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SECTION A: PELVIC ANATOMY & MEASUREMENTS

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Diagonal Conjugate (SN)

• Normal value: 12.5 cm
• It is measured by inserting two fingers vaginally, reaching the sacral promontory, and marking the point where the lower border of symphysis touches the examining hand
• Obstetric conjugate = Diagonal conjugate - 1.5 cm (subtracting for the thickness and inclination of the symphysis)
• If diagonal conjugate < 11.5 cm, the pelvis is likely contracted

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Obstetric Conjugate (2014 SN)

• Normal value: 10 cm (minimum: 10 cm)
• It cannot be measured directly; it is estimated as:
  • Diagonal conjugate - 1.5 cm, OR
  • Anatomical conjugate (true conjugate) - 0.5 to 1 cm
• It is the most important obstetric measurement because the fetal head must pass through this minimum space
• If <10 cm: contraction of pelvic inlet; CPD likely

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Obstetric Outlet (1996 SN)

• Anteriorly: Lower border of symphysis pubis
• Posteriorly: Tip of coccyx
• Laterally: Ischial tuberosities

1. Anterior triangle: Base = bi-ischial diameter; Apex = pubic arch
2. Posterior triangle: Base = bi-ischial diameter; Apex = tip of coccyx

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Plane of Least Pelvic Dimension (1995 SN)

• Anteriorly: Lower border of symphysis pubis
• Posteriorly: Junction of S4 and S5 vertebrae
• Laterally: Ischial spines (most important landmark)

• The bi-spinous diameter (10.5 cm) is the smallest diameter of the entire pelvis - hence "plane of least dimension"
• Prominent ischial spines = android tendency; may obstruct internal rotation
• Spines are palpated vaginally to assess engagement (station 0 = spines level)
• Midpelvic contraction is the most common cause of deep transverse arrest

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Lower Uterine Segment (LUS) (1995 SN)

• The isthmus (0.5 cm in non-pregnant state, between internal os and body of uterus) begins to form the LUS at ~12 weeks
• By term, the LUS is 7-10 cm long and extremely thin (2-3 mm)

• Passive, non-contractile segment (unlike the upper segment which is actively contractile)
• Thin, vascular, and easily stretched
• Contains the retraction ring (physiological) at its upper border during normal labour
• Becomes thinner as labour progresses

• Lower segment caesarean section (LSCS): incision made here - less vascular, heals well, lower risk of rupture in subsequent pregnancy
• Placenta praevia: placenta implanted over LUS
• Pathological retraction ring (Bandl's ring): visible groove between upper and LUS in obstructed labour - sign of impending rupture
• Rupture: LUS is the commonest site of uterine rupture (due to thinness)

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SECTION B: FETAL HEAD AND BIRTH INJURIES

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Caput Succedaneum (2016, 2012, 2011, 2009 SN)

• The registered part of the scalp (within the cervical os) is subject to atmospheric pressure while the rest of the head is under uterine pressure
• This pressure differential causes exudation of serum/blood into the subcutaneous tissue
• It is NOT confined to one bone - crosses suture lines freely

• Benign and self-limiting
• No treatment needed
• The degree of caput may indicate duration/intensity of labour

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Cephalohematoma (2017, 2015 SN)

• Results from rupture of diploic veins during delivery (forceps, vacuum, prolonged labour)
• Blood collects between the periosteum and the outer table of skull

• Conservative - no aspiration (risk of infection)
• Observe for jaundice and anemia
• Most resolve spontaneously in 6-8 weeks
• If calcification occurs, cosmetic concern only - usually remodels

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Internal Rotation (2016 SN)

• At the level of the ischial spines (plane of least dimension), the head must rotate
• In LOA/ROA vertex presentation: The head enters the inlet in the transverse diameter
• As the head descends to the level of spines, the occiput rotates anteriorly (45° in LOA; 135° in ROP)
• The sagittal suture now lies in the AP diameter of the outlet
• This rotation is facilitated by the gutter shape of the levator ani muscles which guide the fetal head

• The levator ani muscles slope downward and forward, forming a gutter
• The occiput (the most dependent part) slips into the gutter and is directed anteriorly

• LOA/ROA (45° position at inlet): rotation of 45°
• LOT/ROT (transverse at inlet): rotation of 90°
• LOP/ROP (posterior at inlet): rotation of 135°

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Non-Engagement of Head in Primigravida at Term (1997 SN)

• Large fetal head / macrosomia
• Hydrocephalus
• Abnormal presentation (face, brow, shoulder)
• Deflexion attitude

• Contracted pelvis (most important)
• Android or anthropoid pelvis with android tendencies
• Pelvic tumors (e.g., large fibroids in lower segment)
• Pelvic kidney

• Placenta praevia (most common cause - prevents engagement)
• Low-lying placenta

• Pendulous abdomen (head floats away from pelvis)
• Uterine malformations (e.g., subseptate uterus)
• Polyhydramnios (head floats)
• Fibromyoma in lower segment

• Asynclitism (deflection laterally)

• USG: to check fetal weight, presentation, placental location, AFI, structural anomalies
• Pelvic assessment/clinical pelvimetry
• X-ray pelvimetry if needed

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SECTION C: NORMAL LABOUR (2018 LQ)

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Definition of Normal Labour

"Labour is called normal when the fetus presenting by vertex is delivered spontaneously in less than 18 hours without undue maternal or fetal trauma."

1. Spontaneous onset - commences on its own at term
2. Term pregnancy - gestational age 37-42 completed weeks
3. Single fetus
4. Vertex presentation
5. No CPD - fetus size compatible with maternal pelvis
6. Duration - completed within 18 hours (some say 24 hrs)
7. Spontaneous delivery - no operative interference
8. No complications - to mother or baby

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Mechanism of Normal Labour (Left Occiput Anterior - LOA)

1. Engagement

• Definition: When the biparietal diameter (BPD = 9.5 cm) passes through the pelvic inlet
• At engagement, the presenting part is at the level of ischial spines (station 0)
• The head enters in the left oblique diameter of the inlet in LOA
• The sagittal suture lies in the left oblique diameter; occiput points to left iliopectineal eminence

2. Descent

• Occurs throughout labour, most rapidly in the second stage
• Caused by: uterine contractions, abdominal muscle action, weight of fetus
• The head descends with flexion occurring simultaneously

3. Flexion

• As head meets resistance of pelvic floor, the chin flexes onto the chest
• The suboccipitobregmatic diameter (9.5 cm) replaces the occipitofrontal (11.5 cm)
• Flexion reduces the presenting diameter - makes delivery easier

4. Internal Rotation

• Occurs at the level of ischial spines
• The occiput rotates 45° anteriorly (in LOA) to come under symphysis pubis
• Sagittal suture now lies in the AP diameter of outlet
• Caused by the sloping levator ani forming a gutter

5. Crowning

• When the widest diameter of the head distends the vulva and does not recede between contractions
• Perineum at maximum stretch

6. Extension

• With the occiput under the symphysis pubis (hypomochlion), the head extends around the symphysis
• Delivered in order: occiput, bregma, forehead, face, chin
• Extension is caused by the resistance of the pelvic floor

7. Restitution

• After delivery of the head, the head rotates 45° back to its natural position relative to the shoulders
• In LOA: the occiput rotates back to the left (undoing internal rotation)

8. External Rotation (Second Rotation)

• The shoulders were in the oblique diameter at entry; they now undergo internal rotation to AP diameter
• This rotation is transmitted to the delivered head, which rotates a further 45° (occiput now points to left thigh)
• Total: head has now rotated 90° from under the symphysis

9. Lateral Flexion and Delivery of Shoulders

• Anterior shoulder delivered first by lateral flexion of trunk downward
• Posterior shoulder delivered by lifting trunk upward
• Trunk and legs follow easily

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Second Stage of Labour (2006 SN)

• Primigravida: Up to 2 hours (extended to 3 hours with epidural)
• Multigravida: Up to 1 hour (extended to 2 hours with epidural)

1. Passive (latent) phase: Full dilation but no urge to push; fetal descent continues
2. Active phase: Expulsive contractions with bearing-down efforts

• Contractions: 3-5 per 10 minutes, each lasting 60-90 seconds
• Ferguson reflex: fetal head on pelvic floor stimulates oxytocin release → expulsive urge
• Perineum distends, anus gapes, labia part

• Maternal position: dorsal/lithotomy/upright
• Encourage pushing with contractions (Valsalva maneuver)
• Monitor FHR after each contraction (normal 110-160 bpm)
• Episiotomy if needed (to prevent perineal tears)
• Support perineum (Ritgen's maneuver for head delivery)
• Delivery of shoulders, cord clamping (after 1-2 minutes ideally)

• Prolonged second stage (CPD, malposition, poor maternal effort)
• Fetal distress (cord compression, head compression)
• Perineal lacerations, PPH

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SECTION D: ECTOPIC PREGNANCY

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Ectopic Pregnancy - Definition, C/F, Diagnosis & Management (2008, 1997, 1993 LQ)

Definition

• Tubal (98%): Ampullary 55%, Isthmic 25%, Fimbrial 17%, Interstitial 3%
• Non-tubal (2%): Ovarian, Abdominal, Cervical, Cornual, Heterotopic

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Aetiological Factors (1997 LQ)

1. Pelvic Inflammatory Disease (PID) - most common cause (salpingitis - Chlamydia, gonorrhea) - tubal mucosal damage and cilia dysfunction
2. Previous ectopic pregnancy - recurrence rate 10-15%
3. Previous tubal surgery (salpingoplasty, salpingostomy, tubal ligation reversal)
4. Use of IUCD - prevents intrauterine implantation but not tubal
5. Progestogen-only pill (mini-pill) - slows tubal motility
6. Assisted reproductive techniques (ART/IVF) - multiple embryo transfer
7. Endometriosis - tubal involvement
8. Congenital tubal abnormalities - diverticula, hypoplasia
9. Peritubal adhesions - post-appendicitis, post-laparotomy
10. Uterine fibroids - compressing tube
11. History of appendicitis / pelvic surgery

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Clinical Features

A. Acute (Ruptured) Ectopic (1993, 1997 LQ - Acute Ectopic)

• Missed period (amenorrhea of 6-8 weeks)
• Sudden severe lower abdominal pain (knife-like, starts in one iliac fossa, becomes generalized)
• Shoulder tip pain (diaphragm irritation by hemoperitoneum - referred pain)
• Vomiting, syncope, collapse

• Shocked patient: pallor, rapid weak pulse, low BP, cold clammy skin
• Abdominal: guarding, rigidity, tenderness (board-like in catastrophic rupture)
• Rebound tenderness
• Shifting dullness (hemoperitoneum)
• Vaginal examination: Cervical excitation (Chandelier sign), tenderness and bogginess in posterior fornix (blood in POD), uterus pushed to one side, adnexal mass (may not be palpable in shock)

B. Subacute (Tubal Abortion / Chronic Ectopic)

• Recurrent episodes of pain and slight bleeding
• Gradual onset
• Pelvic mass (organized hematoma - "frozen pelvis")
• Low-grade fever

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Diagnosis

1. Urine/Serum beta-hCG:
   • Positive in virtually all ectopic pregnancies
   • Serial serum beta-hCG: In normal IUP, doubles every 48 hrs; in ectopic, rise is sluggish (<66% rise in 48 hrs)
   • Discriminatory zone: If beta-hCG >1500-2000 mIU/mL and no IUP on TVS → ectopic likely
2. Transvaginal Ultrasound (TVS):
   • Empty uterus + adnexal mass = high suspicion
   • "Tubal ring" sign (ring of fire)
   • Free fluid in POD (hemoperitoneum)
   • Absence of intrauterine sac when beta-hCG >1500
3. Serum progesterone: <5 ng/mL = non-viable pregnancy; >25 ng/mL = likely normal IUP
4. Culdocentesis: Aspiration of non-clotting blood from POD (now largely replaced by TVS)
5. Laparoscopy: Gold standard for diagnosis (and treatment)
6. Endometrial curettage (D&C): Absence of chorionic villi = ectopic (Arias-Stella reaction present)
7. CBC: Low Hb, raised WBC (peritoneal irritation)

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Management

1. Conservative (Medical) Management - Methotrexate

• Hemodynamically stable
• Unruptured ectopic
• Mass <3.5 cm (some say <4 cm)
• No fetal cardiac activity
• Beta-hCG <5000 mIU/mL (some say <3000)
• No contraindication to methotrexate
• Patient willing for close follow-up

• Single dose IM: 50 mg/m² body surface area
• Multi-dose protocol: 1 mg/kg IM on days 1,3,5,7 alternating with folinic acid (leucovorin) 0.1 mg/kg on days 2,4,6,8
• Monitor beta-hCG on day 4 and day 7; should fall >15% between day 4-7
• If insufficient fall, repeat dose or surgical intervention

2. Surgical Management

• Ruptured ectopic (emergency)
• Hemodynamic instability
• Failed medical management
• Contraindication to methotrexate
• Heterotopic pregnancy
• Beta-hCG >5000
• Mass >3.5 cm / fetal cardiac activity

• Salpingostomy (linear salpingostomy): Longitudinal incision, conceptus removed, tube left to heal by secondary intention - preferred if contralateral tube damaged; risk of persistent trophoblast
• Salpingectomy: Tube excised - preferred if tube severely damaged, recurrent ectopic in same tube, or future fertility not desired

• Salpingectomy - emergency procedure in rupture with massive hemorrhage
• Auto-transfusion of collected blood if uncontaminated
• Control hemorrhage, restore circulation

• Rhesus D immunoglobulin if Rh-negative
• Monitor beta-hCG post-salpingostomy (risk of persistent trophoblast)

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Uses of Methotrexate in Gynecology (2006 SN)

1. Ectopic pregnancy (most common use): Medical management of unruptured tubal ectopic (as above)
2. Gestational Trophoblastic Disease (GTD):
   • Primary treatment for low-risk GTD (hydatidiform mole post-evacuation with rising hCG)
   • Invasive mole and non-metastatic choriocarcinoma: Single-agent MTX
   • Gestational choriocarcinoma: Part of EMA-CO regimen (high-risk)
3. Persistent trophoblast after conservative surgery for ectopic
4. Cervical ectopic pregnancy: Local or systemic MTX
5. Heterotopic pregnancy: Selective feticide of ectopic sac
6. Interstitial/cornual ectopic: MTX ± potassium chloride injection
7. Abdominal/ovarian ectopic: Adjunctive MTX

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SECTION E: PROM AND RELATED CONDITIONS

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Complications of PROM (SN)

Maternal Complications:

1. Chorioamnionitis (most serious) - ascending infection: fever, tachycardia, uterine tenderness, foul-smelling liquor
2. Puerperal sepsis / Endometritis
3. Abruption placenta - (associated)
4. Caesarean section rate increased
5. Failed induction of labour
6. Dry labour - dystocia, cord complications
7. Retained placenta

Fetal/Neonatal Complications:

1. Cord prolapse - especially with non-engaged head
2. Cord compression - oligohydramnios compresses cord
3. Neonatal sepsis / Pneumonia - ascending infection; Streptococcus Group B most dangerous
4. Prematurity complications (if PPROM): RDS, IVH, NEC, retinopathy
5. Pulmonary hypoplasia - prolonged severe oligohydramnios (especially before 20 weeks)
6. Potter sequence - deformities from oligohydramnios: flattened facies, limb deformities, pulmonary hypoplasia
7. Fetal distress - cord compression, infection
8. Perinatal mortality - especially in PPROM

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Management of Premature Labour (2004 LQ)

Diagnosis:

• Regular uterine contractions (at least 4 in 20 minutes or 8 in 60 minutes)
• Cervical changes: effacement and/or dilatation ≥2 cm
• Exclude false labour (Braxton Hicks)

Assessment:

• Gestational age (USG biometry)
• Fetal condition (CTG, BPP)
• Cause identification (USG for placenta, liquor, fetal anomaly; HVS, urine C&S)
• Cervical length on TVS (<25 mm = high risk)
• Fetal fibronectin (positive = predictive of preterm birth)

Management:

A. Tocolysis (to delay delivery for 48-72 hrs to allow steroid effect):

1. Beta-sympathomimetics: Ritodrine, Salbutamol, Terbutaline - side effects: tachycardia, hypotension, hypokalemia
2. Calcium channel blockers: Nifedipine (10 mg oral, preferred) - fewer side effects
3. Prostaglandin synthetase inhibitors: Indomethacin (before 32 weeks only; risk of premature closure of ductus arteriosus)
4. Oxytocin antagonists: Atosiban (IV) - most specific, fewer side effects
5. Magnesium sulfate: (also neuroprotective for fetus <32 weeks)

B. Antenatal Corticosteroids (VITAL - reduce RDS, IVH, NEC):

• Betamethasone 12 mg IM x2 doses, 24 hrs apart (preferred)
• OR Dexamethasone 6 mg IM x4 doses, 12 hrs apart
• Give between 24-34 weeks (benefit up to 36+6 weeks for respiratory morbidity)
• Maximum benefit 24 hrs after first dose; effective for 7 days

C. Antibiotic prophylaxis:

• If PPROM associated: Erythromycin (ORACLE trial) 250 mg QID x10 days
• GBS prophylaxis: IV Penicillin G or Ampicillin intrapartum if GBS+

D. Cervical cerclage:

• Rescue cerclage if cervix <25 mm and previous PTL/loss
• Emergency cerclage if prolapsing membranes with dilated cervix <24 weeks

E. Magnesium sulfate for neuroprotection:

• Give if <32 weeks: 4g IV loading, then 1g/hr maintenance until delivery (reduces cerebral palsy)

Prevention of Premature Labour:

1. Identification of high-risk cases: Previous PTL, uterine anomalies, multiple pregnancy, cervical incompetence
2. Cervical cerclage: Elective at 12-14 weeks in cervical incompetence
3. Progesterone therapy: Vaginal micronized progesterone 200-400 mg/night from 16-24 weeks in women with short cervix (<25 mm) or previous PTL - reduces recurrence
4. Treatment of infections: UTI, BV (Metronidazole), STIs
5. Avoid risk factors: Smoking cessation, adequate nutrition, avoid strenuous work
6. Folic acid supplementation
7. Pessary (Arabin): Cervical pessary in short cervix <25 mm
8. Management of polyhydramnios, fibroids
9. Regular antenatal care

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Preterm Labour (1993 SN)

• Unknown (idiopathic) - 50%
• PPROM
• Multiple pregnancy
• Polyhydramnios
• Placenta praevia / abruption
• Incompetent cervix
• Uterine anomalies (septum, bicornuate)
• Infections (UTI, BV, chorioamnionitis)
• Fetal anomalies
• Previous preterm labour
• Extremes of maternal age, low socioeconomic status, smoking

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Intrauterine Fetal Death (IUFD) & Spalding Sign (1996, 1983 SN)

Spalding Sign (1996 SN)

• Liquefaction and shrinkage of fetal brain after death
• Loss of turgor of scalp and brain contents

Intrauterine Fetal Death (IUFD) - 1983 SN

• Maternal: Hypertension, diabetes, severe anemia, antiphospholipid syndrome, infections (TORCH), Rh isoimmunization, cord accidents, IUGR
• Fetal: Congenital anomalies, chromosomal (trisomy), hydrops fetalis
• Placental: Abruption, infarcts, cord accidents (true knot, prolapse)
• Unknown - 25-40%

• Cessation of fetal movements
• No fetal heart sounds
• USG: absence of cardiac activity (definitive)
• X-ray: Spalding sign, Robert's sign (if delayed diagnosis)

• DIC (Disseminated Intravascular Coagulation) - develops after 4-5 weeks; fibrinogen levels fall progressively
• Sepsis
• Psychological trauma

• Confirm diagnosis (USG)
• Explain to patient
• Check coagulation profile (fibrinogen, PT, PTT, platelet count)
• Induction of labour:
  • Prostaglandin E2 (misoprostol, dinoprostone) - first trimester/early second trimester
  • Prostaglandin E2 gel + oxytocin infusion - late second/third trimester
  • Mifepristone 200 mg followed by misoprostol 36-48 hrs later
• Deliver placenta, examine for clues
• Postpartum: Lactation suppression (Cabergoline)
• Investigate cause (fetal karyotype, maternal thrombophilia screen, TORCH, autopsy)
• Psychological support, counselling
• Advise minimum 6 months before next pregnancy

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QUICK REFERENCE SUMMARY TABLE

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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