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OBSTETRICS & GYNAECOLOGY - II Year

Complete Exam-Ready Answers: Q.215 to Q.246

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Q.215 - Clinical Features (C/F) of Uterine Anomalies

• Class I: Hypoplasia/Agenesis (Mayer-Rokitansky-Kuster-Hauser syndrome)
• Class II: Unicornuate uterus
• Class III: Didelphys uterus (double uterus, double cervix)
• Class IV: Bicornuate uterus
• Class V: Septate uterus (most common)
• Class VI: Arcuate uterus
• Class VII: DES-related uterus (T-shaped)

1. Primary amenorrhoea - in complete agenesis (MRKH syndrome)
2. Recurrent pregnancy loss (RPL) - most common presentation; septate uterus causes 35% of RPL
3. Preterm labour - due to reduced uterine volume
4. Malpresentations - transverse/oblique lie, breech
5. Dysmenorrhoea - especially in obstructed hemi-uterus (unicornuate with non-communicating horn)
6. Infertility
7. Cryptomenorrhoea - in cases with outflow obstruction
8. Dyspareunia - in vaginal septal defects
9. Associated renal anomalies - horseshoe kidney, absent kidney (check always!)

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Q.216 - Functions of Ovarian Hormones

A) OESTROGEN (Estradiol - E2)

1. Uterus: Promotes endometrial proliferation; myometrial hypertrophy; increases oxytocin sensitivity
2. Cervix: Increases mucus quantity, makes it thin, watery, spinnbarkeit (ferning pattern)
3. Vagina: Cornification of vaginal epithelium; maintains acidic pH
4. Fallopian tube: Increases ciliary activity; promotes ovum transport
5. Breast: Ductal growth and development
6. Bone: Inhibits osteoclast activity; maintains bone density
7. Cardiovascular: Increases HDL, decreases LDL; vasodilation
8. Hypothalamic-pituitary axis: Low dose - negative feedback; high sustained level - positive feedback (LH surge)
9. Secondary sex characteristics: Female hair distribution, fat deposition
10. Tanner staging: Breast development (thelarche)

B) PROGESTERONE

1. Uterus: Converts proliferative endometrium to secretory endometrium; decreases myometrial contractility
2. Cervix: Thick, viscid, scanty mucus - non-ferning ("hostile" mucus)
3. Breast: Lobular-alveolar development (for lactation)
4. Body temperature: Raises basal body temperature (BBT) by 0.3-0.5°C after ovulation
5. Negative feedback on hypothalamus/pituitary - suppresses LH/FSH
6. Maintains pregnancy - prevents premature labour
7. Stimulates respiratory centre - increases rate and depth of breathing

C) ANDROGENS (Testosterone, DHEA)

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Q.217 - HPO Axis (Hypothalamic-Pituitary-Ovarian Axis)

Components:

• Arcuate nucleus secretes GnRH (Gonadotropin-Releasing Hormone) = LHRH
• GnRH is released in pulsatile fashion (every 60-90 mins in follicular phase)
• Pulsatile release is essential - continuous GnRH causes downregulation
• Regulated by: kisspeptin neurons (stimulate), dopamine and opioids (inhibit)

• GnRH stimulates release of FSH (Follicle Stimulating Hormone) and LH (Luteinizing Hormone)
• Both are glycoprotein hormones with alpha subunit (common) + beta subunit (specific)

• FSH stimulates follicular growth and estrogen production (granulosa cells)
• LH stimulates theca cell androgen production; triggers ovulation; maintains corpus luteum

Feedback Mechanisms:

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Q.218 - Menstruation: Phases, Hormonal, Ovarian, Uterine Changes

A) PHASES OF MENSTRUAL CYCLE

B) HORMONAL CHANGES

• FSH rises → recruits cohort of follicles
• Dominant follicle secretes rising estrogen
• Estrogen causes LH surge on Day 13-14
• Ovulation occurs 36-38 hours after LH peak

• Corpus luteum forms → secretes progesterone + estrogen
• If no pregnancy: corpus luteum degenerates (day 23-24) → progesterone falls → menstruation

C) OVARIAN CHANGES

1. Days 1-5: Atresia of previous cycle's follicles
2. Days 5-14 (Follicular): Cohort of 6-12 follicles recruited; dominant follicle selected; Graafian follicle reaches 20-25 mm
3. Day 14 (Ovulation): LH surge → follicle ruptures → oocyte released (secondary oocyte in metaphase II)
4. Days 15-25 (Luteal): Corpus luteum forms from granulosa/theca cells; secretes progesterone + estrogen + inhibin A
5. Days 26-28: Corpus albicans forms if no pregnancy

D) UTERINE (ENDOMETRIAL) CHANGES

1. Menstrual phase: Functional layer shed; spiral arteries constrict → ischaemia → shedding; prostaglandins mediate this
2. Proliferative phase: Estrogen drives regeneration; glands are straight and narrow; stroma is compact; pseudostratified epithelium
3. Secretory phase: Progesterone effect; glands become tortuous with subnuclear vacuoles (early); then secretions in lumen; spiral arteries elongate; stroma becomes decidualized
4. Ischemic phase: Withdrawal of progesterone; coiling of spiral arteries; ischaemia

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Q.219 - Tanner's Classification (Sexual Maturity Rating - SMR)

Breast Development (Female):

Pubic Hair (Both sexes):

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Q.220 - Precocious Puberty - Causes and Diagnostic Features

Classification & Causes:

• Idiopathic (most common in girls - 80%)
• CNS tumours (hypothalamic hamartoma, astrocytoma, glioma)
• CNS insults: irradiation, hydrocephalus, NF-1, head trauma

• McCune-Albright syndrome (GNAS1 mutation) - classically: precocious puberty + polyostotic fibrous dysplasia + cafe-au-lait spots
• Ovarian tumours (granulosa cell tumour - most common estrogen-secreting)
• Adrenal tumours / Congenital Adrenal Hyperplasia (CAH)
• Iatrogenic (exogenous estrogen/androgen)
• Hypothyroidism (Van Wyk-Grumbach syndrome)

Diagnostic Features:

1. History: Age of onset of pubic hair, breast development, menarche
2. Anthropometry: Height and weight (growth acceleration early, early epiphyseal fusion → short final height)
3. Bone age X-ray: Advanced bone age (wrist X-ray)
4. Hormonal investigations:
   • Serum LH, FSH, estradiol
   • GnRH stimulation test: LH > 5 IU/L = central type
   • LH:FSH ratio > 1 = central
5. Imaging: MRI brain (hypothalamus/pituitary), pelvic USS
6. Thyroid function - rule out hypothyroidism

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Q.221 - Delayed Puberty - Causes and Characteristic Features

Causes:

• Normal variant; family history; growth will occur later

• Kallmann syndrome: GnRH deficiency + anosmia (olfactory bulb aplasia)
• Hypopituitarism: Tumours (craniopharyngioma), irradiation
• Chronic illness: Anorexia nervosa, malnutrition, excessive exercise, IBD
• Hypothyroidism, Hyperprolactinaemia

• Turner syndrome (45,X) - most common
• Premature ovarian insufficiency (POI)
• Chemotherapy/radiation gonadal damage
• Galactosaemia

Characteristic Features:

1. Short stature (especially Turner syndrome)
2. Absent/minimal breast development
3. Absent/sparse pubic/axillary hair
4. Primary amenorrhoea
5. Infantile genitalia
6. Webbed neck, shield chest (Turner's)
7. Anosmia (Kallmann's)
8. Bone age delayed (wrist X-ray)

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Q.222 - Puberty Menorrhagia - Causes and Diagnostic Features

Causes:

1. Anovulatory cycles (most common) - immature HPO axis, no corpus luteum, no progesterone → unopposed estrogen → irregular shedding
2. Coagulation disorders - von Willebrand disease (15-20% of adolescent heavy bleeding), ITP, platelet dysfunction
3. Hypothyroidism
4. Hyperprolactinaemia
5. Uterine/structural: Fibroids (rare at this age), endometrial polyp
6. Infections: PID (less common at menarche)

Diagnostic Features:

1. History: Age at menarche, cycle length, duration of flow, passage of clots, pad/tampon count
2. Haematological:
   • CBC - anaemia (Hb, MCV)
   • Platelet count
   • Coagulation profile: PT, aPTT
   • Von Willebrand factor, Ristocetin cofactor
3. Hormonal: TSH, T4; FSH, LH; prolactin
4. Pelvic USS: Uterine/ovarian pathology
5. Clinical: PBAC score (Pictorial Blood Assessment Chart) > 100 = heavy

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Q.223 - Amenorrhoea

• Primary amenorrhoea: No menstruation by age 15 with normal secondary sex characteristics, or by age 13 without secondary sex characters
• Secondary amenorrhoea: Cessation of menstruation for ≥3 months in a previously regular cycle, or ≥6 months in irregular cycles

Classification of Primary Amenorrhoea:

• Androgen Insensitivity Syndrome (AIS) - 46,XY; absent uterus; absent pubic hair
• 17-alpha-hydroxylase deficiency

• Turner syndrome (45,X) - most common
• Hypogonadotropic hypogonadism
• Constitutional delay

• MRKH syndrome (Mayer-Rokitansky-Kuster-Hauser) - 46,XX; absent uterus/vagina
• AIS (46,XY)

• Outflow tract obstruction: Imperforate hymen, transverse vaginal septum
• Hypothalamic/pituitary causes (PCOS, hyperprolactinaemia)

Causes of Secondary Amenorrhoea:

1. Pregnancy (must always be excluded first - urine/serum hCG)
2. Hypothalamic: Stress, weight loss, excessive exercise, anorexia nervosa → GnRH suppression
3. Pituitary: Hyperprolactinaemia (most common pituitary cause), Sheehan's syndrome, pituitary tumours
4. Ovarian: PCOS (most common overall), premature ovarian insufficiency (POI), surgical removal
5. Uterine: Asherman's syndrome (intrauterine adhesions post-D&C)
6. Thyroid/Adrenal: Hypothyroidism, Cushing's syndrome, CAH

Investigations:

• Urine hCG (rule out pregnancy)
• FSH, LH, prolactin, estradiol, TSH
• Karyotype (primary amenorrhoea)
• Pelvic USS
• MRI pituitary (if high prolactin)
• Progesterone withdrawal test (tests outflow tract)

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Q.224 - Cryptomenorrhoea - Causes

Causes (Anatomical Obstruction):

1. Imperforate hymen (most common) - bulging bluish-purple membrane at introitus; haematocolpos
2. Transverse vaginal septum - at junction of upper 1/3 and lower 2/3 vagina
3. Cervical stenosis - post-surgical, post-inflammatory
4. Vaginal atresia
5. Cervical atresia - rare

Consequences:

• Haematocolpos: Blood in vagina
• Haematometra: Blood in uterus
• Haematosalpinx: Blood in fallopian tube
• Haematoperitoneum

Features:

• Primary amenorrhoea + cyclical pelvic pain
• Lower abdominal mass (collected blood)
• Imperforate hymen: bulging membrane, purple-blue tinge
• USS/MRI confirms diagnosis

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Q.224(b) - Hypomenorrhoea - Causes

Causes:

1. Intrauterine adhesions (Asherman's syndrome) - most common; post-D&C, post-endometritis
2. Cervical stenosis - obstructs outflow
3. Hypoestrogenism - premature ovarian failure, hypothalamic amenorrhoea
4. Thyroid disorders - hypothyroidism or hyperthyroidism
5. Oral contraceptive pills (OCP) - suppresses endometrial proliferation
6. Progestogen-only pills / Mirena IUS
7. Tuberculosis of endometrium
8. Anxiety/stress

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Q.225 - Oligomenorrhoea - Causes

Causes:

1. PCOS (most common) - hyperandrogenism, anovulation, polycystic ovaries
2. Hypothyroidism
3. Hyperprolactinaemia - elevated prolactin suppresses GnRH pulsatility
4. Hypothalamic dysfunction - stress, exercise, weight loss
5. Perimenopause - declining ovarian reserve
6. Cushing's syndrome - hypercortisolism suppresses GnRH
7. Androgen excess - CAH, androgen-secreting tumours

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Q.226 - Polymenorrhoea - Causes

Causes:

1. Short luteal phase - corpus luteum insufficiency; early progesterone withdrawal
2. Follicular phase shortening - accelerated follicular development (common in perimenopause)
3. Hyperthyroidism
4. Anovulation - irregular, frequent cycles
5. Pelvic inflammatory disease (PID) - inflammation shortens cycle
6. IUCD (copper coil) - can alter cycle
7. Endometriosis

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Q.227 - Metrorrhagia - Causes

Causes:

1. Cervical pathology: Cervical ectropion (most common), cervical polyp, cervical carcinoma
2. Endometrial pathology: Endometrial polyp, endometrial hyperplasia, endometrial carcinoma
3. Hormonal causes: Breakthrough bleeding on OCP, anovulation, progesterone deficiency
4. Uterine fibroids (submucous)
5. PID / Endometritis
6. Ovulation bleeding (Mittelschmerz)
7. Thyroid dysfunction
8. Coagulation disorders
9. IUCD
10. Post-coital bleeding - cervical cause until proven otherwise

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Q.228 - AUB (Abnormal Uterine Bleeding) - Classify, Causes, Investigations, General Management, Homoeopathic Remedies

Definition:

FIGO Classification - PALM-COEIN:

• P - Polyp
• A - Adenomyosis
• L - Leiomyoma (Fibroids)
• M - Malignancy & hyperplasia

• C - Coagulopathy
• O - Ovulatory dysfunction (most common cause - anovulation)
• E - Endometrial (primary endometrial disorder)
• I - Iatrogenic (medications: OCP, anticoagulants, antipsychotics)
• N - Not yet classified

Investigations:

1. CBC - anaemia
2. Coagulation profile - PT, aPTT, platelet, vWF
3. Hormonal: TSH, prolactin, FSH, LH, testosterone
4. Pelvic USS (first-line imaging)
5. Saline infusion sonography (SIS) - for intracavitary lesions
6. Endometrial biopsy - women > 35 years or risk factors for endometrial cancer
7. Hysteroscopy - gold standard for intracavitary lesions

General Management:

1. Medical:
   • Tranexamic acid (antifibrinolytic) - reduces blood loss 40-50%
   • NSAIDs (mefenamic acid) - reduces loss 20-30%
   • Combined OCP - regulates cycle
   • Progestins (MPA, norethindrone) - anovulatory AUB
   • Levonorgestrel-IUS (Mirena) - most effective medical treatment; reduces loss 90%
   • GnRH agonists - for fibroids or preoperative
2. Surgical:
   • Endometrial ablation (suitable for no future fertility)
   • Hysteroscopic polypectomy / myomectomy
   • Hysterectomy - definitive treatment

Homoeopathic Remedies (for reference):

• Phosphorus - profuse, bright red bleeding
• China - weakness from blood loss, dark clots
• Sabina - mixed bright and dark blood; fibroid-related
• Thlaspi bursa-pastoris - menorrhagia + cramping
• Trillium pendulum - profuse flooding
• Ipecac - bright red bleeding with nausea

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Q.229 - Metropathia Haemorrhagica - Causes

Pathophysiology:

• Anovulation → no corpus luteum → no progesterone → prolonged unopposed estrogen → endometrial hyperplasia → cystic changes (Swiss cheese pattern) → irregular heavy bleeding

Causes (of underlying anovulation):

1. PCOS - most common cause in reproductive age
2. Perimenopause - declining ovarian reserve, anovulatory cycles
3. Hypothalamic dysfunction - stress, weight fluctuation
4. Hypothyroidism
5. Hyperprolactinaemia
6. Obesity - peripheral estrogen excess (adipose aromatisation)

Features:

• Period of amenorrhoea followed by heavy prolonged bleeding
• Uterus slightly enlarged
• Endometrial biopsy shows cystic glandular hyperplasia
• Treatment: progesterone (to oppose estrogen), D&C, or endometrial ablation

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Q.230 - Dysmenorrhoea

Classification:

• No underlying pelvic pathology
• Due to excess prostaglandin F2-alpha (PGF2α) → uterine hypercontractility → ischaemia → pain
• Onset: 6-12 months after menarche; young women 15-25 years
• Pain: Cramping, lower abdomen + lower back; onset 1-2 hours before or with flow; lasts 1-2 days; may have nausea, diarrhoea, headache

• Due to underlying pelvic pathology
• Causes: Endometriosis (most common), Adenomyosis, Fibroids (submucous), PID, IUCD (copper), Cervical stenosis, Mullerian anomalies
• Pain: Starts 1-2 weeks before period; may persist after; deep dyspareunia often present; worsens with age

Management of Primary Dysmenorrhoea:

• NSAIDs (ibuprofen, mefenamic acid) - first line; inhibit prostaglandin synthesis
• Combined OCP - suppresses ovulation; reduces prostaglandin levels
• Heat application - local heat to abdomen
• Exercise

Management of Secondary:

• Treat underlying cause (e.g., laparoscopic excision for endometriosis)

Homoeopathic Remedies for Membranous Dysmenorrhoea (Q.232):

• Caulophyllum - spasmodic labour-like pains; dysmenorrhoea with small ineffective contractions
• Viburnum opulus - crampy pains radiating to thighs; scanty flow
• Colocynthis - violent cramping pains; relieved by pressure and bending double
• Magnesia phosphorica - crampy pains; better by heat, pressure, bending double
• Chamomilla - unbearable pain; angry, irritable patient; clotted dark blood

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Q.231 - Mittelschmerz Syndrome - Causes

Causes/Mechanism:

1. Follicular distension - rapidly expanding Graafian follicle distends the ovarian capsule
2. Peritoneal irritation - release of follicular fluid and blood at ovulation irritates the peritoneum
3. Prostaglandins - released from follicular fluid cause smooth muscle contraction and pain
4. Tubal peristalsis - increased fallopian tube motility at ovulation

Features:

• Unilateral lower abdominal pain (alternates sides each month)
• Duration: few minutes to 48 hours
• May have mild vaginal spotting (ovulation bleeding)
• Self-limiting; no treatment usually needed
• Diagnosis: clinical (mid-cycle timing)

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Q.233 - PMS (Premenstrual Syndrome) - Causes, Clinical Features, General Management

Definition:

Causes:

1. Progesterone sensitivity/excess in luteal phase
2. Serotonin deficiency - dropping estrogen reduces serotonin → mood symptoms
3. Aldosterone excess - causes fluid retention and bloating
4. Endorphin withdrawal - opioid withdrawal-like symptoms
5. Vitamin B6 deficiency - involved in serotonin synthesis
6. Psychological factors - stress amplifies symptoms
7. GABA sensitivity - allopregnanolone (progesterone metabolite) modulates GABA-A receptors

Clinical Features (appear day 14-28, resolve with menstruation):

• Breast tenderness (mastalgia)
• Abdominal bloating, weight gain
• Headache / migraine
• Fatigue
• Pelvic pain/cramps
• Oedema of hands/feet
• Acne, appetite changes (carbohydrate craving)

• Irritability, anger
• Anxiety, tension
• Mood swings, depression
• Difficulty concentrating
• Sleep disturbances

Investigations:

• Prospective symptom diary (2 cycles minimum) - confirms cyclical pattern
• Rule out: depression, anxiety disorder, thyroid disease

General Management:

1. Lifestyle: Regular aerobic exercise; low salt, low caffeine diet; adequate sleep
2. NSAIDs - for pain and dysmenorrhoea
3. SSRIs (fluoxetine, sertraline) - for PMDD; most effective; can be taken only in luteal phase
4. Vitamin B6 (pyridoxine) 50-100mg/day
5. Calcium carbonate 1000-1200mg/day
6. Combined OCP - suppresses ovulation
7. GnRH agonists - for severe cases (creates medical menopause)
8. Diuretics (spironolactone) - for fluid retention/bloating
9. Cognitive Behavioural Therapy (CBT)

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Q.234 - Menopause: Pathophysiology, Anatomical Changes, C/F, Menopausal Syndrome, Metabolic Changes

Definition:

Pathophysiology:

1. With ageing, ovarian follicular reserve depletes
2. Fewer follicles → less inhibin B → FSH rises (earliest hormonal change)
3. Fewer follicles → less estradiol production
4. LH also rises (loss of negative feedback)
5. FSH > 40 IU/L + amenorrhoea → menopause
6. Residual estrogen comes from peripheral aromatisation of androgens (in adipose tissue) → estrone (E1) becomes dominant estrogen

Anatomical Changes:

1. Ovaries: Atrophy; no follicles; fibrous tissue
2. Uterus: Shrinks; endometrium atrophies
3. Vagina: Atrophy, rugae disappear; mucosa becomes thin, pale, dry
4. Vulva: Labia minora shrinks; clitoral atrophy
5. Breasts: Glandular tissue replaced by fat
6. Pubic hair: Sparse
7. Urinary tract: Urethral atrophy; shorter urethra; urge incontinence

Clinical Features (Menopausal Syndrome):

• Hot flushes - sudden warmth over face/neck/chest; last 1-5 minutes; affect 75% of women
• Night sweats - nocturnal hot flushes; disrupt sleep
• Palpitations

• Mood swings, irritability
• Anxiety, depression
• Insomnia, fatigue
• Memory and concentration difficulty

• Vaginal dryness, dyspareunia, pruritus vulvae
• Urinary frequency, urgency, recurrent UTIs
• Stress/urge incontinence

• Decreased libido, anorgasmia

Metabolic Changes:

1. Bone: Rapid bone loss (3-5% per year in first 5 years); risk of osteoporosis and fractures (hip, vertebral, Colles')
2. Cardiovascular: Loss of estrogen protective effect → increased LDL, decreased HDL → atherosclerosis risk rises
3. Lipid profile: Elevated total cholesterol, LDL, triglycerides; reduced HDL
4. Weight gain: Central obesity; increased insulin resistance → metabolic syndrome
5. Skin: Decreased collagen → wrinkles; reduced skin thickness
6. Cognitive: Increased risk of Alzheimer's disease

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Q.235 - Perimenopause and Artificial Menopause

Perimenopause (Climacteric):

• The transitional period before and just after menopause (usually 2-8 years)
• Ovarian function begins to decline; cycles become irregular
• FSH starts rising; estrogen fluctuates
• Vasomotor symptoms begin
• Ends 12 months after last menstrual period

Artificial Menopause:

1. Surgical: Bilateral oophorectomy (most common) - called "surgical menopause"
2. Radiation: Pelvic radiotherapy ablates ovarian function
3. Chemotherapy: Alkylating agents, cyclophosphamide → ovarian failure
4. GnRH agonists - reversible medical menopause (used for endometriosis, fibroids, IVF)

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Q.236 - Causes of Delayed and Premature Menopause

Delayed Menopause (after age 55):

1. Nulliparity
2. Obesity (peripheral estrogen production)
3. Genetics / family history
4. High estrogen exposure

Premature Menopause / Premature Ovarian Insufficiency (POI):

1. Chromosomal: Turner syndrome, Fragile X premutation (FMR1)
2. Autoimmune (most common acquired cause) - associated with autoimmune thyroid disease, Addison's disease, DM Type 1
3. Iatrogenic: Radiotherapy, chemotherapy, bilateral oophorectomy
4. Genetic mutations: BRCA mutations (associated with POI)
5. Viral infections: Mumps oophoritis
6. Idiopathic (majority)

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Q.237 - Post-menopausal Bleeding (PMB) - Causes, Investigations, D/D, Homoeopathic Remedies

Definition:

RULE: Post-menopausal bleeding = Endometrial carcinoma until proven otherwise

Causes (in order of frequency):

1. Atrophic vaginitis/endometritis (most common cause, ~30%)
2. Endometrial carcinoma (10-15%) - most important to exclude
3. Endometrial polyp
4. Endometrial hyperplasia (pre-malignant)
5. Cervical carcinoma / polyp
6. Hormone replacement therapy (HRT) - breakthrough bleeding
7. Ovarian tumours (estrogen-secreting - granulosa cell tumour)
8. Vaginal trauma
9. Coagulation disorders
10. Vulval carcinoma

Investigations:

1. Pelvic USS (transvaginal) - first line; endometrial thickness > 4-5 mm is suspicious
2. Endometrial biopsy (Pipelle) - mandatory; rules out malignancy
3. Hysteroscopy + D&C - gold standard; direct visualisation + biopsy
4. Pap smear - for cervical cause
5. CBC, coagulation profile
6. Serum CA-125 (if ovarian tumour suspected)

Differential Diagnosis:

• Endometrial carcinoma vs. Polyp vs. Atrophic vaginitis vs. Cervical carcinoma vs. HRT bleeding vs. Ovarian tumour

Homoeopathic Remedies:

• Phosphorus - bright red profuse bleeding; tall, thin woman
• China - weakness from blood loss; dark clots
• Crocus sativus - dark, stringy, thread-like clotted blood
• Trillium pendulum - profuse flooding; sensation of hip bones falling apart
• Fraxinus Americana - uterine fibroids causing post-menopausal bleeding

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Q.238 - Uterine Prolapse: Causes, Classification, Degrees, C/F, D/D, Complications, General Management

Definition:

Causes:

1. Weakness of pelvic floor muscles - levator ani injury (childbirth)
2. Difficult/prolonged labour - esp. prolonged 2nd stage
3. Multiple pregnancies - repeated stretching
4. Grand multiparity
5. Raised intra-abdominal pressure - chronic cough, constipation, obesity, heavy lifting
6. Menopause - estrogen deficiency → loss of collagen in supports
7. Congenital weakness - nulliparous prolapse (rare; associated with spina bifida, sacral agenesis)
8. Sacral nerve injury

Supports of the Uterus:

• Main support: Cardinal (Mackenrodt's) ligament = lateral cervical ligament (most important)
• Uterosacral ligaments
• Levator ani muscle (pelvic diaphragm)
• Pubocervical fascia, rectovaginal fascia

Degrees/Grades of Uterine Prolapse:

Clinical Features:

1. Dragging/bearing down sensation in pelvis - "something coming down"
2. Lump/protrusion at vulva (visible in 3rd degree)
3. Backache - worse with prolonged standing
4. Urinary symptoms: Frequency, urgency, retention, stress incontinence (often coexists with cystocele)
5. Bowel symptoms: Constipation, incomplete evacuation (with rectocele)
6. Sexual dysfunction: Dyspareunia
7. Decubitus ulcer on cervix (chronic prolapse)
8. Hypertrophy and elongation of cervix

Differential Diagnosis:

• Elongation of cervix (cervix protrudes without descent of body)
• Cervical fibroid polyp
• Vaginal cyst
• Cystocele/Rectocele alone
• Procidentia

Complications:

1. Decubitus ulcer - risk of infection, bleeding
2. Urinary tract infection, hydronephrosis
3. Uterine hypertrophy
4. Incarceration of prolapse (oedema)
5. Psychological/social effects

General Management:

• Pelvic floor exercises (Kegel's) - for 1st degree or mild
• Pessary (ring pessary) - for elderly, unfit for surgery, pregnant
• Estrogen cream (post-menopausal)
• Treat precipitating causes (cough, constipation)

• Manchester/Fothergill operation - amputation of cervix + repair; for 2nd-3rd degree in women desiring to retain uterus
• Pelvic floor repair (colporrhaphy): Anterior repair (cystocele), posterior repair (rectocele)
• Vaginal hysterectomy + pelvic floor repair - definitive; for 3rd degree
• Sacrocolpopexy - for vault prolapse

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Q.239 - Rectocele and Cystocele (Degrees)

Cystocele:

• Grade I: Bulge stays in vagina
• Grade II: Bulge reaches the introitus
• Grade III: Bulge protrudes beyond the introitus

Rectocele:

• Grade I: Rectocele stays in vagina
• Grade II: Rectocele reaches introitus
• Grade III: Protrudes beyond introitus

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Q.240 - Procidentia

• Large mass hanging from vulva
• Decubitus ulceration on cervix (common)
• Urinary problems (urinary retention - kinking of urethra)
• Constipation
• Oedema of prolapsed tissue
• Hypertrophy and elongation of cervix

• Reduction of prolapse + ring pessary (if temporarily needed)
• Vaginal hysterectomy + anterior and posterior colporrhaphy (definitive)

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Q.241 - Pessary Treatment: Indications and Contraindications

Types of Pessaries:

• Ring pessary - most commonly used; for 1st and 2nd degree prolapse
• Shelf pessary / Gellhorn - for 3rd degree / procidentia
• Hodge pessary - for retroversion of uterus
• Donut pessary - for 3rd degree prolapse
• Cube pessary - for vault prolapse, 3rd degree

Indications:

1. Elderly women unfit for surgery
2. Awaiting surgery (temporary)
3. Patient who desires more pregnancies
4. Pregnancy with prolapse
5. Severe medical illness (contra to surgery)
6. Patient's refusal for surgery
7. 1st and 2nd degree prolapse in young women (ring pessary)

Contraindications:

1. Acute pelvic infection / PID
2. Severe ulceration of prolapse
3. Allergy to pessary material
4. Very small or tight vaginal introitus (cannot be inserted)
5. Poor compliance (patient unable to manage pessary hygiene)

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Q.242 - Surgical Management of Genital Prolapse

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Q.243 - Retroversion of Uterus: Causes, Types, C/F, Degrees, D/D, Homoeopathic Remedies

Definition:

Incidence: 20% of women (often normal variant)

Degrees:

• 1st degree: Fundus points directly upward (vertical)
• 2nd degree: Fundus in posterior pouch of Douglas (behind, above)
• 3rd degree: Fundus in rectouterine pouch, cervix pointing upward

Types:

1. Mobile (congenital) - idiopathic; uterus freely movable; no pathology; most common (80%)
2. Fixed (acquired/pathological) - uterus fixed by adhesions

Causes of Fixed Retroversion:

1. Endometriosis - adhesions in pouch of Douglas (most common)
2. PID / Chronic salpingo-oophoritis - adhesions
3. Fibroids (posterior)
4. Ovarian cysts (behind uterus)
5. Previous pelvic surgery
6. Pelvic tuberculosis

Clinical Features:

• Usually asymptomatic (mobile retroversion)
• Dysmenorrhoea - dragging lower back pain during menses
• Dyspareunia (deep) - especially in fixed type
• Backache - chronic, lumbar
• Infertility - if associated with endometriosis
• Urinary symptoms - frequency
• On bimanual examination: fundus felt in posterior fornix; cervix points anteriorly

Differential Diagnosis:

• Ovarian cyst in pouch of Douglas
• Retroverted pregnant uterus
• Fibroid in posterior position
• Pelvic mass

Homoeopathic Remedies:

• Lilium tigrinum - bearing down in retroversion; better by supporting perineum; irritable
• Sepia - bearing down sensation; indifferent to loved ones; backache
• Aletris farinosa - weakness, prolapse tendency, anaemia
• Fraxinus Americana - fibroid-related retroversion

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Q.244 - Inversion of Uterus: Etiology, Types, Clinical Features

Definition:

Etiology:

1. Mismanagement of 3rd stage of labour - most common; undue cord traction
2. Fundal pressure on uncontracted uterus (Credé's manoeuvre incorrectly applied)
3. Spontaneous - rarely
4. Fundal placenta with short umbilical cord
5. Uterine atony with adherent placenta
6. Submucous fibroid at fundus (chronic non-puerperal inversion - rare)

Types:

1. Incomplete (1st degree): Fundal dimple - fundus inverted but does not pass internal os
2. Complete (2nd degree): Fundus passes through internal os but not beyond external os
3. Prolapsed (3rd degree): Fundus protrudes beyond external os/introitus
4. Total inversion: Vagina also inverted

• Acute: Immediately after delivery
• Subacute: 24 hours to 4 weeks postpartum
• Chronic: > 4 weeks (non-puerperal)

Clinical Features:

1. Sudden severe lower abdominal pain
2. Profound shock (neurogenic - due to stretching of peritoneum) out of proportion to blood loss
3. Severe haemorrhage (blood from placental site)
4. Absence of uterus on abdominal palpation
5. Dark red, granular mass at or beyond introitus (complete)
6. Placenta may still be attached
7. No fundus palpable abdominally (dimple instead)

Management:

1. Call for help; IV access; fluids; blood transfusion
2. O'Sullivan's hydrostatic method - warm saline infused into vagina to reduce inversion
3. Johnson's manoeuvre - manual replacement (palm-first method) under anaesthesia
4. Surgical: Huntington's procedure (abdominal); Haultain's operation (incises cervical ring)

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Q.245 - Turner Syndrome

Definition:

Karyotype:

• 45,X (monosomy X) - 57% (classic)
• Mosaics (45,X/46,XX) - 29% - milder features
• Structural X abnormalities - 14%: isochromosome Xq, ring chromosome, deletions

Incidence: 1 in 2,500 phenotypic female births

Clinical Features (by system):

• Short stature (most consistent finding) - below 3rd percentile
• Final height: ~143 cm without treatment
• Loss of SHOX gene (pseudoautosomal region Xp22) → short stature

• Webbed neck (pterygium colli) - lymphedema-related
• Low posterior hairline
• Small mandible, high arched palate
• Prominent ears, low-set ears
• Shield-shaped (broad) chest
• Widely spaced nipples

• Cubitus valgus (increased carrying angle at elbow)
• Short 4th metacarpal
• Lymphedema of hands and feet (especially at birth)
• Nail hypoplasia

• Bicuspid aortic valve (most common - 30-50%)
• Coarctation of aorta
• Aortic dissection risk

• Horseshoe kidney (most common renal anomaly)
• Duplicated collecting system
• Rotational anomalies

• Primary amenorrhoea (90%)
• Streak gonads (ovaries replaced by fibrous tissue)
• Infantile genitalia, absent pubic/axillary hair
• Infertility (most cases)
• Some mosaics may have spontaneous puberty and even fertility

• Autoimmune thyroid disease (Hashimoto's) - 50%
• Diabetes mellitus (Type 2)
• Osteoporosis (from estrogen deficiency)

• Normal IQ but visual-spatial difficulties
• "Space-form blindness"

• Multiple pigmented naevi (melanocytic naevi)
• Keloid tendency

Investigations:

1. Karyotype - diagnostic; look for Y chromosome (gonadoblastoma risk)
2. FSH, LH - very high (hypergonadotropic hypogonadism)
3. Estradiol - very low
4. Thyroid function tests
5. Echocardiogram - cardiac anomalies
6. Renal USS
7. Bone age, DEXA scan

Management:

1. Growth Hormone (GH) therapy - started early; improves final height
2. Estrogen replacement - at age 12-13 for puberty induction; low dose initially, then combined HRT
3. Cardiac surveillance - echo every 1-2 years; avoid pregnancy (aortic dissection risk)
4. Thyroid monitoring - annual TSH
5. Prophylactic gonadectomy if Y chromosome material detected (gonadoblastoma prevention)
6. Psychological support, fertility options (egg donation)

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Q.246 - True Hermaphrodites and Types

Definition:

Karyotype:

• Most common: 46,XX (60%)
• 46,XY (10%)
• Mosaic 46,XX/46,XY (chimaera) - 30%

Gonads:

• Ovotestis - most common gonad (combined ovarian and testicular tissue in same gonad)
• One ovary + one testis
• Bilateral ovotestes

Types (by gonadal arrangement):

1. Lateral type: One ovary on one side; one testis on other side
2. Bilateral type: Ovotestis on both sides
3. Unilateral type (most common): Ovotestis on one side + either ovary or testis on the other

Clinical Features:

• External genitalia ambiguous (most common presentation)
• Predominantly female appearance with varying degrees of virilisation
• Presence of uterus usually (if 46,XX)
• Hypospadias, bifid scrotum
• Cryptorchidism
• Inguinal hernia (may contain gonad)
• Often raised as females

Investigations:

1. Karyotype
2. Hormonal profile - testosterone, AMH, estrogen
3. Pelvic USS/MRI - to map internal organs
4. Gonadal biopsy - definitive; shows both ovarian follicles AND seminiferous tubules histologically

Management:

1. Gender assignment (multidisciplinary team)
2. Remove discordant gonadal tissue (risk of malignancy in Y-containing gonads)
3. Appropriate hormonal therapy
4. Reconstructive surgery of genitalia
5. Psychological support
6. Fertility preservation (if possible)

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Quick Reference Index

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• For LQA (Long Questions): Write definition, classification, causes, features, investigations, management with subheadings - use the full answer above
• For SQA (Short Questions): Cover definition + classification + 4-5 causes/features + management in brief
• For MCQ: Focus on: PALM-COEIN, Tanner stages, 45,X karyotype, Mackenrodt's ligament, PGF2α in dysmenorrhoea, progesterone - secretory endometrium, decubitus ulcer in procidentia

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OBSTETRICS & GYNAECOLOGY — SAQ FORMAT

Q.215 to Q.246

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Q.215 - Clinical Features of Uterine Anomalies

• Class I: Hypoplasia/Agenesis (MRKH syndrome)
• Class II: Unicornuate
• Class III: Didelphys (double uterus + double cervix)
• Class IV: Bicornuate
• Class V: Septate (most common)
• Class VI: Arcuate
• Class VII: DES-related (T-shaped)

1. Primary amenorrhoea (agenesis - MRKH)
2. Recurrent pregnancy loss (RPL) - septate uterus is #1 cause
3. Preterm labour
4. Malpresentations (breech, transverse lie)
5. Dysmenorrhoea (obstructed hemi-uterus)
6. Infertility
7. Cryptomenorrhoea (outflow obstruction)
8. Dyspareunia (vaginal septal defects)
9. Associated renal anomalies (horseshoe/absent kidney - always check!)

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Q.216 - Functions of Ovarian Hormones

A) Oestrogen (E2 - Estradiol)

B) Progesterone

C) Androgens

• Pubic and axillary hair (adrenarche)
• Precursors for estrogen synthesis
• Libido

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Q.217 - HPO Axis (Hypothalamic-Pituitary-Ovarian Axis)

Components:

• Secretes GnRH (= LHRH) in pulsatile fashion (every 60-90 min)
• Pulsatile release essential; continuous → downregulation
• Stimulated by: Kisspeptin
• Inhibited by: Dopamine, opioids, prolactin

• GnRH → releases FSH + LH (glycoproteins; common alpha subunit, specific beta)

• FSH → follicular growth + estrogen production
• LH → androgen production; triggers ovulation; maintains corpus luteum

Feedback Mechanisms:

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Q.218 - Menstruation: Phases, Hormonal, Ovarian, Uterine Changes

Phases:

Hormonal Changes:

• Follicular: FSH rises → recruits follicles → estrogen rises → LH surge (day 13-14) → ovulation (36-38 hrs after LH peak)
• Luteal: Corpus luteum → progesterone + estrogen; if no pregnancy → corpus luteum degenerates → P falls → menstruation

Ovarian Changes:

1. Days 1-5: Follicle atresia
2. Days 5-14: Dominant Graafian follicle (20-25 mm) selected
3. Day 14: Ovulation (secondary oocyte in metaphase II released)
4. Days 15-25: Corpus luteum secretes progesterone + estrogen + inhibin A
5. Days 26-28: Corpus albicans (if no pregnancy)

Uterine (Endometrial) Changes:

1. Menstrual: Functional layer shed; spiral arteries constrict → ischaemia; PGs mediate shedding
2. Proliferative: Estrogen → regeneration; straight glands; pseudostratified epithelium
3. Secretory: Progesterone → tortuous glands; subnuclear vacuoles; secretions in lumen; spiral arteries elongate
4. Ischaemic: Progesterone withdrawal → coiling of spiral arteries → ischaemia

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Q.219 - Tanner's Classification (Sexual Maturity Rating)

Breast Development (B):

Pubic Hair (PH):

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Q.220 - Precocious Puberty: Causes and Diagnostic Features

Causes:

• Idiopathic (80% in girls - most common)
• CNS tumours (hypothalamic hamartoma, glioma)
• CNS insults: hydrocephalus, irradiation, NF-1

• McCune-Albright syndrome (GNAS1 mutation): precocious puberty + polyostotic fibrous dysplasia + cafe-au-lait spots
• Granulosa cell tumour (ovarian)
• Adrenal tumours / CAH
• Hypothyroidism (Van Wyk-Grumbach)
• Exogenous estrogen/androgen

Diagnostic Features:

1. Growth acceleration + early epiphyseal fusion → short final height
2. Bone age X-ray (wrist) - advanced
3. Hormonal: LH, FSH, estradiol; LH > 5 IU/L on GnRH stimulation test = central; LH:FSH ratio > 1 = central
4. Pelvic USS - ovarian cyst/tumour
5. MRI brain - hypothalamic/pituitary lesion
6. TSH - rule out hypothyroidism

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Q.221 - Delayed Puberty: Causes and Characteristic Features

Causes:

• Normal variant; positive family history

• Kallmann syndrome: GnRH deficiency + anosmia
• Craniopharyngioma / hypothalamic tumours
• Anorexia nervosa, malnutrition, excessive exercise
• Hypothyroidism, hyperprolactinaemia

• Turner syndrome (45,X) - most common cause in girls
• Premature ovarian insufficiency (POI)
• Chemotherapy/radiation damage

Characteristic Features:

1. Short stature
2. Absent/minimal breast development
3. Sparse pubic/axillary hair
4. Primary amenorrhoea
5. Infantile genitalia
6. Webbed neck, shield chest (Turner's)
7. Anosmia (Kallmann's)
8. Delayed bone age on X-ray

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Q.222 - Puberty Menorrhagia: Causes and Diagnostic Features

Causes:

1. Anovulatory cycles - most common; immature HPO axis; no progesterone → unopposed estrogen → irregular heavy shedding
2. Von Willebrand disease - 15-20% of adolescent heavy bleeding
3. ITP, platelet dysfunction, coagulopathy
4. Hypothyroidism
5. Hyperprolactinaemia
6. PCOS
7. Structural: Endometrial polyp, fibroid (rare)

Diagnostic Features:

1. PBAC score (Pictorial Blood Assessment Chart) > 100 = heavy
2. CBC - anaemia (low Hb, MCV)
3. Coagulation: PT, aPTT, platelet count
4. vWF assay, Ristocetin cofactor - rule out vWD
5. Hormonal: TSH, prolactin, FSH, LH
6. Pelvic USS - structural causes

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Q.223 - Amenorrhoea

• Primary: No menstruation by age 15 (with normal 2° sex chars) or by 13 (without)
• Secondary: No menstruation for ≥3 months (regular cycle) or ≥6 months (irregular)

Classification of Primary Amenorrhoea:

Causes of Secondary Amenorrhoea:

1. Pregnancy - EXCLUDE FIRST (urine hCG)
2. PCOS - most common
3. Hypothalamic: Stress, weight loss, exercise, anorexia
4. Pituitary: Hyperprolactinaemia (most common pituitary cause), Sheehan's syndrome
5. Ovarian: Premature ovarian insufficiency (POI)
6. Uterine: Asherman's syndrome (post-D&C adhesions)
7. Thyroid/Adrenal: Hypothyroidism, Cushing's, CAH

Investigations:

• Urine hCG, FSH, LH, prolactin, estradiol, TSH
• Karyotype (primary)
• Pelvic USS
• MRI pituitary (high prolactin)
• Progesterone withdrawal test (tests outflow patency)

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Q.224a - Cryptomenorrhoea: Causes

Causes (Anatomical Obstruction):

1. Imperforate hymen - most common; bluish-purple bulging membrane at introitus → haematocolpos
2. Transverse vaginal septum - at upper 1/3-lower 2/3 junction
3. Cervical stenosis - post-surgical/inflammatory
4. Vaginal atresia
5. Cervical atresia - rare

Consequences:

• Haematocolpos (blood in vagina)
• Haematometra (blood in uterus)
• Haematosalpinx (blood in tube)
• Haematoperitoneum

Features: Primary amenorrhoea + cyclical pelvic pain + lower abdominal mass

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Q.224b - Hypomenorrhoea: Causes

Causes:

1. Asherman's syndrome (intrauterine adhesions) - post-D&C, most common
2. Cervical stenosis
3. Hypoestrogenism (POI, hypothalamic amenorrhoea)
4. Hypothyroidism / hyperthyroidism
5. OCP use (suppresses endometrial proliferation)
6. Progestogen-only pill / Mirena IUS
7. Endometrial tuberculosis
8. Anxiety/stress

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Q.225 - Oligomenorrhoea: Causes

Causes:

1. PCOS - most common; hyperandrogenism, anovulation
2. Hypothyroidism
3. Hyperprolactinaemia - suppresses GnRH pulsatility
4. Hypothalamic dysfunction - stress, exercise, weight loss
5. Perimenopause - declining ovarian reserve
6. Cushing's syndrome
7. CAH, androgen-secreting tumours

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Q.226 - Polymenorrhoea: Causes

Causes:

1. Short luteal phase - corpus luteum insufficiency; early progesterone withdrawal
2. Short follicular phase - accelerated follicular development (perimenopause)
3. Hyperthyroidism
4. Anovulation
5. PID - inflammation shortens cycle
6. Copper IUCD
7. Endometriosis

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Q.227 - Metrorrhagia: Causes

Causes:

1. Cervical ectropion - most common
2. Cervical polyp / carcinoma
3. Endometrial polyp / hyperplasia / carcinoma
4. Submucous fibroid
5. Breakthrough bleeding on OCP
6. Anovulation / progesterone deficiency
7. PID / Endometritis
8. Ovulation bleeding (Mittelschmerz)
9. Thyroid dysfunction
10. Coagulation disorders
11. Copper IUCD

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Q.228 - AUB (Abnormal Uterine Bleeding)

PALM-COEIN Classification (FIGO):

• P = Polyp
• A = Adenomyosis
• L = Leiomyoma (fibroid)
• M = Malignancy / Hyperplasia

• C = Coagulopathy (vWD, ITP)
• O = Ovulatory dysfunction (most common - anovulation)
• E = Endometrial disorder
• I = Iatrogenic (OCP, anticoagulants, antipsychotics)
• N = Not yet classified

Investigations:

1. CBC (anaemia), Coagulation profile
2. TSH, prolactin, FSH, LH, testosterone
3. Pelvic USS (first-line imaging)
4. Saline infusion sonography (intracavitary lesions)
5. Endometrial biopsy (> 35 yrs or risk factors)
6. Hysteroscopy (gold standard for intracavitary lesions)

General Management:

• Tranexamic acid - reduces loss 40-50% (antifibrinolytic)
• NSAIDs (mefenamic acid) - reduces loss 20-30%
• Combined OCP - cycle regulation
• Progestins - anovulatory AUB
• Levonorgestrel IUS (Mirena) - most effective medical; reduces loss 90%
• GnRH agonists - for fibroids/preop

• Endometrial ablation (no future fertility)
• Hysteroscopic polypectomy / myomectomy
• Hysterectomy - definitive

Homoeopathic Remedies:

• Phosphorus - bright red profuse bleeding
• Sabina - mixed bright + dark blood; fibroid
• Thlaspi bursa-pastoris - menorrhagia + cramping
• Trillium pendulum - profuse flooding
• China - weakness from blood loss; dark clots
• Ipecac - bright red bleeding with nausea

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Q.229 - Metropathia Haemorrhagica: Causes

Causes of Underlying Anovulation:

1. PCOS - most common in reproductive age
2. Perimenopause - anovulatory cycles
3. Hypothalamic dysfunction - stress, weight loss
4. Hypothyroidism
5. Hyperprolactinaemia
6. Obesity - excess peripheral estrogen (adipose aromatisation)

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Q.230 - Dysmenorrhoea

Primary Dysmenorrhoea:

• No underlying pelvic pathology
• Cause: Excess PGF2α → uterine hypercontractility → ischaemia → pain
• Onset: 6-12 months after menarche; young women 15-25 yrs
• Pain: Crampy, lower abdomen + back; starts 1-2 hrs before flow; lasts 1-2 days
• Associated: Nausea, diarrhoea, headache

Secondary Dysmenorrhoea:

• Underlying pelvic pathology
• Causes: Endometriosis (most common), adenomyosis, submucous fibroid, PID, copper IUCD, cervical stenosis
• Pain: Starts 1-2 weeks before period; persists after; deep dyspareunia; worsens with age

Management of Primary:

1. NSAIDs (ibuprofen, mefenamic acid) - first line; inhibit PG synthesis
2. Combined OCP - suppresses ovulation
3. Heat application; exercise

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Q.231 - Mittelschmerz Syndrome: Causes

Causes/Mechanism:

1. Follicular distension - rapidly expanding Graafian follicle stretches ovarian capsule
2. Peritoneal irritation - release of follicular fluid + blood at ovulation irritates peritoneum
3. Prostaglandins - from follicular fluid → smooth muscle contraction
4. Tubal peristalsis - increased fallopian tube motility at ovulation

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Q.232 - Homoeopathic Remedies for Membranous Dysmenorrhoea

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Q.233 - PMS (Premenstrual Syndrome)

Causes:

1. Progesterone sensitivity in luteal phase
2. Serotonin deficiency (falling estrogen reduces serotonin)
3. Aldosterone excess → fluid retention
4. Endorphin withdrawal
5. Vitamin B6 deficiency (cofactor for serotonin synthesis)
6. GABA-A receptor sensitivity to allopregnanolone

Clinical Features (Day 14-28; resolve with period):

• Breast tenderness (mastalgia)
• Abdominal bloating, weight gain
• Headache/migraine
• Fatigue, oedema
• Acne, carbohydrate craving

• Irritability, anger
• Anxiety, depression, mood swings
• Insomnia, poor concentration

General Management:

1. Aerobic exercise; low salt, low caffeine diet
2. NSAIDs (for pain)
3. SSRIs (fluoxetine/sertraline) - most effective; can be given only in luteal phase
4. Vitamin B6 50-100 mg/day
5. Calcium carbonate 1000-1200 mg/day
6. Combined OCP (suppresses ovulation)
7. GnRH agonists (severe cases)
8. Spironolactone (for bloating/fluid retention)
9. Cognitive Behavioural Therapy (CBT)

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Q.234 - Menopause: Pathophysiology, Anatomical Changes, C/F, Menopausal Syndrome, Metabolic Changes

Pathophysiology:

1. Ageing → depletes ovarian follicular reserve
2. Fewer follicles → less inhibin B → FSH rises (earliest hormonal change)
3. Less estradiol produced → LH also rises (loss of negative feedback)
4. FSH > 40 IU/L + 12 months amenorrhoea = menopause
5. Residual estrogen from peripheral aromatisation → estrone (E1) becomes dominant

Anatomical Changes:

1. Ovaries: Atrophy; fibrous; no follicles
2. Uterus: Shrinks; endometrium atrophies
3. Vagina: Thin, pale, dry; rugae disappear
4. Vulva: Labia minora shrinkage
5. Breast: Glandular → fatty tissue
6. Pubic hair: Sparse
7. Urethra: Atrophy; urge incontinence

Clinical Features / Menopausal Syndrome:

• Hot flushes (sudden warmth; face/neck/chest; 1-5 min)
• Night sweats
• Palpitations

• Mood swings, irritability
• Anxiety, depression
• Insomnia, fatigue
• Memory/concentration difficulty

• Vaginal dryness, dyspareunia, pruritus
• Urinary frequency, urgency, recurrent UTIs
• Stress/urge incontinence

• Decreased libido, anorgasmia

Metabolic Changes:

1. Bone: Rapid loss (3-5%/year first 5 yrs); osteoporosis → hip, vertebral, Colles' fractures
2. CVS: ↑LDL, ↓HDL → atherosclerosis
3. Lipids: ↑Total cholesterol, LDL, triglycerides
4. Weight: Central obesity; insulin resistance → metabolic syndrome
5. Skin: ↓Collagen → wrinkles
6. Cognitive: ↑Risk of Alzheimer's

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Q.235 - Perimenopause and Artificial Menopause

Perimenopause (Climacteric):

• Transitional period 2-8 years before and just after menopause
• Cycles become irregular; FSH rises; estrogen fluctuates
• Vasomotor symptoms begin
• Ends 12 months after last menstrual period

Artificial Menopause:

1. Surgical: Bilateral oophorectomy - most common; called "surgical menopause"
2. Radiation: Pelvic radiotherapy
3. Chemotherapy: Alkylating agents, cyclophosphamide
4. GnRH agonists - reversible medical menopause

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Q.236 - Causes of Delayed and Premature Menopause

Delayed Menopause (after age 55):

• Nulliparity
• Obesity (peripheral estrogen production)
• Genetics / family history
• High prolonged estrogen exposure

Premature Menopause / Premature Ovarian Insufficiency (POI):

1. Chromosomal: Turner syndrome (45,X), Fragile X premutation (FMR1)
2. Autoimmune - most common acquired cause; associated with Hashimoto's, Addison's, DM Type 1
3. Iatrogenic: Radiotherapy, chemotherapy, bilateral oophorectomy
4. Genetic: BRCA mutations
5. Viral: Mumps oophoritis
6. Idiopathic (majority)

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Q.237 - Post-Menopausal Bleeding: Causes, Investigations, D/D, Homoeopathic Remedies

Causes (frequency order):

1. Atrophic vaginitis/endometritis - most common (~30%)
2. Endometrial carcinoma - most important to exclude
3. Endometrial polyp
4. Endometrial hyperplasia (pre-malignant)
5. Cervical carcinoma / polyp
6. HRT breakthrough bleeding
7. Ovarian tumour (granulosa cell - estrogen-secreting)
8. Vaginal trauma / ulcer
9. Coagulation disorders
10. Vulval carcinoma

Investigations:

1. Transvaginal USS - first line; endometrial thickness > 4-5 mm suspicious
2. Endometrial biopsy (Pipelle) - mandatory; rules out malignancy
3. Hysteroscopy + D&C - gold standard; direct visualisation + biopsy
4. Pap smear - cervical cause
5. CBC, coagulation profile
6. Serum CA-125 (ovarian tumour suspected)

D/D:

Homoeopathic Remedies:

• Phosphorus - bright red profuse bleeding; thin, tall woman
• China - weakness from blood loss; dark clots
• Crocus sativus - dark, stringy, thread-like clotted blood
• Trillium pendulum - profuse flooding; hip bones sensation
• Fraxinus Americana - fibroid-related post-menopausal bleeding

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Q.238 - Uterine Prolapse: Causes, Classification, Degrees, C/F, D/D, Complications, General Management

Causes:

1. Difficult/prolonged labour (injury to levator ani)
2. Grand multiparity / multiple pregnancies
3. Chronic raised intra-abdominal pressure (chronic cough, constipation, obesity)
4. Menopause - estrogen deficiency → loss of collagen
5. Congenital weak supports (nulliparous prolapse - rare)
6. Sacral nerve injury

Degrees:

Clinical Features:

1. Dragging/bearing down sensation - "something coming down"
2. Visible lump at vulva (3rd degree)
3. Backache (worse with prolonged standing)
4. Urinary: frequency, urgency, retention, stress incontinence
5. Bowel: constipation, incomplete evacuation (with rectocele)
6. Dyspareunia
7. Decubitus ulcer on cervix (chronic)
8. Cervical hypertrophy + elongation

Differential Diagnosis:

• Cervical elongation (body not descended)
• Cervical fibroid polyp
• Vaginal cyst
• Cystocele/rectocele alone

Complications:

1. Decubitus ulcer → infection, bleeding
2. Urinary tract infection; hydronephrosis
3. Uterine hypertrophy
4. Oedema/incarceration of prolapse

General Management:

• Pelvic floor exercises (Kegel's) - 1st degree / mild
• Ring pessary - elderly, unfit for surgery, pregnant
• Topical estrogen cream (post-menopausal)
• Treat precipitating causes

• Manchester/Fothergill operation - amputation of cervix + repair; retains uterus
• Anterior colporrhaphy - cystocele repair
• Posterior colporrhaphy + perineorrhaphy - rectocele repair
• Vaginal hysterectomy + pelvic floor repair - definitive; 3rd degree/procidentia
• Sacrocolpopexy - vault prolapse

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Q.239 - Rectocele and Cystocele (Degrees)

Cystocele:

• Grade I: Bulge stays within vagina
• Grade II: Bulge reaches introitus
• Grade III: Protrudes beyond introitus

Rectocele:

• Grade I: Stays in vagina
• Grade II: Reaches introitus
• Grade III: Protrudes beyond introitus

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Q.240 - Procidentia

• Large mass hanging from vulva
• Decubitus ulceration on cervix
• Urinary retention (urethral kinking)
• Constipation
• Oedema of prolapsed tissue
• Hypertrophy + elongation of cervix

• Temporary: Reduction + ring pessary
• Definitive: Vaginal hysterectomy + anterior + posterior colporrhaphy

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Q.241 - Pessary Treatment: Indications and Contraindications

Types of Pessary:

Indications:

1. Elderly unfit for surgery
2. Awaiting surgery (temporary measure)
3. Patient desiring more pregnancies
4. Prolapse during pregnancy
5. Severe medical illness (contraindication to surgery)
6. Patient refusal of surgery
7. 1st-2nd degree in young women

Contraindications:

1. Acute PID / pelvic infection
2. Severe ulceration of prolapsed tissue
3. Very tight/small vaginal introitus
4. Allergy to pessary material
5. Poor patient compliance (unable to maintain hygiene)

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Q.242 - Surgical Management of Genital Prolapse

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Q.243 - Retroversion of Uterus: Causes, Types, C/F, Degrees, D/D, Homoeopathic Remedies

Degrees:

1. 1st degree: Fundus points directly upward (vertical)
2. 2nd degree: Fundus in posterior pouch of Douglas
3. 3rd degree: Fundus in rectouterine pouch; cervix points anteriorly

Types:

1. Mobile (congenital) - idiopathic; freely movable; no pathology; most common (80%)
2. Fixed (acquired/pathological) - uterus fixed by adhesions

Causes of Fixed Retroversion:

1. Endometriosis - most common; adhesions in pouch of Douglas
2. PID / Chronic salpingo-oophoritis - adhesions
3. Posterior fibroids
4. Ovarian cysts behind uterus
5. Previous pelvic surgery
6. Pelvic tuberculosis

Clinical Features:

• Usually asymptomatic (mobile type)
• Dysmenorrhoea - dragging backache during menses
• Deep dyspareunia (especially fixed type)
• Chronic backache (lumbar)
• Infertility (if associated endometriosis)
• Per vaginum: Fundus in posterior fornix; cervix points anteriorly

Differential Diagnosis:

• Ovarian cyst in pouch of Douglas
• Retroverted gravid uterus
• Posterior fibroid
• Pelvic abscess

Homoeopathic Remedies:

• Lilium tigrinum - bearing down in retroversion; relieved by supporting perineum; irritable, hurried
• Sepia - bearing down; indifferent; backache; better by exercise
• Aletris farinosa - weakness, prolapse tendency, anaemia
• Fraxinus Americana - fibroid-related retroversion with bearing down

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Q.244 - Inversion of Uterus: Etiology, Types, Clinical Features

Etiology:

1. Mismanagement of 3rd stage of labour - most common; undue cord traction on uncontracted uterus
2. Fundal pressure incorrectly applied (Credé's manoeuvre)
3. Fundal placenta with short umbilical cord
4. Uterine atony + adherent placenta
5. Submucous fundal fibroid (chronic non-puerperal inversion)

Types:

Clinical Features:

1. Sudden severe lower abdominal pain
2. Profound shock (neurogenic - peritoneal stretching) disproportionate to blood loss
3. Severe haemorrhage from placental site
4. No uterine fundus palpable abdominally (dimple instead)
5. Dark red granular mass at/beyond introitus (complete)
6. Placenta may still be attached
7. Bradycardia (vasovagal)

Management:

1. IV access; fluids; blood transfusion
2. O'Sullivan's hydrostatic method - warm saline into vagina; hydrostatic pressure reduces inversion
3. Johnson's manoeuvre - manual reduction under anaesthesia (palm-first method)
4. Surgical: Huntington's procedure (abdominal traction); Haultain's operation (incises cervical ring)

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Q.245 - Turner Syndrome

Karyotype:

• 45,X - 57% (classic)
• Mosaic 45,X/46,XX - 29% (milder)
• Structural X abnormalities - 14% (isochromosome Xq, ring X, deletions)
• Incidence: 1 in 2,500 phenotypic female births
• Most common single chromosomal disorder in humans (most abort spontaneously)

Clinical Features:

• Short stature (most consistent; SHOX gene loss on Xp22)
• Final height ~143 cm without treatment

• Webbed neck (pterygium colli)
• Low posterior hairline
• Shield-shaped broad chest; widely spaced nipples
• Small mandible; high arched palate

• Cubitus valgus (increased carrying angle)
• Short 4th metacarpal
• Lymphoedema of hands + feet (at birth)
• Nail hypoplasia

• Bicuspid aortic valve (30-50%) - most common
• Coarctation of aorta
• Risk of aortic dissection (especially in pregnancy)

• Horseshoe kidney (most common renal anomaly)
• Duplicated collecting system

• Primary amenorrhoea (90%)
• Streak gonads (fibrous; no follicles)
• Infantile genitalia; absent pubic/axillary hair
• Infertility (most cases)

• Autoimmune thyroid disease (Hashimoto's) - 50%
• Diabetes mellitus Type 2
• Osteoporosis

• Normal IQ; but visual-spatial difficulties ("space-form blindness")

• Multiple pigmented naevi; keloid tendency

Investigations:

1. Karyotype - diagnostic; check for Y chromosome (gonadoblastoma risk)
2. FSH, LH - very high (hypergonadotropic hypogonadism)
3. Estradiol - very low
4. TFTs (annual)
5. Echocardiogram
6. Renal USS
7. Bone age, DEXA scan

Management:

1. Growth Hormone therapy - early initiation improves final height
2. Estrogen replacement - at 12-13 yrs for puberty induction; then combined HRT
3. Cardiac surveillance - echo every 1-2 yrs; avoid pregnancy (aortic dissection risk)
4. Annual TFTs
5. Prophylactic gonadectomy if Y chromosome material found (prevents gonadoblastoma → dysgerminoma)
6. Psychological support; egg donation for fertility

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Q.246 - True Hermaphrodites and Types

Karyotype:

• 46,XX - most common (60%)
• 46,XY - 10%
• Mosaic 46,XX/46,XY (chimera) - 30%

Gonads:

• Ovotestis - most common (combined ovarian + testicular tissue in one gonad)
• One ovary + one testis
• Bilateral ovotestes

Types (by gonadal arrangement):

Clinical Features:

• Ambiguous external genitalia (most common presentation)
• Predominantly female appearance + variable virilisation
• Uterus usually present (if 46,XX)
• Hypospadias, bifid scrotum, cryptorchidism
• Inguinal hernia (may contain gonadal tissue)
• Often raised as female

Investigations:

1. Karyotype
2. Hormonal profile: testosterone, AMH, estrogen, LH, FSH
3. Pelvic USS/MRI - internal organ mapping
4. Gonadal biopsy - definitive; both ovarian follicles AND seminiferous tubules on histology

Management:

1. Multidisciplinary team (MDT) - gender assignment
2. Remove discordant gonadal tissue (malignancy risk in Y-containing gonads)
3. Appropriate hormonal therapy
4. Reconstructive surgery of genitalia
5. Psychological support
6. Fertility preservation (if possible)

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EXAM TIPS - How to Score Maximum in SAQs

• Most important uterine support = Cardinal (Mackenrodt's) ligament
• Primary dysmenorrhoea mechanism = excess PGF2α
• Most common cause of AUB = Anovulatory dysfunction (O in COEIN)
• Most common karyotype in Turner = 45,X
• Most consistent feature of Turner = Short stature
• PMB rule = Endometrial carcinoma until proven otherwise
• Procidentia = 3rd degree prolapse + inverted vagina
• Ovotestis = most common gonad in True hermaphrodites
• Most common cause of fixed retroversion = Endometriosis
• Perimenopause hormone: FSH rises first