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1. PUBERTY

• Breast development → Pubic hair → Axillary hair → Growth spurt → Menarche

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2. ENDOCRINOLOGY IN PUBERTY

• Gonadal steroids and gonadotropins are low until age 6–8 yrs due to Gonadostat (highly sensitive negative feedback of oestrogen on hypothalamo-pituitary system)
• As puberty approaches, this negative feedback is gradually lost
• Hormone cascade: GnRH → FSH + LH → Oestradiol → Secondary sexual characters
• GnRH pulses = pulsatile gonadotropin secretion (first at night, then by day)
• Adrenarche (~7 yrs): Adrenal glands increase sex steroid synthesis (DHEA, DHAS, androstenedione)
• Gonadarche: ↑ GnRH → ↑ FSH/LH → follicular development → ↑ oestrogen
• Leptin (from adipose tissue): also involved in puberty initiation and menarche

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3. PRECOCIOUS PUBERTY

• GnRH Dependent (80%): Constitutional (most common), Juvenile primary hypothyroidism, CNS lesions (tumour/trauma/infection)
• Incomplete forms: Premature thelarche, Premature pubarche, Premature menarche
• GnRH Independent (Ovarian): Granulosa/Theca/Leydig cell tumour, McCune-Albright syndrome
• GnRH Independent (Adrenal): Hyperplasia, Tumour
• McCune-Albright: Sexual precocity + polyostotic fibrous dysplasia + café-au-lait spots; treat with aromatase inhibitors

• Suppresses FSH/LH → down-regulates HPO axis
• Reverses breast development, arrests puberty progression
• Given as monthly depot injection; maintain oestradiol <10 pg/mL
• Used till age 11 years

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4. DELAYED PUBERTY

• Hypergonadotropic Hypogonadism: Gonadal dysgenesis (45 XO/Turner's), pure gonadal dysgenesis, ovarian failure
• Hypogonadotropic Hypogonadism: Constitutional delay, Chronic illness/malnutrition, Kallmann's syndrome, intracranial tumours
• Eugonadism: Müllerian agenesis, imperforate hymen, transverse vaginal septum, androgen insensitivity

• Mature 2° characters → Müllerian agenesis/dysgenesis
• Asynchronous pubic hair → Androgen insensitivity syndrome
• Immature → ↑FSH (karyotype) OR Low/Normal FSH (sellar CT/MRI) OR ↑TSH (hypothyroidism)

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GYNECOLOGY EXAM NOTES

Source: DC Dutta's Textbook of Gynecology | Ch. 14 & 15

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TOPIC 1: PRIMARY DYSMENORRHEA (SPASMODIC)

Definition

• Incidence: 15–20% of all women with incapacitation
• With NSAIDs and oral contraceptives, marked relief of symptoms occurs

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Etiopathology — Causes of Pain

• Mostly confined to adolescents
• Almost always confined to ovulatory cycles
• Pain is usually cured following pregnancy and vaginal delivery
• Pain is related to dysrhythmic uterine contractions and uterine hypoxia

Key Mechanisms (High Yield MCQ)

• In ovulatory cycles, under action of progesterone → PGF2α and PGE2 are synthesized from secretory endometrium
• PGF2α is a strong vasoconstrictor → causes ischaemia (angina) of myometrium
• Either ↑ production of PG OR ↑ sensitivity of myometrium to normal PG → ↑ myometrial contraction ± dysrhythmia
• Possible cause of pain = Junctional Zone (JZ) change → dysperistalsis and hyperactivity

• Most important mechanism of primary dysmenorrhea
• Subendometrial myometrium (JZ) is structurally and functionally different from outer myometrium
• Marked hyperperistalsis of JZ in women with endometriosis and adenomyosis
• JZ changes: irregular thickening, hyperplasia of smooth muscle, less vascularity = Junctional Zone Hyperplasia

• Overactivity of sympathetic nerves → hypertonicity of circular fibres of isthmus and internal os
• Relief of pain following dilatation of cervix or following vaginal delivery = damage to adrenergic neurons

• ↑ Vasopressin released during menstruation → ↑ uterine hyperactivity and dysrhythmic contractions → ischaemia and hypoxia → pain
• Explains persistence of pain even with anti-prostaglandin drugs
• Vasopressin also ↑ PG synthesis and ↑ myometrial activity directly

• Causes myometrial smooth muscle contractions, especially in JZ endometrium
• Endothelins in endometrium can induce PGF2α
• Local myometrial ischaemia caused by endothelins and PGF2α aggravates uterine dysperistalsis and hyperactivity

• Concentration is found high
• Leukotrienes and PAFs are vasoconstrictors that stimulate myometrial contractions

• Tension and anxiety during adolescence → lower the pain threshold

FLOWCHART: Progesterone → PGF2α synthesis → Endothelin + Leukotrienes + PAFs → Reduced blood flow + ↑ Myometrial contractions (JZ) ± dysrhythmia → PAIN

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Patient Profile

• Predominantly adolescent girls
• Usually appears within 2 years of menarche
• More common in girls from affluent society
• Mother or sister may be dysmenorrhoeic (genetic predisposition)

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Clinical Features

• Pain begins a few hours before or just with onset of menstruation
• Lasts usually a few hours, may extend to 24 hours; seldom persists beyond 48 hours
• Character: spasmodic, confined to lower abdomen; may radiate to back and medial aspect of thighs
• Systemic: nausea, vomiting, fatigue, diarrhea, headache, tachycardia
• Vasomotor: pallor, cold sweats, occasional fainting; syncope in severe cases
• Abdominal and pelvic examination: no abnormal findings
• Ultrasound: very useful, not invasive

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Differentiating Features: Primary vs Secondary

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Treatment

General Measures

• Explanation, reassurance, simple psychotherapy
• Continue usual activities including sports
• During menses: keep bowel empty; mild analgesics and antispasmodics
• HABIT-FORMING drugs (pethidine, morphine) must NOT be prescribed

Drug Treatment (Table 14.1)

DRUG OF CHOICE: PSIs/NSAIDs are FIRST LINE. OCP is drug of choice when contraception is also required.

• PSIs reduce intrauterine pressure significantly; reduce PG synthesis via COX enzyme inhibition
• Used orally for 2–3 days starting with onset of period; continued for 3–6 cycles
• Contraindications to PSI therapy: allergy to aspirin, gastric ulceration, history of asthma

1. Wanting contraceptive precaution
2. With heavy periods
3. Unresponsive or having contraindications to anti-prostaglandin drugs

Surgical Treatment

• TENS (Transcutaneous Electrical Nerve Stimulation): results not better than analgesics
• LUNA (Laparoscopic Uterine Nerve Ablation): NOT found beneficial
• LPSN (Laparoscopic Presacral Neurectomy): cuts sensory pathways via T11–T12; NOT helpful for adnexal pain (T9–T10)
• Dilatation of cervical canal: under anaesthesia; not commonly done; late sequela = cervical incompetence

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TOPIC 2: SECONDARY DYSMENORRHEA (CONGESTIVE)

Definition

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Patient Profile

• Usually in their thirties; more often parous; unrelated to social status

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Causes (Table 14.2)

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Clinical Features

• Pain is dull, situated in back and in front without radiation
• Appears 3–5 days PRIOR to period and relieves with onset of bleeding
• No systemic discomfort (unlike primary)
• Discomfort may exist even between periods
• Abdominal/vaginal examination usually reveals pathology

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Investigations

• Transvaginal sonography: detects most pelvic pathology (leiomyoma, adenomyosis)
• Saline infusion sonography: submucous fibroid, polyps
• Laparoscopy: endometriosis — both diagnostic and therapeutic
• Hysteroscopy: both diagnostic and therapeutic

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Special Types

Ovarian Dysmenorrhea

• Right ovarian vein crosses ureter at right angle
• Premenstrual pelvic congestion → engorgement in vein → pressure on ureter → stasis → infection → pyelonephritis → pain
• Important cause of UNILATERAL dysmenorrhea
• Pain referred to area innervated by T10 to L1 segments
• Diagnosis: pelvic venography, Doppler scan, CT, MRI, angiography
• Treatment: MPA 50 mg daily × 4 months; hysterectomy in parous women advancing in age

Mittelschmerz's Syndrome (Ovular/Midcycle Pain)

• Ovular pain — midmenstrual period
• Situated in hypogastrium or iliac fossa (side of ovulating ovary); does NOT change side
• Lasts < 12 hours; may have slight vaginal bleeding or mucoid discharge
• Probable causes: (i) tension of Graafian follicle prior to rupture; (ii) peritoneal irritation by follicular fluid; (iii) contraction of tubes and uterus
• Treatment: assurance and analgesics; obstinate cases — make cycle anovular with OCP

Pelvic Congestion Syndrome

• Disturbance in autonomic nervous system → gross vascular congestion with pelvic varicosities
• Congestive dysmenorrhea without demonstrable pelvic pathology
• Patient complains of vague pelvic discomfort + backache + pelvic pain with long standing position ± dyspareunia
• May have menorrhagia or epimenorrhea; uterus bulky and boggy
• Diagnosis: pelvic venography, Doppler — vessels compressed with intraperitoneal pressure but reappear as pressure reduced
• Treatment: MPA 50 mg daily × 4 months; hysterectomy in parous women

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TOPIC 3: PREMENSTRUAL SYNDROME (PMS / PMDD)

Definition (ACOG Criteria — ALL must be fulfilled)

PMS is a psychoneuroendocrine disorder of unknown etiology, noticed just prior to menstruation, occurring regularly in the luteal phase of each ovulatory menstrual cycle, with a large number of symptoms during the last 7–10 days of the menstrual cycle.

ACOG Criteria:

1. No organic lesion
2. Regularly occurs during luteal phase of each ovulatory menstrual cycle
3. Symptoms severe enough to disturb life style or require medical help
4. Symptom-free period during rest of the cycle

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Pathophysiology (Hypotheses)

• Altered ratio starting from midluteal phase → diminished progesterone level

• Serotonin: important neurotransmitter; decreased synthesis in luteal phase in PMS sufferers → explains why SSRIs work
• Endorphins: PMS symptom complex thought to be due to withdrawal of endorphins from CNS during luteal phase
• GABA (γ-aminobutyric acid): suppresses anxiety level in brain; GABA agonists are effective

• TRH, prolactin, renin, aldosterone, prostaglandins — mentioned but nothing conclusive
• Pyridoxine (Vit B6): corrects tryptophan metabolism, especially 'pill'-associated depression

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Symptomatology (Table 14.4)

MOST USEFUL DIAGNOSTIC TOOL: Patient's symptom diary documented over 2–3 cycles (Table 14.4)

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Treatment (Table 14.5)

Non-pharmacological

• Assurance, yoga, stress management, dietary manipulation
• Avoidance of salt, caffeine and alcohol especially in second half of cycle

Non-hormonal Drugs

Hormonal Drugs

Surgical

• Hysterectomy + bilateral oophorectomy — last resort in established cases approaching menopause

KEY POINTS:

• SSRI (fluoxetine) is DOC
• GnRH agonist therapy results are DRAMATIC
• Women with PMDD show NO deficit in cognitive function in the luteal phase
• Exact etiology UNKNOWN

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TOPIC 4: ABNORMAL UTERINE BLEEDING (AUB)

Definition

Normal Menstruation

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Patterns of AUB — Definitions

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Menorrhagia — Detailed Notes

Causes

• Fibroid uterus, Adenomyosis, Pelvic endometriosis, IUCD in utero
• Chronic tubo-ovarian mass, Tubercular endometritis (early cases)
• Retroverted uterus — congestion, Granulosa cell tumour
• Endometrial polyp, Cervical stenosis

• Liver dysfunction (cirrhosis) — failure to conjugate/inactivate oestrogens
• Congestive cardiac failure, Severe hypertension

• Hypothyroidism, Hyperthyroidism

• ITP, Leukaemia, Von Willebrand's disease, Platelet deficiency (thrombocytopenia)

• Disturbed hypothalamo-pituitary-ovarian-endometrial axis
• Emotional upset

Diagnosis

• Long duration of flow, passage of big clots, use of increased number of thick sanitary pads, pallor, low Hb
• Transvaginal sonography: most pelvic pathology detected

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Polymenorrhea

• Cycle reduced to < 21 days; constant at that frequency
• Causes: DUB (adolescence, preceding menopause, post-delivery/abortion); PID; ovarian endometriosis
• Treatment: hormone treatment as outlined in DUB

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Metrorrhagia

• Irregular, acyclic bleeding; amount variable
• Malignancy must be excluded prior to any definitive treatment

• Carcinoma cervix, Mucous polyp of cervix
• Vascular ectopy of cervix (especially pregnancy/pill use)
• Infections — chlamydial or tubercular cervicitis
• Cervical endometriosis

• Urethral caruncle, Ovular bleeding
• Breakthrough bleeding in pill use
• IUCD in utero, Decubitus ulcer

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Oligomenorrhea

• Intervals > 35 days; constant at that frequency

• Age-related: adolescence and preceding menopause
• Weight-related: obesity
• Stress and exercise related
• Endocrine disorders: PCOS (most common), Hyperprolactinemia, Hyperthyroidism
• Androgen producing tumours: ovarian, adrenal
• Tubercular endometritis — late cases
• Drugs: Phenothiazines, Cimetidine, Methyldopa

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Hypomenorrhea

• Scanty bleeding < 2 days

• Local: uterine synechiae or endometrial tuberculosis
• Endocrinal: OCPs, thyroid dysfunction, premenopausal period
• Systemic: malnutrition

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RAPID REVISION — HIGH YIELD EXAM POINTS

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• Primary dysmenorrhea: full etiopathology table (PGF2α, JZ, Vasopressin, Endothelins, PAF) with the pain flowchart
• Patient profile + clinical features side-by-side
• Primary vs Secondary differentiating features table
• Complete drug treatment table with doses (NSAIDs, OCP, Dydrogesterone, LNG-IUS)
• Surgical options (TENS, LUNA, LPSN, cervical dilatation)
• Secondary dysmenorrhea: causes, special conditions (Ovarian dysmenorrhea, Mittelschmerz's, Pelvic congestion), investigations

• PMS: ACOG criteria, pathophysiology hypotheses, full symptomatology table
• Complete PMS treatment table (Fluoxetine DOC, GnRH agonists, Spironolactone, Danazol, OCP)
• AUB: normal menstruation values, all 5 patterns with definitions + cut-offs
• Menorrhagia causes (pelvic/systemic/endocrinal/haematological/functional)
• Contact bleeding, acyclic and intermenstrual bleeding causes
• Final rapid revision MCQ table with 27 key exam facts

• No pelvic pathology, adolescents, ovulatory cycles only
• Pain AT onset of menses, spasmodic/colicky, lasts <48 hrs
• Systemic symptoms present (N/V/D/headache)
• Pain-free between periods
• Relieved by pregnancy & vaginal delivery
• Cause: PGF2α → JZ dysperistalsis → ischaemia → pain
• Rx: NSAIDs first line, then OCP/LNG-IUS

• Pelvic pathology PRESENT, women in 30s, parous
• Pain starts 3-5 days BEFORE menses, dull/non-radiating
• Systemic symptoms usually ABSENT
• Discomfort may persist between periods
• Examination reveals pathology
• Causes: Endometriosis, Adenomyosis, Fibroids, IUCD, Cervical stenosis
• Special types: Ovarian dysmenorrhea, Mittelschmerz's, Pelvic congestion syndrome

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