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How to Use These Answers for Exam Preparation

• Diagonal conjugate = 12.5 cm (only pelvic measurement done clinically; subtract 1.5 cm = obstetric conjugate)
• Caput vs Cephalohematoma: Caput crosses sutures + present at birth + resolves 24-48 hrs; Cephalo does NOT cross sutures + appears after 12-24 hrs + lasts 6-8 weeks
• Mechanism of labour = 9 steps; internal rotation at ischial spines is the key step
• MTX for ectopic: 50 mg/m² single dose IM; hCG <5000, mass <3.5 cm, no cardiac activity
• PPROM complications: Chorioamnionitis, cord prolapse, neonatal sepsis, pulmonary hypoplasia
• Spalding sign = overlapping skull bones on X-ray = IUFD (appears 5-7 days after death)
• Betamethasone 12 mg x2 doses 24 hrs apart for fetal lung maturity in preterm (<34 weeks)

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SECTION 1: PRIMARY AMENORRHOEA (SN / LQ)

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Definition

• Age 14 years with no secondary sexual characteristics (breast development, pubic/axillary hair), OR
• Age 16 years with normal secondary sexual characteristics present

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Classification & Causes

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A. SSC Absent + Uterus Present

• Kallmann syndrome (GnRH deficiency + anosmia) - most important
• Constitutional delay of puberty (most common cause of primary amenorrhoea overall)
• Hypothalamic suppression: anorexia nervosa, excessive exercise, stress, chronic illness
• Space-occupying lesions: craniopharyngioma, glioma

• Hypopituitarism (Sheehan's, pituitary tumors)
• Isolated FSH/LH deficiency
• Hyperprolactinemia (prolactinoma)

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B. SSC Absent + Uterus Absent (or abnormal)

• Turner syndrome (45,XO) - most important; streak gonads, short stature, webbed neck, shield chest, widely spaced nipples, primary amenorrhoea
• Gonadal dysgenesis (46,XX or 46,XY)
• Swyer syndrome (46,XY pure gonadal dysgenesis) - XY female with streak gonads; normal female external genitalia, tall stature, no SSC
• Premature ovarian failure
• Resistant ovary syndrome

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C. SSC Present + Uterus Absent

• Androgen insensitivity syndrome (AIS / Testicular feminization) - 46,XY; normal female external genitalia, good breast development, absent/scanty pubic & axillary hair, blind vaginal pouch, no uterus, no fallopian tubes; testes intra-abdominal
• Mayer-Rokitansky-Kuster-Hauser (MRKH) syndrome - 46,XX; absent uterus and upper vagina; normal ovaries and SSC; most common cause of amenorrhoea with absent uterus in otherwise normal female

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D. SSC Present + Uterus Present (Outflow Tract Obstruction)

• Imperforate hymen (most common outflow cause) - cyclic pelvic pain, bluish bulge at introitus, hematocolpos → hematometra → hematosalpinx
• Transverse vaginal septum
• Cervical atresia/stenosis
• Cryptomenorrhoea

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E. SSC Present + Normal Pelvic Anatomy (Endocrine causes)

• PCOS (polycystic ovary syndrome)
• Congenital adrenal hyperplasia (CAH) - 21-hydroxylase deficiency
• Thyroid disorders (hypothyroidism)
• Hyperprolactinemia
• Cushing syndrome

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Investigations

1. History & Examination: Growth, SSC, sense of smell (Kallmann), stigmata of Turner
2. Karyotype (essential in all primary amenorrhoea)
3. Hormonal profile: FSH, LH, Estradiol, Prolactin, TSH, Free T4, DHEAS, Testosterone, Progesterone
4. USG pelvis/abdomen: Uterus, ovaries, streak gonads
5. X-ray wrist: Bone age assessment
6. MRI brain: If pituitary/hypothalamic pathology suspected
7. Diagnostic laparoscopy: Gonadal morphology if gonadal dysgenesis suspected
8. Progesterone withdrawal test: If positive (bleeding) = adequate estrogen + intact outflow

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Management

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SECTION 2: SECONDARY AMENORRHOEA (SN / LQ)

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Definition

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Causes (DC Dutta Classification)

A. Physiological

• Pregnancy (most common cause)
• Lactation (hyperprolactinemia)
• Menopause

B. Hypothalamic causes (most common pathological group)

1. Functional Hypothalamic Amenorrhoea (FHA) - most common:
   • Weight loss / anorexia nervosa / bulimia
   • Excessive exercise (athlete's amenorrhoea)
   • Psychological stress
   • Chronic systemic illness
   • Mechanism: GnRH pulsatility disturbed → low FSH/LH → low estrogen
2. Hypothalamic tumors (craniopharyngioma)
3. Post-pill amenorrhoea (rare; usually resolves in 3-6 months)

C. Pituitary causes

1. Hyperprolactinemia (most common pituitary cause):
   • Prolactinoma (microadenoma/macroadenoma)
   • Drug-induced (phenothiazines, metoclopramide, domperidone, methyldopa, antipsychotics)
   • Hypothyroidism (elevated TRH stimulates prolactin)
   • Mechanism: Prolactin inhibits GnRH pulsatility
2. Sheehan's syndrome (postpartum pituitary necrosis - most important in developing countries):
   • Follows PPH + circulatory collapse
   • Failure of lactation, loss of pubic/axillary hair, fatigue, amenorrhoea
3. Simmond's disease (hypopituitarism from other causes)
4. Pituitary tumors, empty sella syndrome

D. Ovarian causes

1. Premature Ovarian Insufficiency/Failure (POI/POF): Before age 40; high FSH/LH, low estrogen; causes: autoimmune, fragile X premutation, iatrogenic (radiation, chemotherapy), idiopathic
2. PCOS (most common endocrine cause of amenorrhoea in reproductive age):
   • Hyperandrogenism, anovulation, polycystic ovaries (Rotterdam criteria: 2 of 3)
   • LH:FSH ratio >2:1, raised androgens, raised LH
3. Resistant ovary syndrome (Savage syndrome)
4. Radiation/chemotherapy damage

E. Uterine causes (Outflow tract)

1. Asherman's syndrome (Intrauterine adhesions / synechiae):
   • Most important uterine cause
   • Follows vigorous curettage (post-abortal, post-partum), endometritis, uterine TB
   • Diagnosis: Hysterosalpingography (filling defects), hysteroscopy (gold standard)
   • Treatment: Hysteroscopic adhesiolysis + estrogen therapy + IUD/Foley catheter to prevent re-adhesion
2. Cervical stenosis (post-conization, LLETZ)
3. Genital tuberculosis (TB endometritis → Asherman's)

F. Systemic / Endocrine causes

1. Hypothyroidism
2. Hyperthyroidism
3. Cushing syndrome (excess cortisol → inhibits GnRH)
4. Congenital adrenal hyperplasia (late-onset)
5. Severe anemia, malnutrition, chronic renal/hepatic failure

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Investigations

• Prolactin (if elevated → prolactinoma workup)
• TSH (thyroid disease)
• FSH/LH:
  • High FSH/LH → ovarian failure (POI)
  • Low/normal FSH/LH → hypothalamic/pituitary cause
• Estradiol
• Testosterone, DHEAS (if signs of hyperandrogenism)

• Give medroxyprogesterone acetate 10 mg OD x 5 days
• Withdrawal bleed = adequate estrogen, patent outflow → PCOS/hypothalamic likely
• No bleed = either low estrogen OR outflow obstruction → Estrogen-progesterone test

• Conjugated estrogen 1.25 mg/day x 21 days + progesterone last 5 days
• Bleed = outflow intact; etiology is endocrine (hypothalamic/pituitary/ovarian)
• No bleed = outflow obstruction (Asherman's, cervical stenosis)

• USG pelvis (ovarian morphology, endometrial thickness, uterus)
• MRI pituitary (if prolactin high, visual field defects)
• Hysteroscopy / HSG (if Asherman's suspected)

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Management

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SECTION 3: DEFENCE MECHANISMS OF THE FEMALE GENITAL TRACT

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1. Vulva and Vaginal Introitus

• Labial apposition of labia majora physically covers the introitus
• Intact perineum and hymen act as mechanical barriers

2. Vaginal Defence Mechanisms

• Vaginal epithelium: Thick stratified squamous epithelium acts as a physical barrier
• Doderlein's bacilli (Lactobacillus acidophilus):
  • Dominant commensal organisms
  • Break down glycogen in desquamated epithelial cells → lactic acid
  • Maintain vaginal pH at 3.8-4.5 (acidic) - inhibits most pathogens
  • Also produce hydrogen peroxide which is bactericidal
• Acidic pH: Hostile to most pathogenic bacteria (Gonococci, E. coli, Staphylococci)
• Vaginal secretions: Bacteriostatic properties; flow of secretion is self-cleansing

• Postmenopausal state (reduced estrogen → thin epithelium, reduced glycogen, raised pH)
• Broad-spectrum antibiotics (kill Lactobacilli → overgrowth of Candida, BV organisms)
• Excessive douching
• Foreign bodies
• Diabetes mellitus (excess glucose)

3. Cervical Defence Mechanisms

• Cervical mucus plug:
  • Thick, tenacious mucus fills the endocervical canal
  • Contains IgA, lysozyme, lactoferrin, peroxidase - antimicrobial proteins
  • Acts as a mechanical and immunological barrier
  • Becomes permeable only at ovulation (under estrogen influence) and in menstruation (plug shed)
• Alkaline cervical mucus neutralizes descending semen and ascending organisms
• Cervical crypts contain immunoglobulin-secreting plasma cells

4. Uterine Defence

• Endometrial shedding during menstruation removes organisms and infected endometrium
• Endometrial secretions contain IgA, IgG, lysozyme
• Myometrial contractions during menstruation expel organisms
• Endocervical columnar epithelium is normally resistant to many pathogens

5. Tubal Defence

• Ciliary action of fallopian tube epithelium moves secretions downward (away from peritoneum)
• Peristaltic contractions of tube propel ovum/secretions toward uterus
• Peritoneal macrophages at the fimbriated end engulf organisms

6. Peritoneal Defence

• Peritoneum and omentum wall off infection (pelvic peritonitis localized by omentum)
• Peritoneal macrophages and WBCs provide cellular immunity

• Disruption at menstruation/delivery/abortion
• Excess organisms (STI)
• Immunocompromised host (HIV, diabetes, steroids)

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SECTION 4: MODE OF INFECTION IN SALPINGITIS

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1. Ascending (Canalicular) Infection - MOST COMMON

• Organisms travel from the vagina/cervix → endocervical canal → endometrium (endometritis) → fallopian tubes → peritoneum
• Organisms: Neisseria gonorrhoeae, Chlamydia trachomatis (most common), Mycoplasma genitalium
• Facilitated by:
  • Menstruation (mucus plug shed, alkaline blood media)
  • IUCD insertion (string acts as wick)
  • Uterine instrumentation (D&C, hysterosalpingography, hysteroscopy)
  • Post-abortal state
  • Post-partum state
  • Ovulation (cervical os open, mucus less viscid)
  • Sexual intercourse (organisms propelled upward by uterine contractions)

2. Lymphatic Spread

• From parametrium or from adjacent pelvic organs
• Organisms: Streptococci, Staphylococci, E. coli (non-STI organisms)
• Seen after: septic abortion, puerperal sepsis, appendicitis, pelvic surgery
• The lymphatics carry organisms from adjacent organs (appendix, sigmoid) to the tubes and parametrium

3. Haematogenous Spread

• Least common route for PID
• Important exception: Tuberculosis - always reaches the genital tract haematogenously (from a primary focus in the lung)
• Blood carries organisms to the tubes → tubes are the first and most commonly affected organ in genital TB

4. Direct Spread (Contiguous)

• From adjacent organs: acute appendicitis, diverticulitis, Crohn's disease, sigmoid diverticulosis
• Organisms spread through the peritoneum to the pelvic organs

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SECTION 5: PELVIC ABSCESS (1990 LQ)

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Definition

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Aetiology

• Aerobic: Gonococci, Chlamydia, E. coli, Streptococcus, Staphylococcus, Klebsiella
• Anaerobic (majority in TOA): Bacteroides fragilis, Peptostreptococcus, Fusobacterium
• Gram-negative anaerobes predominate in established abscess

1. Previous PID / chronic salpingitis
2. IUCD use
3. Multiple sexual partners / STIs
4. Post-abortal / post-partum sepsis
5. Appendicitis/diverticulitis (secondary spread)
6. Pelvic surgery
7. Immunocompromised states (HIV, diabetes)

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Clinical Features

• Pain: Constant, severe lower abdominal and pelvic pain (bilateral/unilateral)
• Fever: High-grade, spiking temperature with chills/rigors
• Vaginal discharge: Purulent, foul-smelling
• Nausea, vomiting
• Dyspareunia
• Dysuria, frequency (if bladder irritation)
• Tenesmus (if rectal pressure)
• History of previous PID or recent instrumentation

• Toxic, ill-looking patient
• Fever (>38°C), tachycardia
• Lower abdominal tenderness, guarding, rigidity
• Bimanual examination:
  • Cervical excitation tenderness (marked)
  • Uterus tender, fixed
  • Tender pelvic mass in adnexa/POD - ill-defined, doughy, tender
  • Bogginess/fullness in posterior fornix
• If rupture: generalized peritonitis (board-like abdomen, signs of septicemic shock)

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Investigations

1. CBC: Raised WBC (>15,000) with neutrophilia, raised ESR, CRP
2. Cervical/high vaginal swab: C&S, NAAT for Gonococci and Chlamydia
3. Blood cultures (if septicemic)
4. Urine R&M + C&S (exclude UTI)
5. Serum beta-hCG (exclude ectopic)
6. Ultrasound pelvis (TVS preferred):
   • Thick-walled, complex adnexal mass with internal echoes
   • Cog-wheel sign (thickened tube walls)
   • Free fluid in POD
   • Most reliable non-invasive investigation
7. CT scan pelvis: More accurate for defining extent, relationships to adjacent structures; used if USG inconclusive or for surgical planning
8. Diagnostic laparoscopy: Definitive diagnosis (and can aspirate/drain)
9. Culdocentesis (posterior colpotomy for pus): Diagnostic and therapeutic if abscess points into posterior fornix

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Management

A. Conservative (Antibiotic) Management

• IV Cefoxitin 2g q6h + IV Doxycycline 100 mg q12h

• IV Clindamycin 900 mg q8h + IV Gentamicin 1.5 mg/kg q8h (or 5 mg/kg OD)

• IV Ampicillin + IV Metronidazole + IV Gentamicin ("triple therapy")

• IV fluids, analgesics, antipyretics
• Rest, nil orally if peritonism
• Monitor WBC, CRP, temperature curve

B. Interventional (Image-guided Drainage)

• USG-guided or CT-guided percutaneous/transvaginal drainage
• Preferred in stable patients where surgery carries high morbidity
• Aspirate pus, send for C&S, instill antibiotics locally

C. Surgical Management

1. Ruptured/leaking abscess (emergency - peritonitis, septic shock)
2. Failure of antibiotics + drainage (no improvement in 72-96 hrs)
3. Large abscess (>9 cm) not amenable to drainage
4. Diagnostic uncertainty (exclude malignancy, appendicitis)

• If abscess is pointing into posterior fornix (Douglas's pouch)
• Incision in posterior vaginal fornix → drain pus → leave drain in situ
• Indicated only when abscess is midline, adherent to vaginal vault, fluctuant

• Midline incision preferred (better access)
• Procedure: Drain abscess, peritoneal lavage (normal saline)
• Conservative: Unilateral salpingo-oophorectomy (if other tube and ovary normal) - preserve fertility in young patients
• Radical: Total hysterectomy + bilateral salpingo-oophorectomy (BSO) - if bilateral disease, recurrent TOA, perimenopausal patient, or no desire for fertility
• Leave drain in POD
• Post-op IV antibiotics continued

• Drainage, adhesiolysis, peritoneal lavage
• Suitable if technically feasible (no dense adhesions, no rupture)

• Complete 14-day antibiotic course
• Treat partner (for STI cause)
• Follow-up USG after 6 weeks

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SECTION 6: CHRONIC SALPINGITIS (1987 LQ) - Complications & Management

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Definition

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Pathological Changes

• Tubes thickened, fibrous, with peritubal adhesions
• Tubal lumen may be:
  • Hydrosalpinx: Distended with clear fluid (fimbrial end occluded)
  • Pyosalpinx: Distended with pus (persisting from acute phase)
  • Sactosalpinx: Generic term for distended (fluid-filled) tube
• Tubo-ovarian mass (tube + ovary matted together)
• Peritubal and periovarian adhesions ("frozen pelvis" in severe cases)

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Complications of Chronic Salpingitis

1. Infertility (Most common and important)

• Bilateral tubal block (commonest cause of tubal factor infertility)
• Peritubal adhesions prevent oocyte pickup
• Ciliary destruction prevents sperm/ovum transport
• ~15-20% risk per episode of PID; rises to 75% after 3+ episodes

2. Ectopic Pregnancy

• Partial tubal occlusion + damaged cilia → fertilized ovum implants in tube
• Risk increased 6-10 times after one episode of salpingitis

3. Chronic Pelvic Pain (CPP)

• Due to hydrosalpinx, adhesions, pelvic congestion
• Dysmenorrhoea (acquired secondary dysmenorrhoea)
• Dyspareunia (deep)

4. Hydrosalpinx

• Fimbriae sealed, secretion accumulates → tube distends with watery fluid
• May twist (torsion)
• Reduces IVF success rates (toxic fluid refluxes into uterus)

5. Pyosalpinx / Tubo-Ovarian Abscess

• Reactivation of chronic infection → acute-on-chronic flare

6. Pelvic Peritonitis

• Rupture of pyosalpinx → acute peritonitis

7. Tubo-ovarian Mass

• Dense adhesions bind tube, ovary, bowel, omentum

8. Intestinal Obstruction

• Bowel involvement in adhesions

9. Menstrual Disturbances

• Menorrhagia, irregular cycles due to hormonal disruption

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Management of Chronic Salpingitis

A. General Measures

• Treat sexual partner simultaneously
• Investigate for STI (Chlamydia, Gonorrhoea - NAAT from cervix/urine)
• Pelvic rest during acute exacerbations

B. Medical Treatment

• Long-term low-dose antibiotics for recurrent flares
• Doxycycline 100 mg BD for Chlamydia (4-6 weeks in chronic disease)
• NSAIDs for pain (chronic pelvic pain)
• OCP (regularizes cycles, reduces dysmenorrhoea)

C. Management of Complications

• Tubal surgery (tuboplasty):
  • Salpingolysis: Release of peritubal adhesions (laparoscopic)
  • Fimbriolysis/Salpingostomy: Open blocked fimbriated end
  • Tubal cannulation (fluoroscopic/hysteroscopic): For proximal block
  • Success rates poor for distal disease
• IVF-ET: Treatment of choice when tubes are severely damaged; salpingectomy of hydrosalpinx before IVF improves success rates (NICE guideline)

• Salpingectomy (preferred before IVF) or proximal tubal ligation

• Adhesiolysis (laparoscopic)
• LUNA (laparoscopic uterosacral nerve ablation) - limited evidence
• Hysterectomy + BSO (last resort in completed family)

• IV antibiotics → drainage/salpingectomy

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SECTION 7: PELVIC INFLAMMATORY DISEASE (1987 LQ) - Investigations & Management

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Definition

Investigations

A. Minimum Criteria for Diagnosis (CDC):

• Uterine tenderness, OR
• Adnexal tenderness, OR
• Cervical motion (excitation) tenderness

• Temperature >38.3°C
• Abnormal cervical/vaginal mucopurulent discharge
• Presence of WBCs on vaginal wet prep
• Elevated CRP/ESR
• Positive NAAT for gonococci or chlamydia

B. Laboratory Investigations

1. NAAT (Nucleic Acid Amplification Test): Endocervical/vaginal swab for Chlamydia trachomatis and Neisseria gonorrhoeae - most important
2. High vaginal swab (HVS) C&S - for other organisms
3. CBC: Leukocytosis, raised ESR, CRP
4. Blood cultures if severe/septicemic
5. Urine R&M + C&S (exclude UTI)
6. Serum beta-hCG (exclude ectopic pregnancy - critical)
7. HIV, syphilis serology (screen for other STIs)

C. Imaging

1. USG pelvis (TVS): Thickened tubes, free pelvic fluid, TOA; "cogwheel sign" (thickened tube), "incomplete septum sign" (pyosalpinx)
2. MRI pelvis: Superior soft tissue delineation; confirms TOA, differentiates from other masses

D. Invasive Investigations

1. Laparoscopy (gold standard):
   • Direct visualization of tubes (erythema, edema, purulent exudate on tubes)
   • Allows sampling for culture
   • Confirms diagnosis when in doubt; differentiates from appendicitis, ectopic
   • Used when diagnosis uncertain or no response to treatment
2. Endometrial biopsy: Histological evidence of endometritis (plasma cells in endometrium)

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Management of PID

Outpatient (Mild-to-Moderate, No TOA)

• IM Ceftriaxone 500 mg single dose + Oral Doxycycline 100 mg BD x 14 days + Metronidazole 400 mg BD x 14 days

• Oral Ofloxacin 400 mg BD + Metronidazole 400 mg BD x 14 days (only if gonorrhoea prevalence low and NAAT negative)

• Ampicillin + Metronidazole + Doxycycline orally

Inpatient Indications (ADMIT):

1. Diagnosis uncertain (exclude ectopic, appendicitis, ovarian torsion)
2. TOA suspected/confirmed
3. Failure to respond to oral antibiotics in 72 hrs
4. Severe illness (high fever, nausea/vomiting, unable to tolerate oral)
5. Pregnancy
6. Adolescent (compliance concern)
7. HIV-positive patient

Inpatient (IV Regimens)

• IV Cefoxitin 2g q6h + IV Doxycycline 100 mg q12h → oral Doxycycline 100 mg BD + Metronidazole 400 mg BD to complete 14 days

• IV Clindamycin 900 mg q8h + IV Gentamicin (2 mg/kg loading then 1.5 mg/kg q8h) → oral Clindamycin 450 mg QID to complete 14 days

Additional Management

• Partner notification and treatment (trace, test, treat sexual contacts from last 6 months)
• Remove IUCD if no improvement within 72 hrs (controversial - benefit uncertain; remove if TOA or no improvement)
• Analgesia: NSAIDs (diclofenac, ibuprofen)
• Screen for other STIs (HIV, syphilis, hepatitis B)
• Safe sex counselling
• Follow-up at 72 hours to confirm clinical response
• Sexual abstinence until treatment complete + partner treated

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SECTION 8: TUBERCULOSIS OF THE GENITAL TRACT (SN)

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Definition

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Epidemiology

• Very common in India and developing countries
• Accounts for 10-15% of female infertility in India
• A silent disease - often asymptomatic for years
• Most patients are young (15-45 years)

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Route of Infection

• Always haematogenous from a primary pulmonary focus (during primary bacteraemia)
• The fallopian tubes are affected first (blood supply richest) in >90% of cases
• Then spreads to: Endometrium (50-60%), Ovaries (20-30%), Cervix (5-15%), Vagina/vulva (rare)
• Note: Primary genital TB (from direct inoculation - sexual contact with male partner with genital TB) is extremely rare

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Pathology

• Caseating granulomas with Langhans' giant cells + epithelioid cells + central caseation
• Tuberculous follicles
• Endometrium: Caseating granulomas (typically seen in premenstrual endometrium)

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Clinical Features

1. Infertility (primary infertility in 40-60% - most common presentation)
2. Menstrual disturbances:
   • Oligomenorrhoea → amenorrhoea (endometrial destruction/Asherman's)
   • Menorrhagia (early, active disease)
   • Hypomenorrhoea (fibrosis)
3. Chronic pelvic pain / dysmenorrhoea
4. Constitutional symptoms: Low-grade fever, evening rise of temperature, night sweats, weight loss, malaise (classical TB symptoms - often absent in genital TB)
5. Vaginal discharge (if cervical involvement)
6. Pelvic mass (tubo-ovarian mass, ascites)
7. Contact history with TB (household)

• Often minimal
• Pelvic tenderness (adnexal)
• Bilateral adnexal masses (matted, irregular, non-tender in chronic)
• Ascites (peritoneal TB) - "doughy abdomen"
• Cervical erosion/ulcer (if cervical TB)
• Uterus may be small, fixed

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Investigations

A. Bacteriological (Definitive)

1. Menstrual blood culture (MGIT - mycobacteria growth indicator tube): Culture for AFB - best specimen for genital TB
2. Endometrial biopsy / curettage (premenstrual): Histopathology (caseating granulomas) + AFB culture + PCR - Most reliable single investigation
3. Peritoneal fluid AFB culture and PCR (if ascites present)
4. Laparoscopic biopsy of peritoneum/tube for histology

B. Radiological

1. Chest X-ray: Look for primary focus (calcified hilar nodes, old TB lesion, pleural effusion, Ghon focus)
2. HSG (Hysterosalpingography):
   • Multiple filling defects, irregular ragged contour, "pipestem" tubes
   • "Golf club" deformity of tubes
   • Beading of tubes
   • Calcification in tubes
   • Asherman's pattern (intrauterine adhesions)
   • Risk of dissemination (relative contraindication in active TB - defer until treatment started)
3. USG/CT pelvis: Tubo-ovarian mass, ascites, calcification, liver/spleen lesions (miliary)

C. Immunological / Biochemical

1. Mantoux test (Tuberculin skin test): Positive (>10 mm induration at 48-72 hrs) suggests TB exposure; not diagnostic
2. IGRA (Interferon Gamma Release Assay - QuantiFERON-TB Gold): More specific than Mantoux; useful to exclude TB in non-endemic setting
3. PCR for MTB DNA on endometrial tissue/fluid - rapid, sensitive (Xpert MTB/RIF)
4. ESR: Raised (non-specific)
5. CA-125: May be elevated (mimics ovarian cancer) - useful to follow up

D. Diagnostic Laparoscopy

• Direct visualization: Tubercles on tubes, peritoneum, omentum
• Biopsy, peritoneal fluid for AFB culture
• Gold standard for confirmation

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Management

A. Anti-Tubercular Treatment (ATT) - Mainstay

• Isoniazid (H) + Rifampicin (R) + Pyrazinamide (Z) + Ethambutol (E) - 2HRZE

• Isoniazid (H) + Rifampicin (R) - 4HR (total 6 months)
• Extended to 9-12 months for genital TB (as response may be slower)

• Pyridoxine (Vit B6) 10 mg/day with Isoniazid (prevents peripheral neuropathy)
• Prednisolone 40 mg/day (tapering) - for severe peritubal adhesions, peritoneal TB with ascites (reduces fibrosis)

B. Monitoring During ATT

• Monthly LFTs (hepatotoxicity from H, R, Z)
• Baseline LFT, RFT, visual acuity (Ethambutol)
• Urine color turns orange-red (Rifampicin) - counsel patient
• Beta-hCG (if amenorrhoea resolves - may become pregnant during treatment)

C. Surgical Management

1. Tubo-ovarian mass not resolving after 9-12 months of ATT
2. Suspected malignancy
3. Pyosalpinx / abscess formation
4. Fistula formation
5. Persistent pelvic pain / chronic mass

• Must do surgery during/after ATT - never without prior ATT (risk of dissemination)

D. Fertility

• Only 5-15% achieve intrauterine pregnancy after ATT
• Reason: Irreversible tubal damage (fibrosis), endometrial fibrosis (Asherman's), ovarian involvement
• IVF-ET is the recommended option for fertility after successful ATT
• Even IVF success rates lower if endometrial disease (thin endometrium, Asherman's)
• Hysteroscopic adhesiolysis + estrogen priming can improve endometrial receptivity before IVF

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Summary Table: Genital TB vs PID

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Quick Exam Summary