Obs. and Gynae. Forum
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24/10/2022
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07/09/2022
Endometriosis
DEFINITION Presence of endometrial tissue outside the uterus.
AETIOLOGY Suggested theories include: (i) retrograde menstruation (Sampson�s theory), the
passage of endometrial tissue through the fallopian tubes into the pelvis during
menstruation; (ii) metaplasia of coelomic epithelium into endometrial glands (Meyer�s
theory); (iii) vascular and lymphatic dissemination; (iv) immune; (v) genetic.
ASSOCIATIONS/RISK FACTORS Nulliparity, family history, short menstrual cycle, long
periods.
EPIDEMIOLOGY Affects 10–15% of women of reproductive age.
HISTORY Cyclical dysmenorrhoea (starting premenstrually and reaching peak at onset of
menstruation), dyspareunia, chronic pelvic pain, infertility. Rarely symptoms of involvement
of other organs/distant sites: cyclical haematuria, PR bleed, epistaxis, haemoptysis.
EXAMINATION
Vaginal: (Often unremarkable) pelvic tenderness, immobile uterus, tender uterosacral
ligaments, palpable uterosacral nodules.
PATHOLOGY/PATHOGENESIS Ectopic endometrial tissue induces a chronic, inflammatory
reaction. Can cause fibrosis/adhesions. Classic ‘Powder-burn’ or ‘gun-shot’ lesions seen on
pelvic surfaces. On the o***y, an endometriotic cyst can form which enlarges with blood
during each menstrual cycle (endometrioma/chocolate cyst).
INVESTIGATIONS
USS: Endometrioma, differential diagnosis.
Laparoscopy: Gold standard for diagnosis.
MANAGEMENT
Medical: Analgesia (NSAIDs), suppression of ovulation (COCP, progestogens, Mirena IUS,
GnRH analogues).
Surgical: Laparoscopic ablation/excision of lesions, adhesiolysis, ovarian cystectomy, rarely
TAH/BSO (last resort).
COMPLICATIONS Ovarian cyst accident (endometrioma), infertility, chronic pelvic pain,
adhesions, s*xual dysfunction.
PROGNOSIS Medical management improves symptoms in 80–90%, but recurs if treatment
stopped. Symptoms subside in pregnancy and menopause.
04/09/2022
Dysmenorrhoea
DEFINITION Painful menstruation.
AETIOLOGY
Primary: Occurs in the absence of pathology
Secondary: Identifiable underlying pathology.
ASSOCIATIONS/RISK FACTORS
Primary: Time period shortly after menarche.
Secondary: Endometriosis, adenomyosis, PID, pelvic congestion syndrome, menorrhagia,
fibroids.
EPIDEMIOLOGY Affects 45–95% of women of reproductive age.
Primary: Commonly young girls soon after establishing me**es.
Secondary: Any time after menarche, commonly in 20s or 30s.
HISTORY Spasmodic cramping lower abdominal pain, may have radiation to thighs/lower
back.
Primary: Onset with menstruation or within 24 hours, resolves within 8–72 hours.
Secondary: May occur prior to and peak with onset of menstruation.
EXAMINATION
Primary: Abdominal/vaginal examination often unremarkable.
Secondary: Findings are specific to underlying cause.
PATHOLOGY/PATHOGENESIS
Primary: Prostaglandin F2a causes uterine hypercontractility and myometrial ischaemia,
uterine contractions cause further ischaemia.
Secondary: Dependent on cause (also likely to be related to prostaglandins).
INVESTIGATIONS
Microbiology: HVS, endocervical/Chlamydia swabs (exclude infection).
Imaging: Pelvic USS (?fibroids, assess endometrium if associated menorrhagia).
Other: Laparoscopy (endometriosis).
MANAGEMENT
Analgesia: NSAIDS (e.g. mefenamic acid), paracetamol and codeine preparations.
Hormonal methods: COCP, progestogens, GnRH analogues (e.g. severe endometriosis).
Surgery: Laparoscopic ablation of endometriosis, hysterectomy rare (severe intractable cases
if family complete).
COMPLICATIONS Limitation of activities of daily living.
PROGNOSIS Primary – excellent with simple methods; secondary – dependent on cause.
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