---

Basic Terminology in Gynaecology

1. Menstrual Cycle Terminology

---

2. Abnormal Uterine Bleeding (AUB) - PALM-COEIN Classification

• PALM (structural): Polyp, Adenomyosis, Leiomyoma, Malignancy/hyperplasia
• COEIN (non-structural): Coagulopathy, Ovulatory dysfunction, Endometrial, Iatrogenic, Not yet classified

---

3. Ovarian/Hormonal Terminology

---

4. Obstetric History Notation

---

5. Vaginal Discharge Terminology

---

6. Anatomical and Structural Terms

---

7. Gynaecological Conditions - Key Terms

---

8. Procedures

---

9. Contraception Terminology

---

---

Sexually Transmitted Infections (STIs): A Comprehensive Discussion

---

1. Definition and Classification

---

2. Etiology

2a. Bacterial STIs

• Gram-negative diplococcus; has tropism for columnar epithelium (endocervix, urethra, rectum, pharynx)
• Immune evasion via antigenic variation of pili and outer membrane proteins
• Control of dissemination requires complement-mediated immunity

• Gram-negative obligate intracellular bacterium
• Serovars D-K: genital tract infections (urethritis, cervicitis, PID)
• Serovars L1-L3: Lymphogranuloma venereum (LGV)
• Exists in two forms: the infectious elementary body (EB) and the replicating reticulate body (RB)

• A motile spirochete; cannot be cultured in vitro
• Causes syphilis; enters via mucosal breaches or abraded skin
• Disseminates haematogenously early in infection

• Gram-negative bacillus causing chancroid
• Produces a cytotoxin causing local tissue destruction

• Intracellular bacterium causing granuloma inguinale (donovanosis)

2b. Viral STIs

• HSV-2 is the predominant cause of genital herpes; HSV-1 increasingly implicated
• Establishes latency in dorsal root ganglia; reactivation causes recurrent disease
• Shedding occurs both symptomatically and asymptomatically

• 200 genotypes; sexually transmitted types classified as low-risk (6, 11 - genital warts) and high-risk (16, 18 - cervical carcinoma)

• Infects basal layer keratinocytes of stratified squamous epithelium

• Retrovirus targeting CD4+ T-lymphocytes; transmitted via sexual contact (especially anal intercourse), blood, and vertically
• STIs (especially ulcerative) dramatically increase HIV transmission risk by disrupting mucosal barriers

• HBV is highly sexually transmissible; transmitted via blood and bodily fluids

2c. Protozoal STI

• Flagellated protozoan; infects squamous epithelium of the vagina, urethra, and Skene's glands
• Only STI with a flagellated motile form visible on wet mount

---

3. Pathology

Gonorrhoea

• Infects columnar and transitional epithelium; produces acute purulent inflammation with neutrophil-rich exudate
• Local tissue invasion can lead to salpingitis with tubal scarring; systemic dissemination causes septic arthritis and dermatitis
• In females, often asymptomatic; the cervix may appear normal or show mucopurulent discharge

Chlamydia

• Intracellular infection; causes a lymphocytic, plasma cell infiltration rather than a neutrophilic exudate
• LGV: causes granulomatous inflammation of lymph nodes with stellate abscesses, progressing to fibrosis and lymphoedema
• Chronic pelvic infection can cause peritubal and periovarian adhesions (Fitz-Hugh-Curtis syndrome when involving the liver capsule)

Syphilis (Treponema pallidum)

• Primary: Chancre - epithelial ulceration with plasma cell and lymphocyte infiltrate, proliferative endarteritis of small vessels
• Secondary: Systemic dissemination; skin shows perivascular lymphocytic infiltrates and epidermal changes
• Tertiary: Gummas (granulomatous necrotic lesions) in any organ; obliterative endarteritis affects the vasa vasorum of the aorta causing aortic aneurysm and aortic regurgitation
• Neurosyphilis: Meningovasculitis, or parenchymatous involvement (tabes dorsalis, general paresis)

Herpes Simplex Virus

• Vesicles contain necrotic epithelial cells, fused multinucleated giant cells, and Cowdry type A intranuclear inclusions
• After primary infection, virus travels retrograde along sensory neurons to dorsal root ganglia where it establishes latency

HPV

• Low-risk types: stimulate koilocytic changes (perinuclear vacuolation of squamous cells) and benign papillomatous proliferation (condyloma acuminata)
• High-risk types: E6 and E7 oncoproteins inactivate p53 and Rb tumour suppressor proteins respectively, promoting malignant transformation

Chancroid (H. ducreyi)

• Soft, painful ulcer; histology shows superficial acute inflammation and necrosis overlying a zone of granulation tissue and mononuclear infiltrate

Bacterial Vaginosis

• Polybacterial dysbiosis of the vaginal microbiome with replacement of hydrogen peroxide-producing Lactobacillus by Gardnerella vaginalis and anaerobes including Prevotella species

---

4. Clinical Features

Gonorrhoea

Chlamydia

• Clinically indistinguishable from gonorrhoea but typically milder
• Mucopurulent cervicitis, urethritis, proctitis
• Reactive arthritis triad (Reiter's syndrome): urethritis + arthritis + conjunctivitis
• Often entirely asymptomatic (hence major reservoir for silent spread)

Syphilis

Genital Herpes (HSV)

• Incubation: <21 days
• Primary episode: clustered vesicles on erythematous base → pustules → shallow painful ulcers → healing by crusting over 2-3 weeks; may have systemic fever, headache, aseptic meningitis
• Only ~20% manifest the classic presentation; 60% have mild/atypical symptoms; 20% are completely asymptomatic
• Viral shedding occurs 20% of days in symptomatic individuals, 10% of days in asymptomatic individuals
• Recurrences shorter (5-7 days) and less severe; prodrome of tingling/burning may precede lesions

HPV

• Condylomata acuminata (genital warts): cauliflower-like, soft, flesh-coloured papillary lesions on external genitalia, perianal region, cervix, vagina
• Often asymptomatic; may cause pruritus, bleeding, or psychological distress
• High-risk HPV: cervical dysplasia (CIN) - usually subclinical until advanced; cervical, vulvar, vaginal, anal, oropharyngeal carcinomas

Trichomonas vaginalis

• Profuse, frothy, yellow-green malodorous vaginal discharge
• Vulval pruritus and burning dysuria
• Pathognomonic "strawberry cervix" (colpitis macularis - punctate haemorrhages of ectocervix) on colposcopy
• Many infections (especially in men) are asymptomatic

Lymphogranuloma Venereum (LGV)

• Small, transient painless ulcer (often missed) followed by inguinal lymphadenopathy ("buboes") that may rupture
• Proctitis and rectal strictures in advanced disease (especially MSM)

Chancroid (H. ducreyi)

• Painful, soft, non-indurated genital ulcer ("soft chancre") - contrast with the painless hard chancre of syphilis
• Inguinal lymphadenopathy (bubo) in 50% of cases; nodes may ulcerate

Granuloma Inguinale (Donovanosis)

• Painless, progressive, beefy-red ulcerative genital lesions
• Pathognomonic Donovan bodies (intracellular organisms in macrophages) on tissue smear

Bacterial Vaginosis (BV)

• Thin, homogeneous, grey-white, fishy-smelling vaginal discharge
• pH >4.5; positive whiff (amine) test; clue cells on wet mount
• Often asymptomatic

---

5. Differential Diagnosis

For Genital Ulcers

• Behcet's disease (recurrent oral and genital ulcers)
• Fixed drug eruption
• Erosive lichen planus
• Squamous cell carcinoma
• Cutaneous leishmaniasis (in endemic regions)

For Vaginal Discharge

---

6. Investigations

General Principles

• Nucleic acid amplification tests (NAATs/PCR) have become the gold standard for most STIs due to superior sensitivity. Can be performed on urine, vaginal swabs, or cervical swabs.
• Culture is still important for antibiotic susceptibility testing (especially for gonorrhoea due to resistance issues)
• All patients diagnosed with one STI should be screened for co-infections

Specific Tests

---

7. Management

Gonorrhoea

• Uncomplicated: Ceftriaxone 500 mg IM single dose (1 g if weight ≥150 kg) PLUS doxycycline 100 mg twice daily for 7 days (to cover co-infection with Chlamydia)
• Fluoroquinolones are no longer recommended due to high rates of resistance
• Disseminated gonococcal infection: Ceftriaxone 1 g IV/IM daily for at least 7 days

Chlamydia

• First-line: Doxycycline 100 mg twice daily for 7 days
• Alternative: Azithromycin 1 g orally single dose

Syphilis

• Primary/Secondary: Benzathine penicillin G 2.4 million units IM single dose
• Latent (early, <1 year): Benzathine penicillin G 2.4 million units IM single dose
• Latent (late, >1 year) / Tertiary: Benzathine penicillin G 2.4 million units IM weekly x 3 doses (total 7.2 million units)
• Neurosyphilis: Aqueous penicillin G 18-24 million units IV daily for 10-14 days
• Penicillin-allergic: Doxycycline 100 mg twice daily for 14 days (primary/secondary) - desensitisation preferred in pregnancy
• Test of cure: Monitor RPR titres at 6 and 12 months; treatment failure = failure of RPR to fall fourfold within 6 months

Genital Herpes (HSV)

• Primary episode: Acyclovir 400 mg three times daily x 7-10 days; or Famciclovir 250 mg three times daily x 7-10 days; or Valacyclovir 1 g twice daily x 7-10 days
• Recurrent episode: Acyclovir 800 mg twice daily x 5 days; or Valacyclovir 500 mg twice daily x 3 days
• Chronic suppression (to reduce frequency and asymptomatic shedding): Acyclovir 400 mg twice daily; or Valacyclovir 500 mg-1 g once daily; or Famciclovir 250 mg twice daily
• Patient counselling: discuss asymptomatic viral shedding, partner disclosure, and avoidance of sex during prodrome/outbreaks

HPV / Genital Warts

• Topical (patient-applied): Imiquimod 5% cream (3x/week for up to 16 weeks); Podophyllotoxin 0.5% solution
• Clinician-applied: Trichloroacetic acid (TCA); Podophyllin resin; Cryotherapy; Laser ablation
• Surgical: Excision for large or refractory warts
• Vaccination: HPV vaccine (Gardasil-9) protects against HPV types 6, 11, 16, 18, 31, 33, 45, 52, 58; recommended for all adolescents (ideally before sexual debut) and up to age 26 (catch-up); approved to age 45 in some populations

Trichomonas vaginalis

• Metronidazole 500 mg twice daily for 7 days (preferred in women)
• Tinidazole 2 g orally single dose (alternative)
• Both partners must be treated; high reinfection rate; re-test within 3 months

Bacterial Vaginosis

• Metronidazole 500 mg twice daily for 7 days or 0.75% vaginal gel once daily for 5 days
• Clindamycin 300 mg twice daily for 7 days (alternative)
• Treatment of male partner does not reduce recurrence

Chancroid

• Azithromycin 1 g orally single dose; or Ceftriaxone 250 mg IM single dose; or Ciprofloxacin 500 mg twice daily for 3 days

LGV

• Doxycycline 100 mg twice daily for 21 days
• Alternative: Azithromycin 1 g weekly for 3 weeks

Granuloma Inguinale (Donovanosis)

• Azithromycin 1 g weekly or 500 mg daily for >3 weeks (and until all lesions healed)
• Alternatives: Doxycycline, TMP-SMX, erythromycin

Pelvic Inflammatory Disease (PID)

• Outpatient (mild-moderate): Ceftriaxone 500 mg IM single dose PLUS doxycycline 100 mg twice daily x 14 days PLUS metronidazole 500 mg twice daily x 14 days
• Inpatient (moderate-severe / TOA suspected): Ceftriaxone 1 g IV q24h PLUS doxycycline 100 mg IV/oral q12h PLUS metronidazole 500 mg IV/oral q8h
• Indications for hospitalisation: tubo-ovarian abscess, failure/intolerance of oral therapy, pregnancy, surgical emergency cannot be excluded

HIV

• Combined antiretroviral therapy (cART) is not curative but suppresses viral load to undetectable levels
• Pre-exposure prophylaxis (PrEP): tenofovir disoproxil/emtricitabine for high-risk individuals
• Post-exposure prophylaxis (PEP): within 72 hours of high-risk exposure

General Principles

• Partner notification and treatment (contact tracing) is essential for all STIs
• Condom promotion remains the single most effective prevention measure
• Screening: All sexually active women <25 years should be screened annually for chlamydia and gonorrhoea; syphilis and HIV screening for high-risk individuals

---

8. Long-Term Complications and Outcomes

Reproductive

• Infertility: Ascending infection with C. trachomatis or N. gonorrhoeae causes salpingitis and peritubal adhesions; each episode of PID increases the risk of tubal-factor infertility - after 3 episodes, up to 40-75% risk
• Ectopic pregnancy: Tubal scarring from salpingitis predisposes to implantation of fertilised ovum in the fallopian tube; risk is increased 6-10-fold after PID
• Chronic pelvic pain: PID can leave adhesions causing persistent pain
• Fitz-Hugh-Curtis syndrome: Perihepatitis from ascending C. trachomatis or N. gonorrhoeae causing right upper quadrant pain and "violin-string" adhesions between liver capsule and anterior abdominal wall

Oncological

• Cervical carcinoma: Persistent high-risk HPV infection (especially types 16 and 18) is the necessary cause of >99% of cervical cancers; also causes vulvar, vaginal, anal, penile, and oropharyngeal cancers
• Hepatocellular carcinoma: Chronic HBV and HCV infection leads to cirrhosis and liver cancer

Neurological

• Neurosyphilis: General paresis (dementia, personality change), tabes dorsalis (lightning pains, sensory ataxia, Argyll Robertson pupils, Charcot joints), meningovasculitis
• HSV meningitis: Recurrent aseptic (Mollaret's) meningitis associated with HSV-2

Cardiovascular

• Cardiovascular syphilis: Aortic aneurysm (ascending aorta), aortic regurgitation, coronary ostial stenosis in tertiary syphilis

Neonatal/Congenital

• Gonorrhoea: Ophthalmia neonatorum (blindness if untreated)
• Chlamydia: Neonatal conjunctivitis and pneumonia
• Syphilis: Congenital syphilis (stillbirth, hydrops, multi-organ disease)
• HSV: Neonatal herpes (generalised disease, encephalitis with high mortality)
• HIV: Vertical transmission to infant

Immunological and Systemic

• HIV facilitation: STIs (especially ulcerative: herpes, syphilis, chancroid) increase HIV transmission risk 2-5-fold by disrupting mucosal barriers; BV also increases HIV acquisition risk
• Reactive arthritis (Reiter's syndrome): Post-chlamydial urethritis in genetically susceptible (HLA-B27+) individuals: arthritis, conjunctivitis, urethritis, mucocutaneous lesions

Social and Psychological

• Stigma and psychological distress, especially with incurable viral infections (HSV, HIV, HPV)
• Recurrent HSV significantly impacts quality of life and relationships

---

Summary Table: Key STI Comparisons

---

---

Systemic Changes in Menopause

---

1. Definition and Hormonal Basis

Hormonal Profile at Menopause

• Oestrogen (17β-oestradiol): falls by up to 90%; residual oestrogen comes from peripheral aromatisation of androstenedione (in adipose tissue, muscle, liver)
• Progesterone: falls to near zero (no corpus luteum formation)
• FSH: rises markedly (loss of negative feedback from inhibin B and oestradiol); FSH ≥25 IU/L is consistent with menopause
• LH: rises moderately; episodic bursts coincide with hot flushes
• Anti-Müllerian hormone (AMH): becomes undetectable (best marker of ovarian reserve)
• Inhibin B: undetectable

Stages of Reproductive Ageing (STRAW Framework)

---

2. Systemic Changes

2a. Vasomotor System - Hot Flushes and Night Sweats

• Loss of ovarian oestrogen leads to dysregulation of the hypothalamic thermoregulatory set point
• Aberrant activation of the tachykinin system (specifically neurokinin B signalling via NK3 receptors in the arcuate nucleus) triggers vasodilation and heat dissipation responses
• Each flush coincides with a large pulsatile LH secretion burst - however, LH itself is not the cause, since flushes persist after hypophysectomy; rather, an estrogen-sensitive event in the hypothalamus simultaneously triggers both LH release and the flush
• Median duration: 7.4 years after the final menstrual period; ~50% of women have symptoms for >10 years; Black women are disproportionately affected with longer duration

• Sudden sensation of warmth spreading from the trunk to the face and neck
• Cutaneous flushing and profuse sweating
• Night sweats causing sleep disruption
• Associated palpitations and anxiety
• Each episode lasts 1-5 minutes; may occur multiple times daily

2b. Genitourinary System - Genitourinary Syndrome of Menopause (GSM)

• Thinning and atrophy of vaginal squamous epithelium
• Reduced vaginal glycogen (less Lactobacillus colonisation) → rise in vaginal pH from ~4.0 to >5.0
• Decreased vaginal secretions and lubrication
• Thinning of urethral and bladder epithelium

• Vaginal dryness, chronic irritation, burning, and itching (vulvovaginal atrophy)
• Dyspareunia (painful intercourse) and post-coital bleeding
• Loss of vaginal rugae; labia minora may become atrophic
• Urinary urgency, frequency, dysuria, and recurrent urinary tract infections
• Urethral caruncle formation
• Sexual dysfunction: reduced libido, arousal, and orgasm

2c. Skeletal System - Osteoporosis and Fracture Risk

• Oestradiol normally suppresses bone resorption by inhibiting osteoclast formation and activity via regulation of the RANK-L / osteoprotegerin axis
• At menopause, falling oestrogen increases RANK-L and decreases osteoprotegerin, tipping the balance toward increased osteoclast activity and accelerated bone resorption
• Oestradiol levels fall by 90% over the menopausal transition, closely paralleling the period of accelerated and progressive bone loss

• Spine: approximately 1.8 to 2.3% per year during early menopause
• Hip: approximately 1.0 to 1.4% per year
• Over 6-10 perimenopausal years: up to 30% loss of trabecular bone and 10% loss of cortical bone
• Results in a 50-100% higher fracture rate compared with premenopausal women

2d. Cardiovascular System

• Lipid profile deteriorates: LDL and triglycerides rise; HDL falls
• Blood pressure rises: loss of oestrogen-mediated vasodilation; increased arterial stiffness
• Central adiposity increases: visceral fat accumulation promotes insulin resistance and the metabolic syndrome
• Inflammatory markers rise: CRP, fibrinogen, and other pro-atherogenic markers increase
• Endothelial dysfunction: reduced nitric oxide production

2e. Central Nervous System - Cognitive and Mood Changes

• Hypogonadism of menopause explains frequent complaints of memory loss, "brain fog," and inability to focus
• Sex differences in hippocampal and temporal lobe structure and function are linked to oestradiol - these change after menopause
• Higher executive functioning in women (pre-menopause) is partly oestrogen-mediated
• Many executive functions spontaneously recover within a few years of the final menstrual period
• Long-term: menopause is associated with increased risk for dementia (including Alzheimer's disease); surgical menopause (bilateral oophorectomy) carries a particularly elevated risk
• The "critical window hypothesis": oestrogen neuroprotection may only be effective if initiated within 5-10 years of the final menstrual period

• Perimenopausal and recently menopausal women have higher rates of anxiety, irritability, and depression compared with premenopausal counterparts
• Especially in women with a history of mood dysfunction (PMS, postnatal depression), or adverse childhood experiences
• The relationship is complex: sleep disruption from hot flushes independently worsens mood
• Not simply "psychological" - abrupt oestrogen withdrawal using GnRH agonists in premenopausal women reproducibly produces mood symptoms

2f. Sleep Architecture

• Increased sleep fragmentation, especially in the second half of the night, with disproportionate disruption of REM sleep
• Nighttime hot flushes and night sweats are a direct cause of nocturnal awakenings
• Independent sleep disorders become more prevalent: obstructive sleep apnoea (worsened by central adiposity), restless legs syndrome, and insomnia
• Chronic poor sleep contributes to mood deterioration, reduced cognitive performance, and metabolic dysfunction

2g. Body Composition and Metabolic Changes

• Weight gain: midlife women gain an average of 2-5 pounds (with wide variation) during the menopausal transition, but this is partly age-related
• Redistribution of fat: shift from gynoid (gluteal-femoral) to android (central/visceral) distribution, regardless of weight change
• Visceral adiposity promotes:
  • Insulin resistance and type 2 diabetes
  • Metabolic syndrome
  • Chronic low-grade inflammation (elevated TNF-α, IL-6, CRP)
• Hypogonadism disrupts adipocyte lipolysis and adipogenesis via adipose oestrogen receptors
• The gut microbiome is also affected by hypogonadism, potentially contributing to weight gain

2h. Skin and Hair

• Skin: collagen content declines after menopause (oestrogen maintains dermal collagen synthesis); skin becomes thinner, drier, and less elastic; wound healing may be impaired
• Hair: pubic and axillary hair thins; paradoxically, androgen excess relative to oestrogen may cause increased facial hair (hirsutism) in some women
• Scalp hair may thin or develop a female-pattern androgenic alopecia pattern
• Skin sebaceous gland activity decreases, contributing to dryness and pruritus

2i. Urological and Pelvic Floor

• Loss of oestrogen weakens pelvic floor support structures
• Stress urinary incontinence (increased with coughing, sneezing, physical activity)
• Urge incontinence and overactive bladder symptoms
• Prolapse of pelvic organs (uterovaginal, cystocele, rectocele) becomes more common with ageing and oestrogen deficiency
• Recurrent urinary tract infections due to urethral mucosal atrophy and loss of protective vaginal flora

2j. Haematological and Coagulation Changes

• Postmenopausal state is associated with a mild pro-thrombotic tendency: increased fibrinogen, factor VII, factor VIII, and reduced fibrinolysis
• This contributes to the elevated cardiovascular risk of the postmenopausal period

---

3. Diagnosis

• FSH ≥25 IU/L (confirmatory, but fluctuates - less useful than clinical criteria alone)
• AMH - undetectable (best proxy for ovarian reserve; does not fluctuate with cycle)
• Oestradiol - very low (<20 pg/mL)
• Thyroid function tests (to exclude hypothyroidism mimicking menopausal symptoms)
• DEXA scan to assess baseline bone mineral density
• Fasting lipids, glucose, and blood pressure screening

---

4. Management Overview

Vasomotor Symptoms

Genitourinary Syndrome

• Local (vaginal) oestrogen: tablets, cream, ring, pessary - minimal systemic absorption; safe long-term
• Vaginal moisturisers and lubricants (over the counter)
• Ospemifene (oral SERM with oestrogenic effects on urogenital epithelium)
• DHEA (prasterone) vaginal insert

Bone Protection

• Adequate calcium (1200 mg/day) and vitamin D (800-1000 IU/day)
• Weight-bearing exercise
• Bisphosphonates (first-line): alendronate, risedronate, zoledronate
• Denosumab (RANK-L inhibitor): second-line
• Hormone therapy: preserves bone density if started within 10 years of FMP, but not given primarily for bone protection due to other risks

Cardiovascular Risk Reduction

• Screening and treatment of hypertension and hyperlipidaemia
• Lifestyle modification (exercise, weight loss, smoking cessation)
• Hormone therapy is not recommended for cardiovascular risk reduction (Women's Health Initiative data)

Risks of Combined Hormone Therapy (WHI trial data)

• Increased coronary heart disease (HR 1.29)
• Increased breast cancer (HR 1.26; significant after 5+ years of use)
• Increased stroke (HR 1.41)
• Increased venous thromboembolism

---

5. Summary: Organ Systems Affected by Menopause

---