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QUESTION 1: Classify AUB based on FIGO and discuss Clinical Features, Diagnosis & Management of Leiomyoma

AUB - FIGO Classification (PALM-COEIN System)

STRUCTURAL (PALM):

NON-STRUCTURAL (COEIN):

• HMB - Heavy menstrual bleeding (>80 mL/cycle)
• HPMB - Heavy and prolonged menstrual bleeding (>8 days)
• IMB - Intermenstrual bleeding
• PCB - Post-coital bleeding
• PMB - Postmenopausal bleeding

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Leiomyoma (Uterine Fibroids) - AUB-L

Clinical Features:

• Most common benign tumor of the uterine myometrium (smooth muscle origin)
• Seen in reproductive age; estrogen-dependent
• Symptoms: menorrhagia (most common), pelvic pressure/heaviness, urinary frequency (if anterior), constipation (if posterior), infertility, dysmenorrhea
• Types by location: Submucosal (most likely to cause bleeding), intramural, subserosal, pedunculated, cervical, broad ligament

Diagnosis:

• Pelvic examination: enlarged, irregular, firm, non-tender uterus
• Transvaginal/Abdominal USG: hypoechoic lesions; confirms size, number, location
• Saline infusion sonohysterography (SIS): best for submucosal fibroids
• MRI pelvis: gold standard for mapping multiple fibroids (especially pre-surgery)
• Hysteroscopy: for submucosal fibroids - diagnostic + therapeutic
• Endometrial biopsy: to exclude malignancy in AUB

Management:

• GnRH agonists (Leuprolide) - shrinks fibroid preoperatively, causes temporary amenorrhea
• Combined OCPs / progestins - control bleeding
• Tranexamic acid + NSAIDs - for HMB
• Levonorgestrel IUD (Mirena) - reduces bleeding
• Selective progesterone receptor modulators (Ulipristal acetate)

• Myomectomy - removes fibroid, preserves uterus; for women desiring fertility
• Hysterectomy - definitive treatment; for completed family
• Uterine artery embolization (UAE) - minimally invasive; 31% eventually need hysterectomy
• Endometrial ablation - for submucosal fibroids causing HMB; 29% need hysterectomy by 60 months
• Hysteroscopic resection - for submucosal fibroids

Source: Berek & Novak's Gynecology; Robbins & Kumar Basic Pathology

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QUESTION 2 (Short Notes):

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i) Follicular Study (Folliculometry)

• Protocol: Baseline scan day 2-3; then every 2-3 days
• Pre-ovulatory follicle (Graafian): 18-24 mm
• Signs of ovulation on USG: sudden reduction in follicle size, free fluid in POD, collapsed follicle
• Uses: Infertility workup, timing of IUI/IVF, diagnosing LUFS (Luteinized Unruptured Follicle Syndrome), monitoring response to ovulation induction (Clomiphene, Gonadotropins)
• LH surge + USG: Ovulation occurs 34-36 hours after LH peak

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ii) Puberty Menorrhagia & Metropathia Hemorrhagica

Puberty Menorrhagia (Dysfunctional Uterine Bleeding at Menarche):

• Occurs within 1-2 years of menarche
• Due to anovulatory cycles - immature HPO axis fails to produce LH surge
• Prolonged estrogen stimulation without progesterone opposition leads to endometrial hyperplasia then irregular shedding
• Features: Heavy, prolonged, irregular bleeding; often no dysmenorrhea (anovulatory)
• Management: Combined OCP (first line), high-dose progestin, tranexamic acid, iron supplementation; exclude coagulation disorder (von Willebrand disease, platelet dysfunction)

Metropathia Hemorrhagica (Cystic Glandular Hyperplasia of Schroeder):

• Seen in perimenopausal women (also at puberty)
• Caused by prolonged anovulation with sustained unopposed estrogen stimulation
• Histology: Cystic, dilated endometrial glands lined by proliferating epithelium ("Swiss cheese" pattern) - i.e., simple endometrial hyperplasia without atypia
• Uterus is slightly enlarged; ovaries show follicular cysts (no corpus luteum)
• Features: Episode of amenorrhea (6-8 weeks) followed by sudden, heavy, prolonged bleeding
• Management: High-dose progestin (Norethisterone 5 mg TDS x 10 days); OCPs; D&C (diagnostic + therapeutic); if recurrent - endometrial ablation or hysterectomy

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iii) PCOS (Polycystic Ovary Syndrome)

1. Oligomenorrhea/Anovulation
2. Clinical/biochemical hyperandrogenism
3. Polycystic ovaries on USG (>12 follicles 2-9 mm in each ovary OR ovarian volume >10 mL)

• Elevated LH:FSH ratio (>2:1)
• Excess LH stimulates theca cells to produce excess androgens
• FSH deficiency → follicles fail to mature → multiple small follicles (2-9 mm "string of pearls")
• Insulin resistance → hyperinsulinemia → more androgen production

• Irregular/absent periods, obesity, acne, hirsutism, alopecia
• Infertility (most common endocrine cause), acanthosis nigricans

• USG: >12 follicles per ovary; ovarian volume >10 mL; "necklace sign"
• Hormones: Elevated LH, testosterone; normal/low FSH; elevated AMH
• Fasting glucose, insulin resistance (HOMA-IR)

• Lifestyle modification (weight loss restores ovulation in many)
• Metformin - improves insulin resistance, restores menstrual cycles
• OCPs - regulate periods, treat hyperandrogenism
• Clomiphene citrate - ovulation induction for fertility
• Letrozole - now preferred over clomiphene for ovulation induction
• Spironolactone/Cyproterone acetate - antiandrogen therapy

Source: Robbins & Kumar Basic Pathology; Swanson's Family Medicine

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iv) Etiology of Uterovaginal (UV) Prolapse

• Primary: Transverse cervical (Cardinal/Mackenrodt's) ligaments, Uterosacral ligaments, Pubocervical fascia
• Secondary: Broad ligaments, Round ligaments, Pelvic floor muscles (levator ani)

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v) Staging of Cervical Carcinoma (FIGO 2018)

Source: Grainger & Allison's Diagnostic Radiology

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vi) Bartholin Cyst

• Arise from occlusion of the Bartholin duct (greater vestibular gland) with accumulation of mucus
• Located at 4 and 8 o'clock positions of the posterior vulva
• Usually asymptomatic when small; painful if infected (Bartholin abscess)

• Rapid, painful inflammatory enlargement; most common pathogen is polymicrobial (E. coli, Staphylococcus); STIs (N. gonorrhoeae, Chlamydia) in younger women
• Features: Exquisitely tender, fluctuant swelling at base of labia minora; dyspareunia, difficulty walking

• Small asymptomatic cyst: Watchful waiting
• Word catheter - stab incision, insert bulb-tipped catheter, inflate balloon with 2-3 mL saline, leave for 4-6 weeks to allow epithelialization of a new duct
• Marsupialisation - surgical creation of permanent opening; preferred for recurrent cysts
• Excision - reserved for postmenopausal women (to exclude carcinoma) or recurrent failure
• Antibiotics for associated cellulitis; anti-gonococcal/chlamydia cover if STI suspected

Source: Berek & Novak's Gynecology; Roberts & Hedges' Clinical Procedures

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vii) Evaluation of Secondary Amenorrhea

Step 1 - Rule out common causes first:

• Pregnancy test (urine hCG) - always first
• History: Weight change, stress, exercise, medications (antipsychotics, OCP)
• Examination: BMI, signs of hyperandrogenism, thyroid, galactorrhea

Step 2 - Investigations:

Classification of Causes:

• Asherman syndrome (post-traumatic synechiae after D&C/infection)

• Primary ovarian insufficiency (POI) / Premature ovarian failure (POF < 40 yrs)
• Post-chemotherapy/radiation; autoimmune oophoritis
• If <25 years or <5 feet: karyotype + FMR1 (Fragile X premutation) testing

• Hyperprolactinemia (most common pituitary cause)
• Sheehan syndrome (postpartum pituitary necrosis)
• Acquired hypopituitarism (tumor, trauma)

• Functional hypothalamic amenorrhea: anorexia, excessive exercise, stress (competitive athletes, underweight women)
• Tumor or infiltrative disease

• Thyroid disease (hypo/hyperthyroidism)
• Cushing syndrome, adrenal disorders
• Drug-induced (antipsychotics, antidepressants, metoclopramide, OCPs)

Sources: Tietz Textbook of Laboratory Medicine; Berek & Novak's Gynecology; Goldman-Cecil Medicine

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DETAILED SHORT NOTES - GYNAECOLOGY

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i) FOLLICULAR STUDY (Folliculometry)

Definition

Anatomy Background

• A primary follicle at the start of the cycle measures ~2-5 mm
• Under FSH stimulation, one follicle becomes dominant (Graafian follicle) and grows at ~2 mm/day
• Pre-ovulatory Graafian follicle size: 18-24 mm (ovulation imminent)
• Ovulation occurs 34-36 hours after the LH surge

Protocol / When to Scan

Normal Findings on TVS

• Dominant follicle: 18-24 mm, thin wall, anechoic content
• Endometrial thickness: 8-12 mm, triple-line (trilaminar) pattern
• Cumulus oophorus: echogenic mound inside follicle (sign of impending ovulation)

• Sudden disappearance or collapse of follicle
• Irregular, echogenic follicle walls post-rupture
• Free fluid in Pouch of Douglas (POD) - follicular fluid
• Corpus luteum formation (thick-walled, hypoechoic structure)

Luteinized Unruptured Follicle Syndrome (LUFS)

• Follicle grows to full size but does NOT rupture
• LH surge occurs, progesterone rises - mimics normal ovulation
• USG: follicle persists beyond expected rupture time, becomes echogenic
• Cause of unexplained infertility

Clinical Uses

1. Infertility workup - confirm ovulatory cycles
2. Timing of intercourse - optimize natural conception
3. Timing of IUI - intrauterine insemination (done 36-40 hrs after hCG trigger)
4. Monitoring ovulation induction - with clomiphene citrate, letrozole, gonadotropins
5. IVF monitoring - superovulation (multiple follicle development monitored)
6. Diagnosing LUFS
7. Trigger injection timing - hCG (Ovidrel) given when dominant follicle ≥18 mm

Ovulation Trigger

• hCG 10,000 IU IM given when follicle 18-22 mm → ovulation expected 36-40 hours later
• Alternatively: GnRH agonist trigger used in IVF cycles to prevent OHSS

Complications of Ovulation Induction (Monitored by Folliculometry)

• Ovarian Hyperstimulation Syndrome (OHSS) - multiple large follicles, ascites, pleural effusion
• Multiple pregnancy - if >3 dominant follicles, cycle cancelled or converted to IVF
• Monitoring prevents these by allowing timely cycle cancellation

Source: Berek & Novak's Gynecology

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ii) PUBERTY MENORRHAGIA AND METROPATHIA HEMORRHAGICA

A. Puberty Menorrhagia (Dysfunctional Uterine Bleeding at Menarche)

Definition

Pathophysiology

• At menarche, the HPO axis is not yet fully mature
• Estrogen rises sufficiently to stimulate endometrial proliferation BUT there is no LH surge → no ovulation → no corpus luteum → no progesterone
• Sustained unopposed estrogen causes continuous, irregular endometrial proliferation
• Eventually, different portions of the endometrium outgrow their blood supply at different times → irregular, asynchronous shedding → heavy, prolonged, unpredictable bleeding
• Without progesterone, coiled arterioles do not develop properly → abnormal fragile vasculature → excessive bleeding

Clinical Features

• Occurs in girls aged 11-16 years, usually within 2 years of menarche
• Heavy, prolonged, painless (anovulatory = no dysmenorrhea) bleeding
• Irregular cycle intervals
• May cause significant anemia (pallor, dizziness, fatigue)
• No structural pathology

Diagnosis

• History + age
• Rule out coagulation disorders (von Willebrand disease - most common in this age group; platelet dysfunction, ITP)
• CBC - assess anemia, platelet count
• Coagulation profile: PT, aPTT, bleeding time, vWF antigen, ristocetin cofactor assay
• TSH, Prolactin - thyroid/pituitary causes
• Pregnancy test (even in teenagers)
• Pelvic USG - to exclude structural pathology

Management

• Reassurance - most anovulatory cycles self-correct within 2-3 years
• Tranexamic acid 1 g TDS during bleeding
• NSAIDs (Mefenamic acid) - reduce prostaglandin-mediated bleeding

• Combined OCP (Ethinyl estradiol 30 mcg + progestin) - first line
• Cyclic progestin (Norethisterone 5 mg BD/TDS for 10-14 days from day 16-25)

• High-dose combined OCP: 2-4 tablets/day for 3-4 days to stop bleeding, then taper
• IV conjugated estrogen (Premarin 25 mg IV) for acute severe bleeding
• Blood transfusion if Hb <7 g/dL
• Iron supplementation
• D&C (rare in adolescents - only if life-threatening and medical therapy fails)

• Cyclic OCPs for 3-6 months
• Levonorgestrel IUS (Mirena) - reduces menstrual blood loss by 90%

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B. Metropathia Hemorrhagica (Cystic Glandular Hyperplasia / Schroeder's Disease)

Definition

Aetiology

• Anovulatory cycles (perimenopausal, occasionally pubertal)
• Persistent follicular cysts secreting continuous estrogen
• No corpus luteum formed → no progesterone → no secretory transformation
• Obesity (peripheral conversion of androgens to estrone in adipose tissue)
• PCOS, granulosa cell tumours (estrogen-secreting)
• Exogenous unopposed estrogen therapy (HRT without progestin)

Pathophysiology

• Prolonged estrogen → endometrial proliferation → simple endometrial hyperplasia without atypia
• Glands become cystic and dilated - classic "Swiss cheese" appearance on histology
• Stroma remains adequate initially
• Eventually, outgrowth of blood supply → irregular, patchy shedding → heavy bleeding
• Ovaries: contain follicular cysts (no corpus luteum - absent due to anovulation)

Clinical Features (Classic Triad)

1. Period of amenorrhea (6-12 weeks) - due to sustained estrogen stimulation keeping endometrium intact
2. Followed by sudden onset of heavy, prolonged bleeding - as endometrium outgrows its blood supply
3. Uterus slightly enlarged and softer than normal; ovaries may be palpably enlarged with cysts

Diagnosis

• History (age: perimenopausal or adolescent)
• Pelvic USG: thickened, echogenic endometrium; follicular cysts in ovaries; no corpus luteum
• Endometrial biopsy / D&C - gold standard: shows simple cystic hyperplasia ("Swiss cheese" pattern)
• Hormone profile: estrogen elevated, progesterone absent/very low, FSH/LH anovulatory

Management

• High-dose progestin: Norethisterone 5 mg TDS x 7-10 days → controlled withdrawal bleed
• High-dose combined OCP (2-4 pills/day tapering over 7 days)

• Cyclic progestin (Provera 10 mg/day for 10-14 days per month) - prevents recurrence and cancer risk
• Combined OCP
• Levonorgestrel IUS - delivers local progestin, prevents hyperplasia

• D&C - diagnostic + therapeutic (removes hyperplastic endometrium)
• Endometrial ablation - for recurrent cases not wanting pregnancy
• Hysterectomy - if severe, recurrent, or atypia found (due to cancer risk)

Important: Untreated simple hyperplasia has ~1% risk of progressing to endometrial carcinoma; with atypia this rises to 8-29%.

Source: Robbins & Kumar Basic Pathology; Textbook of Family Medicine

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iii) POLYCYSTIC OVARY SYNDROME (PCOS)

Definition

Diagnostic Criteria (Rotterdam 2003 - 2 of 3 required):

1. Oligo-ovulation or anovulation (manifested as oligomenorrhea/amenorrhea)
2. Clinical or biochemical hyperandrogenism (hirsutism, acne, alopecia / elevated testosterone)
3. Polycystic ovaries on USG (≥12 follicles 2-9 mm per ovary OR ovarian volume >10 mL)

Pathophysiology

Insulin Resistance
        ↓
Hyperinsulinemia
        ↓
↑ Androgen production by theca cells (↑ LH stimulation)
        ↓
↑ LH : FSH ratio (classically >2:1 or >3:1)
        ↓
Follicles fail to mature → arrested at 2-9 mm (multiple small cysts)
        ↓
No dominant follicle → No LH surge → Anovulation
        ↓
No corpus luteum → No progesterone → Unopposed estrogen
        ↓
Risk of endometrial hyperplasia/carcinoma

• Elevated androgen → peripheral conversion to estrone → positive feedback on LH
• Hyperinsulinemia → reduces SHBG → more free (active) testosterone

Clinical Features

• Oligomenorrhea (cycles >35 days) or amenorrhea
• Anovulatory cycles
• Infertility (most common endocrine cause of infertility)

• Hirsutism (male-pattern hair growth - Ferriman-Gallwey score >8)
• Acne (often adult, jaw/chin distribution)
• Androgenic alopecia (frontal thinning)
• Rarely virilization (clitoromegaly) - suggests tumor

• Obesity (50-70%), especially central/abdominal
• Acanthosis nigricans (dark velvety skin in neck, axilla, groin) - marker of insulin resistance
• Metabolic syndrome (hypertension, dyslipidaemia, impaired glucose tolerance)
• Type 2 diabetes risk (3-7x higher)
• Cardiovascular risk increased

• Depression, anxiety, body image issues

Investigations

Management

• Even 5-10% weight loss restores ovulation in 55-80% of overweight PCOS women
• Reduces androgen, insulin, LH levels
• Low GI diet + aerobic exercise 150 min/week

• Combined OCP (preferred): regulates cycles, suppresses androgens, protects endometrium
  • Drospirenone (anti-androgenic progestin) containing OCPs preferred
• Cyclic progestin (Medroxyprogesterone 10 mg for 12-14 days every 1-3 months) - prevents hyperplasia

• Spironolactone 50-100 mg/day (antiandrogen - blocks androgen receptor)
• Cyproterone acetate (strong antiandrogen + progestin) - used in reverse sequential OCPs (Diane-35)
• Finasteride - 5-alpha reductase inhibitor
• Eflornithine cream - topical for facial hirsutism
• Laser/electrolysis for hair removal

• Metformin 500-1500 mg/day: reduces insulin resistance, restores menstruation, improves fertility; also reduces risk of type 2 diabetes
• Inositol (myo-inositol + D-chiro-inositol) - adjunct

• Letrozole (aromatase inhibitor) - NOW FIRST LINE (higher live birth rate than clomiphene)
  • 2.5-7.5 mg day 3-7 of cycle
• Clomiphene citrate 50-150 mg day 3-7: 60-85% ovulation rate; 15-20% pregnancy/cycle; 50% pregnant by 6 months
• Gonadotropins (FSH injections) - if clomiphene/letrozole fails; requires close monitoring (OHSS risk)
• Laparoscopic Ovarian Drilling (LOD) - electrocautery of ovarian surface destroys androgen-producing theca; restores FSH:LH balance; surgical equivalent of clomiphene; indicated when gonadotropins unavailable or fail; not for poor responders with low AMH

• Annual fasting glucose / HbA1c
• Lipid profile
• Blood pressure
• Endometrial surveillance (if amenorrheic for >3 months, do endometrial biopsy or progestin withdrawal)

Source: Berek & Novak's Gynecology; Robbins & Kumar; Textbook of Family Medicine; Swanson's Family Medicine

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iv) ETIOLOGY OF UTEROVAGINAL (UV) PROLAPSE

Definition

Normal Supports of the Uterus (What Gets Damaged)

• Cardinal (Mackenrodt's) ligaments - most important; transverse cervical ligaments
• Uterosacral ligaments

• Arcus tendinous fasciae pelvis (ATFP)
• Paravaginal fascial attachments

• Perineal body
• Superficial perineal muscles
• Levator ani complex (pubococcygeus, iliococcygeus, puborectalis)

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ETIOLOGY - Classified

1. Obstetric Causes (MOST COMMON)

• Multiparity - repeated childbirth overstretches pelvic floor
• Prolonged/obstructed labour - sustained pressure on supports
• Large baby (macrosomia) - overdistension of pelvic floor
• Precipitate delivery - sudden delivery tears supports
• Instrumental delivery (forceps/ventouse) - traction damages levator ani and fascial supports
• Unrepaired perineal tears (3rd/4th degree) - denervation of levator ani
• Bearing down before full cervical dilation - increases intra-abdominal pressure prematurely
• Delivery by traditional birth attendants without proper technique

2. Hormonal Causes

• Postmenopausal estrogen deficiency - atrophy of collagen and smooth muscle in pelvic supports
• Premature ovarian insufficiency
• Estrogen maintains collagen synthesis in ligaments and fasciae; loss leads to weakening

3. Congenital / Developmental

• Spina bifida - neuropathic bladder + weak pelvic floor
• Connective tissue disorders: Marfan syndrome, Ehlers-Danlos syndrome - defective collagen
• Congenital absence/weakness of pelvic floor muscles
• Nulliparous prolapse (rare, usually associated with CTD)

4. Causes Increasing Intra-Abdominal Pressure (IAP)

• Chronic cough (COPD, asthma, TB, smoking) - repetitive straining
• Chronic constipation - repeated Valsalva manoeuvre during straining
• Ascites - continuous raised IAP
• Obesity - chronic raised IAP + estrogen excess causing progesterone resistance
• Heavy occupational lifting - farmer women, labourers
• Pelvic masses - fibroid, ovarian cyst pushing uterus down

5. Iatrogenic

• Wertheim's / radical hysterectomy - division of uterosacral and cardinal ligaments → vault prolapse
• Simple hysterectomy without vault suspension → enterocele, vault prolapse
• Post-sacrospinous fixation without anterior repair

6. Neurological

• Spinal cord injury (L1-L2 level)
• Peripheral neuropathy (diabetic)
• Pudendal nerve damage during childbirth

7. Race / Ethnicity

• Less common in Asian and African women (stronger pelvic floor musculature, different collagen composition)
• More common in Caucasian women

Classification of Prolapse

• Cystocoele - anterior vaginal wall + bladder descent
• Urethrocoele - urethra descent
• Rectocoele - posterior vaginal wall + rectum descent
• Enterocoele - small bowel herniating into posterior vaginal wall (between rectum and vagina)
• Uterine prolapse - descent of uterus
• Vault prolapse - after hysterectomy

• 1st degree - Descent within vagina, cervix does not reach introitus
• 2nd degree - Cervix at the introitus
• 3rd degree (Procidentia) - Entire uterus outside the introitus; vagina inverted

Management Principles

• Conservative: Pelvic floor exercises (Kegel's), ring pessary (for elderly/unfit)
• Surgical: Pelvic floor repair (anterior/posterior colporrhaphy), Manchester repair (amputation of cervix + pelvic floor repair), vaginal hysterectomy + pelvic floor repair, sacrospinous fixation

Source: Berek & Novak's Gynecology; Campbell Walsh Wein Urology

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v) STAGING OF CERVICAL CARCINOMA (FIGO 2018)

Background

• Cervical carcinoma is staged clinically by FIGO (unlike endometrial which is surgically staged)
• The 2018 FIGO revision now also incorporates imaging and pathological findings (lymph node status)

FIGO 2018 Staging Table

Key MRI Findings (Grainger & Allison)

• Stage IB: Intermediate signal mass on T1WI; loss of normal low-signal stroma
• IIB: Disruption of low-signal cervical stromal ring; spiculated tumour-parametrium interface; uterine vessel encasement
• IIIA: Disruption of low-signal vaginal wall by high-signal tumour in lower 1/3
• IIIB: Tumour within 3 mm of pelvic sidewall; hydronephrosis
• IVA: Loss of perivesical/perirectal fat planes; disruption of normal low-signal bladder/rectal mucosa

Treatment Principles by Stage

Histological Types

• Squamous cell carcinoma - 70-75% (from squamocolumnar junction / transformation zone)
• Adenocarcinoma - 20-25% (glandular; HPV 18 associated; poorer prognosis)
• Adenosquamous - 3-5%

HPV Connection

• HPV 16 (squamous) and HPV 18 (adenocarcinoma) responsible for ~70% cases
• Prevention: HPV vaccination (Gardasil 9, Cervarix), cervical screening (Pap smear/HPV testing)

Source: Grainger & Allison's Diagnostic Radiology

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vi) BARTHOLIN CYST

Anatomy

• Bartholin's glands (greater vestibular glands) are paired, pea-sized glands located at the 4 o'clock and 8 o'clock positions of the posterior vaginal introitus
• They drain via small ducts (2.5 cm long) opening at the inner surface of the labia minora
• Function: secrete mucus for vaginal lubrication, especially during sexual arousal

Pathogenesis

• Occlusion of the Bartholin duct (not the gland itself initially) due to trauma, infection, or inflammation
• Secretions accumulate → mucus-filled cyst forms
• Infection of accumulated content (by bacteria) → Bartholin abscess

Causative Organisms (Abscess)

• Polymicrobial (most common): E. coli, Staphylococcus, Streptococcus, anaerobes
• STIs: Neisseria gonorrhoeae, Chlamydia trachomatis (especially in younger women)
• Note: gonorrhoea/chlamydia screen mandatory in sexually active women with Bartholin abscess

Clinical Features

• Usually asymptomatic if small (<1-2 cm)
• Smooth, soft, non-tender, fluctuant swelling at base of labia minora
• May cause dyspareunia or discomfort when large

• Rapidly enlarging, acutely painful swelling
• Marked tenderness, erythema, warmth, oedema of overlying skin
• Dyspareunia, difficulty walking or sitting
• Fever and systemic symptoms in severe cases
• May spontaneously rupture (temporary relief, often recurs)

Differential Diagnosis

• Sebaceous cyst, lipoma, fibroma of vulva
• Skene's duct cyst (near urethral meatus)
• Gartner's duct cyst (lateral vaginal wall)
• In postmenopausal women: Bartholin gland carcinoma (must exclude - any new Bartholin lump in women >40 years warrants biopsy)

Management

• Sitz baths, watchful waiting (may resolve spontaneously)

1. Word catheter (most common, outpatient procedure):
   • Incision: Small stab wound (1.5 cm) through mucosa at inner labia minora
   • Bulb-tipped catheter (Word catheter) inserted into cavity
   • Balloon inflated with 2-3 mL saline
   • Catheter left in place 4-6 weeks → epithelialization of a new permanent duct opening
   • Simple, quick, effective; high success rate (~80%)
2. Marsupialization (preferred for recurrent cysts):
   • Elliptical incision over cyst wall
   • Cyst wall sutured to skin edges → creates permanent opening
   • Performed under local/regional anaesthesia
   • Lower recurrence rate than Word catheter
3. Excision of Bartholin gland:
   • Complete surgical removal of gland
   • Reserved for: recurrent failure, postmenopausal women (exclude carcinoma), suspicion of malignancy
   • Higher complication rate: scarring, haematoma, fibrosis, loss of secretion → dyspareunia
4. Antibiotics:
   • Not effective alone for abscess (poor penetration into purulent collection)
   • Used as adjuncts if surrounding cellulitis, fever, or STI identified
   • Cefixime + Doxycycline (if gonorrhoea/chlamydia suspected)
   • Amoxicillin-clavulanate for polymicrobial cover

Source: Berek & Novak's Gynecology; Roberts & Hedges' Clinical Procedures in Emergency Medicine

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vii) EVALUATION OF SECONDARY AMENORRHEA

Definition

• Secondary amenorrhea: Absence of menstruation for ≥3 consecutive months in a woman with previously regular cycles, OR ≥6 months in a woman with previously irregular cycles.
• Differs from primary amenorrhea (never menstruated by age 15/16 with/without secondary sexual characteristics).

Prevalence

• Affects approximately 3-4% of reproductive-age women (excluding pregnancy)

Causes (Compartment-Based Classification)

Step-by-Step Evaluation

Step 1: History

• Menstrual history: last period, cycle history, contraceptive use
• Weight changes (gain/loss), eating habits, exercise level
• Stress, psychological history
• Galactorrhea → hyperprolactinemia
• Hot flashes, night sweats → ovarian failure (POI)
• Headache, visual field changes → pituitary tumour
• Hirsutism, acne, weight gain → PCOS or CAH
• Recent pregnancy, postpartum haemorrhage, D&C → Sheehan's, Asherman's
• Medications: antipsychotics, antiemetics, OCPs recently stopped

Step 2: Physical Examination

• BMI and weight
• Signs of androgen excess: hirsutism (Ferriman-Gallwey score), acne, clitoromegaly
• Galactorrhea (gently express breast secretion)
• Thyroid enlargement
• Cushingoid features (buffalo hump, central obesity, purple striae)
• Visual fields (bitemporal hemianopia → pituitary macro-adenoma)
• Pelvic exam: uterine size, cervical os patency

Step 3: Initial Investigations

Step 4: Interpret FSH/LH Results

Step 5: Progestin Challenge Test

• Give Medroxyprogesterone acetate 10 mg/day x 10 days (or Norethisterone 5 mg BD x 5 days)
• Withdrawal bleed within 2-7 days = POSITIVE:
  • Adequate estrogen present, uterus intact, ovulatory tract open
  • Cause is anovulation (PCOS, hypothalamic anovulation)
• No withdrawal bleed = NEGATIVE:
  • Either low estrogen (pituitary/hypothalamic failure or POI) OR
  • Outflow tract obstruction (Asherman syndrome, cervical stenosis)
  • Proceed to estrogen-progestin challenge

Step 6: Estrogen-Progestin Challenge (if progestin challenge negative)

• Give Conjugated estrogen 1.25 mg/day x 21 days + Medroxyprogesterone 10 mg x 5 days
• Bleed = outflow tract patent, low estrogen state (central/pituitary/ovarian cause)
• No bleed = Asherman syndrome (intrauterine adhesions / uterine outflow obstruction)

Step 7: Further Investigations Based on Results

Management Overview by Cause

Source: Tietz Textbook of Laboratory Medicine; Berek & Novak's Gynecology; Goldman-Cecil Medicine; Textbook of Family Medicine

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SHORT NOTES — GYNAECOLOGY

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i) FOLLICULAR STUDY (Folliculometry)

• Day 2-3: Baseline scan (AFC, ovarian volume, rule out cysts)
• Day 8-10: First monitoring scan
• Daily scans when follicle >14 mm
• Pre-ovulatory follicle: 18-24 mm

• Follicle disappears or collapses
• Free fluid in Pouch of Douglas
• Corpus luteum formation (thick-walled, hypoechoic)
• Endometrium: trilaminar, 8-12 mm (optimal)

• Time intercourse / IUI / hCG trigger
• Monitor ovulation induction (Clomiphene, Letrozole, Gonadotropins)
• Diagnose LUFS (follicle grows but never ruptures — cause of unexplained infertility)
• IVF superovulation monitoring

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ii) PUBERTY MENORRHAGIA & METROPATHIA HEMORRHAGICA

A. Puberty Menorrhagia

• Immature HPO axis → no LH surge → anovulation → no progesterone
• Unopposed estrogen → continuous endometrial proliferation → asynchronous, irregular shedding → heavy bleeding

• Exclude coagulation disorders (von Willebrand disease — most common in teens)
• CBC, coagulation profile, TSH, pregnancy test, pelvic USG

• Mild (Hb >10): Tranexamic acid, NSAIDs
• Moderate (Hb 8-10): Combined OCP or cyclic progestin (Norethisterone 5 mg TDS x 10 days)
• Severe (Hb <8): High-dose OCP (4 pills/day tapering), IV estrogen, blood transfusion if needed; iron supplementation

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B. Metropathia Hemorrhagica

1. Amenorrhea (6-12 weeks)
2. Sudden onset heavy prolonged bleeding
3. Slightly enlarged soft uterus; follicular cysts in ovaries (no corpus luteum)

• Acute: Norethisterone 5 mg TDS x 10 days → controlled withdrawal bleed
• Long-term: Cyclic progestin 4x/year OR combined OCP OR LNG-IUS
• D&C: diagnostic + therapeutic
• Endometrial ablation / hysterectomy for recurrent cases

Note: Untreated → ~1% risk of endometrial carcinoma (higher if atypia present)

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iii) PCOS (Polycystic Ovary Syndrome)

1. Oligo/anovulation
2. Clinical/biochemical hyperandrogenism
3. Polycystic ovaries on USG (≥12 follicles 2-9 mm OR volume >10 mL)

• Insulin resistance → hyperinsulinemia → ↑ androgen production by theca cells
• ↑ LH : FSH ratio (>2:1) → arrested follicular development → multiple small cysts
• No dominant follicle → anovulation → unopposed estrogen → endometrial hyperplasia risk

• Irregular/absent periods, infertility (most common endocrine cause)
• Hirsutism, acne, androgenic alopecia
• Obesity, acanthosis nigricans (insulin resistance marker)
• Long-term: T2DM, metabolic syndrome, cardiovascular risk, endometrial carcinoma

• USG: "necklace sign" / ≥12 follicles / ovarian volume >10 mL
• LH:FSH >2:1; ↑ testosterone; ↓ SHBG; ↑ AMH
• Fasting glucose + insulin (HOMA-IR); HbA1c; lipid profile
• Exclude: thyroid disease (TSH), hyperprolactinemia, CAH (17-OHP)

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iv) ETIOLOGY OF UTEROVAGINAL PROLAPSE

• Cardinal (Mackenrodt's) ligaments — most important
• Uterosacral ligaments
• Levator ani muscles (especially pubococcygeus)
• Pubocervical and rectovaginal fascia

• 1st: Descent within vagina, cervix doesn't reach introitus
• 2nd: Cervix at introitus
• 3rd (Procidentia): Entire uterus outside introitus

• Conservative: Pelvic floor (Kegel) exercises, ring pessary
• Surgical: Pelvic floor repair, Manchester repair, vaginal hysterectomy + pelvic floor repair

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v) STAGING OF CERVICAL CARCINOMA (FIGO 2018)

• IA1: Cone biopsy or simple hysterectomy
• IA2-IB2: Radical hysterectomy (Wertheim's) + pelvic lymph node dissection
• IB3-IVA: Concurrent cisplatin-based chemoradiation
• IVB: Palliative chemotherapy ± bevacizumab

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vi) BARTHOLIN CYST

• Cyst: Smooth, soft, non-tender swelling at base of labia; may cause dyspareunia if large
• Abscess: Acutely painful, rapidly enlarging, tender, erythematous; fever; difficulty walking/sitting

Important: Any new Bartholin swelling in a woman >40 years → biopsy to exclude Bartholin gland carcinoma.

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vii) EVALUATION OF SECONDARY AMENORRHEA

• TSH → hypothyroidism/hyperthyroidism
• Prolactin → hyperprolactinemia
• FSH + LH + Estradiol → localise level of problem

• High FSH (>40) → Ovarian failure (POI) → karyotype if <25 yrs; FMR1 screening
• Low FSH + Low E2 → Hypothalamic/pituitary cause → MRI brain/pituitary
• Normal FSH + Normal E2 → Anovulation (PCOS, thyroid) or outflow tract problem

• Norethisterone 5 mg BD x 5 days
• Bleed (+): Adequate estrogen, intact uterus → anovulatory cause (PCOS, hypothalamic)
• No bleed (-): Low estrogen state OR Asherman syndrome → proceed to estrogen-progestin challenge

• Bleed: Outflow patent → low estrogen (central/ovarian cause)
• No bleed: Asherman syndrome → hysteroscopy (gold standard for diagnosis + treatment)

• Elevated prolactin → MRI pituitary (prolactinoma)
• High androgens → 17-OHP (CAH), DHEAS (adrenal tumour)
• Suspected Cushing → overnight dexamethasone suppression test

• PCOS → Metformin + OCP
• Hyperprolactinemia → Cabergoline (dopamine agonist)
• Hypothyroidism → Levothyroxine
• POI → HRT (bone + cardiovascular protection); donor egg IVF for fertility
• Asherman → Hysteroscopic adhesiolysis + postoperative estrogen
• Functional hypothalamic → Weight restoration, reduce exercise, psychological support

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