surgery may restore natural conception.

Severe adhesions: IVF is usually the best solution.

Recurrence is common, so surgical results are sometimes temporary.

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A condition where semen enters the bladder instead of exiting through the urethra

during ejaculation.

The result: little to no semen is expelled (sometimes called “dry orgasm”).

Accounts for a small percentage of male infertility but is important to recognize.

Normal Ejaculation Physiology

At orgasm, bladder neck contracts which prevents semen from flowing backward.

Prostate, seminal vesicles, and vas deferens expel semen forward through the urethra.

In retrograde ejaculation, the bladder neck fails to close causing semen flows into the bladder.

Causes

Nerve Damage

• Diabetes mellitus (diabetic neuropathy), this is the most common cause.

• Multiple sclerosis, spinal cord injuries.

Surgery involving bladder neck/prostate

Transurethral resection of the prostate (TURP).

Radical pelvic surgery (bladder, prostate, retroperitoneal lymph nodes).

The persistent inability to achieve or maintain an erection sufficient for satisfactory sexual performance.

ED is one of the most common male sexual disorders and can lead to infertility when intercourse is not possible or incomplete.

Persistent or recurrent ejaculation with minimal sexual stimulation, before or shortly after penetration, and earlier than desired, leading to distress or infertility.

Most common male sexual dysfunction (affects ~20–30% of men).

Types

Lifelong (primary): present since sexual debut.

Acquired (secondary): develops later in life, often due to stress, ED, or medical conditions.

Causes

Psychological: performance anxiety, depression, relationship issues.

Biological: hypersensitivity of penile nerves, serotonin receptor imbalance, thyroid disorders, prostatitis.

Associated with ED (men with erectile issues may rush intercourse).

How It Causes Infertility

Ejaculation may occur before penetration causing no sperm deposited in vagina.

Ejaculation too soon after penetration causes reduced chance of depositing sperm deep enough near the cervix.

Anxiety/avoidance behavior causes reduced intercourse frequency during fertile window.

Diagnosis

Clinical (based on sexual history).

Intravaginal Ejaculatory Latency Time (IELT): <1 min = severe PE.

Management

Behavioral therapies – stop-start technique, squeeze technique.

Medications

• SSRIs (dapoxetine, paroxetine, sertraline).

• Topical anesthetics (lidocaine spray/cream).

Psychosexual counseling.

Assisted reproduction (collecting sperm for IUI/IVF if intercourse impossible).

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Persistent difficulty, delay, or inability to achieve orgasm/ejaculation despite adequate stimulation and erection.

Less common than PE, but can severely impact fertility.

Causes

Psychological

• Anxiety, trauma, depression, relationship conflict.

Neurological

• Spinal cord injuries, multiple sclerosis, diabetic neuropathy.

Medications

• SSRIs, antipsychotics, opioids, alcohol, recreational drugs.

Endocrine

• Hypogonadism (low testosterone), thyroid disorders.

Post-surgical

• Pelvic/prostate surgery affecting nerves.

  How It Causes Infertility

Man may be able to have intercourse and erection but fails to ejaculate which means no sperm reaches cervix.

In some cases, semen is produced but orgasm is absent, leading to coital dissatisfaction and reduced frequency.

Diagnosis

Sexual/medical history.

Review medications.

Endocrine and neurological evaluation if needed.

Management

Address cause – adjust offending drugs, treat low testosterone, manage diabetes.

Sex therapy – behavioral techniques, psychological counseling.

Medical options – dopamine agonists, PDE5 inhibitors (if coexisting ED).

Assisted Ejaculation techniques

• Penile vibratory stimulation (PVS).

• Electroejaculation (EEJ).

• Semen collected for IUI/IVF/ICSI.

  Fertility Insight

Premature Ejaculation: Fertility possible if some semen reaches vagina, but severe PE may need treatment or ART.

Anorgasmia: Directly prevents semen delivery; usually requires assisted ejaculation or sperm retrieval for fertility treatments.

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A congenital (present at birth) condition in which both vas deferens ducts fail to develop, so sperm cannot be transported from the testes to the urethra.

Affects about 1–2% of infertile men, and is strongly associated with cystic fibrosis (CF) gene mutations.

Causes & Associations

Genetic link (CFTR mutations):

• ~80–90% of men with CBAVD carry at least one mutation in the CFTR gene.

• Some have clinical cystic fibrosis, while others are otherwise healthy but infertile.

Developmental anomaly:

• Vas deferens fails to form during embryogenesis.

• Often associated with absent or hypoplastic seminal vesicles.

Other associations:

• Unilateral renal agenesis (missing kidney) in some cases.

• Congenital absence of other parts of Wolffian duct system.

  Pathophysiology

Testes produce sperm normally.

Epididymis and vas deferens are absent causing obstructive azoospermia.

Ejaculate volume is very low because seminal vesicles (often absent) contribute majority of semen.

Clinical Features

Normal puberty, sexual function, and erections.

Infertility despite normal sexual activity.

Low semen volume, azoospermia on semen analysis.

On exam:

• Vas deferens not palpable in scrotum.

• Testes are usually normal in size and consistency.

  Investigations

Semen Analysis

• Azoospermia.

• Low volume, acidic pH, absent fructose (if seminal vesicles also absent).

Physical Exam

• Absent vas deferens on palpation.

Genetic Testing

• CFTR mutation screening (essential for patient and partner).

• If both partners carry mutations, there is a 25% chance of child with cystic fibrosis.

Imaging

• Scrotal ultrasound or MRI may confirm absent vas deferens/seminal vesicles.

• Renal ultrasound (to check for renal agenesis).

  Management

Counseling

• Genetic counseling for couple is mandatory (CFTR mutation risk).

Fertility Options

• Natural conception impossible (since no vas deferens).

• Assisted Reproductive Technology (ART):

  • Surgical sperm retrieval (from testis or epididymis via TESE, PESA, or MESA).

  • Combine with ICSI (Intracytoplasmic Sperm Injection).

• IUI is not possible (no sperm in ejaculate).

Partner genetic testing

• If partner carries CFTR mutation, consider preimplantation genetic testing (PGT) inorder not for the defect be transferred to the offspring or donor gametes to avoid CF in offspring.

  Fertility Insight

CBAVD men produce sperm normally, but delivery is blocked.

With sperm retrieval + ICSI, pregnancy rates are excellent.

Main challenge is genetic risk of CF which must be addressed before treatment.

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A disorder where the hypothalamus or pituitary gland fails to produce enough GnRH, LH, or FSH, leading to low testosterone and impaired spermatogenesis.

It is a form of secondary hypogonadism (problem lies “upstream,” not in the testes).

A chromosomal disorder where males have an extra X chromosome (47,XXY instead of 46,XY).

Leads to testicular failure (primary hypergonadotropic hypogonadism), impaired spermatogenesis, and infertility.

Occurs in about 1 in 600 male births.

Genetics

Karyotype: 47,XXY (most common).

Variants: 48,XXXY, mosaic forms (46,XY/47,XXY).

Mosaic cases may have milder features and higher fertility potential.

Pathophysiology

Seminiferous tubules undergo fibrosis and hyalinization, resulting in severe loss of germ cells.

Leydig cell dysfunction leads to low testosterone.

Feedback loop: Low testosterone causes elevated LH and FSH (hypergonadotropic hypogonadism).

Result: Small, firm testes, gynecomastia, and azoospermia.

Clinical Features

General

Tall stature (long arms and legs due to delayed epiphyseal closure).

Reduced muscle mass, sparse facial and body hair.

Gynecomastia (increased risk of breast cancer).

Infertility (almost universal in non-mosaic cases).

Genital

Small, firm testes (usually <5 mL).

Small penis in some cases.

Azoospermia (no sperm in semen).

Decreased libido, erectile dysfunction (in severe testosterone deficiency).

Developmental/Behavioral

Learning difficulties (especially language and reading).

Social/behavioral problems (sometimes mild).

Investigations

Hormonal profile

• Low Testosterone.

• High FSH and High LH (primary testicular failure).

Semen analysis

• Azoospermia (rarely severe oligospermia in mosaic cases).

Genetic testing

• Karyotype (47,XXY).

• Y-chromosome microdeletion testing if sperm retrieval attempted.

Other

• Breast exam/mammography (gynecomastia → ↑ breast cancer risk).

• Bone density scan (osteoporosis risk).

  Management

Hormone replacement

Testosterone therapy: improves virilization, libido, bone density, muscle mass.

Note: not used if actively trying for fertility, as TRT suppresses spermatogenesis further.

Small deletions (loss of genetic material) on the Y chromosome long arm (Yq11) that remove genes essential for spermatogenesis.

These deletions cause no or low sperm count

Found in about 10–15% of men with non-obstructive azoospermia and 5–10% with severe oligospermia (low sperm count).

Clinical Features

Normal male external genitalia.

Testicular size may be normal or reduced.

Primary infertility due to azoospermia/severe oligospermia.

Often no other systemic abnormalities.

Investigations

Semen Analysis

• Severe oligospermia (<5 million/mL) or azoospermia.

Hormonal Profile

• Variable. May show elevated FSH if testicular failure.

Genetic Testing

• Y-chromosome microdeletion analysis (PCR-based testing of AZF regions).

• Usually ordered for men with azoospermia or sperm count <5 million/mL.

  Management

No curative treatment — deletions cannot be repaired.

Fertility options depend on deletion type:

• Donor sperm or adoption required.

• Possible sperm retrieval via TESE in up to ~50–70% of men → used for ICSI (Intracytoplasmic Sperm Injection).

Genetic Counseling

• YCMD is passed to all male offspring if ICSI is successful.

• Sons will likely face the same infertility issues.

• Couples may consider preimplantation genetic testing (PGT) to avoid tramission of offspring to offspring.

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Cystic Fibrosis (CF) is an autosomal recessive genetic disorder caused by mutations in the CFTR gene (Cystic Fibrosis Transmembrane Conductance Regulator).

Beyond lung and pancreatic disease, CF is a major genetic cause of male infertility due to congenital bilateral absence of the vas deferens (CBAVD).

Around 97–98% of men with CF are infertile, but usually not sterile (they produce sperm, but it cannot be transported).

Pathophysiology

A CFTR gene mutation causes abnormal chloride channel function, leading to thick secretions in multiple organs.

In the male reproductive tract:

Thick secretions during development cause obstruction and atrophy of the vas deferens.

This results in congenital bilateral absence of the vas deferens (CBAVD), meaning there is no connection between the testes and the ejaculatory ducts.

The testes produce sperm normally, but the ejaculate lacks sperm, leading to obstructive azoospermia.

The seminal vesicles may also be absent or underdeveloped, resulting in low ejaculate volume.

Clinical Features

General CF symptoms (classic form):

Chronic cough, recurrent lung infections.

Pancreatic insufficiency (steatorrhea, malabsorption).

Poor growth, diabetes, liver disease.

Genital/Reproductive:

Infertility (almost universal in males).

Small or absent vas deferens on exam/ultrasound.

Normal libido and erections.

Normal spermatogenesis (testes usually normal size).

Very low semen volume, azoospermia.

Some men present with isolated CBAVD without lung/pancreatic disease, due to milder CFTR mutations.

Investigations

Semen analysis

• Low volume, azoospermia.

Physical examination

• Absent or atrophic vas deferens (palpable along spermatic cord).

Genetic testing

• CFTR mutation analysis recommended for all men with CBAVD.

• Partner testing is crucial to assess risk of CF in offspring.

Imaging (scrotal/abdominal ultrasound, MRI)

• May confirm absent vas deferens/seminal vesicles.

  Management

Fertility options

• Surgical sperm retrieval (e.g., MESA – microsurgical epididymal sperm aspiration, PESA, or TESE).

• Retrieved sperm used in IVF with ICSI (intracytoplasmic sperm injection).

• Success rates are good since spermatogenesis is normal.

Genetic counseling

• Both partners must undergo CFTR mutation testing.

• If female partner is a carrier we have a 25% chance of child with CF.

• Preimplantation genetic testing (PGT) or donor gametes may be considered.

General CF care (if systemic disease present)

• Pulmonary, nutritional, and metabolic management.

  Fertility Insight

Men with cystic fibrosis (CF) mutations are almost always infertile because of congenital bilateral absence of the vas deferens (CBAVD), but sperm retrieval combined with intracytoplasmic sperm injection (ICSI) makes biological fatherhood possible.

The major concern is genetic transmission, with a risk of passing cystic fibrosis (CF) or congenital bilateral absence of the vas deferens (CBAVD) to offspring. This requires partner testing and genetic counseling.

In summary:

CFTR mutations cause Cystic Fibrosis and CBAVD in men, leading to obstructive azoospermia.

Testes make sperm normally, but no transport.

Fertility is achievable with surgical sperm retrieval and ICSI, but genetic counseling and partner testing are mandatory.

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INVESTIGATION

• Semen analysis

• Sperm chromatin structure Assay

• Male hormonal Assay

• Scrotal scan and rectal scan to rule out obstruction along the path where sperm cells flows.

• Genetic Test : Karyotyping

  TREATMENT

Refrain from all risk factors mentioned above

Hormonal drugs like clomid, human menopausal gonadotropin, Human Chorionic gonadotropin injections can be used if it is an hormonal cause

Fertility supplements like carnitine, zinc, magnesium

Removal of varicocele, surgical management of undescended testes.

IVF, ICSI, Testicular sperm aspiration/extraction, Percutaenous epididymal aspiration

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Prevalence: Affects about 15% of all men and up to 40% of men evaluated for infertility.

Side: More common on the left side due to anatomical differences in vein drainage, but it can affect both sides.

Age of Onset: Often develops during puberty.

Causes:

Faulty or weak valves in the spermatic vein → blood backs up → vein dilates.

Left renal vein compression (nutcracker effect) may also contribute.

Symptoms:

Many cases are asymptomatic (found during infertility evaluation or routine exam).

Some men may notice:

• A dull, aching scrotal pain (worse after standing/exercise, relieved when lying down).

• Testicular atrophy (affected testicle smaller).

• A "bag of worms" feel on palpation of the scrotum.

  Complications:

Male infertility: Varicoceles can impair sperm production and function due to:

• Increased scrotal temperature

• Oxidative stress

• Impaired blood flow and oxygen supply

Testicular growth arrest in adolescents.

Diagnosis:

Physical examination: Graded based on palpability/visibility (Grade I–III).

Scrotal ultrasound with Doppler: Confirms diagnosis and measures reflux/vein diameter.

Treatment:

Not all varicoceles need treatment (if asymptomatic and fertility is not a concern).

Indications for treatment:

• Infertility with abnormal semen parameters

• Testicular atrophy in adolescents

• Symptomatic pain

Options:

• Surgical ligation (varicocelectomy) – open, laparoscopic, or microsurgical (preferred due to fewer recurrences).

• Percutaneous embolization – minimally invasive, blocks blood flow to varicocele.