Gynaecology Flashcards
(96 cards)
Average blood loss in a menstrual cycle
37-43ml
Normal menstrual cycle
Days 1-4: menses
Days 5-13:
- Follicular phase ovarian cycle: follicles develop, one follicle becomes dominant
- Proliferative phase uterine cycle: endometrial proliferation
Day 14: ovulation
Days 15-28:
- Luteal phase ovarian cycle: formation of corpus luteum
- Secretory phase uterine cycle: endometrial changes to secretory lining under the influence of progesterone
Hormones involved in the menstrual cycle and at which points
Days 5-13: rise in FSH -> development of follicles -> secretion of oestrogen
Day 14: when there is sufficient oestrogen, this causes a surge of LH to be released -> ovulation
Days 15-28: progesterone secreted by corpus luteum. if fertilisation does not occur then the corpus luteum will degenerate and progesterone levels fall. Oestrogen levels rise during this period.
Differential diagnoses for IMB and PCB
Cervical bleeding: ectropion, polyps, malignancy, cervicitis
Intra-uterine: polyps, submucous fibroids, endometrial hyperplasia, endometrial malignancy, endometriosis
Hormonal: breakthrough bleeding
Investigations for PCB and IMB
High vaginal swab and endocervical swabs (STIs) Cervical smear (CIN, cancer) Pelvic USS (polyps, fibroids) Hysteroscopy and endometrial biopsy Laparoscopy
How much blood defines menorrhagia?
Signs/symptoms
Causes of menorrhagia
> 80ml/cycle
60-70% get anaemia
May have menstrual pain, lethargy, breathlessness, affects QoL
Causes:
- Systemic: thyroid disease, clotting disorders
- Iatrogenic: IUD, IUS, POP, implant, depo, anticoag
- Local pathology: dysfunctional uterine bleeding, fibroids, endometrial polyps, endometrial carcinoma, endometriosis, PID
Dysfunctional uterine bleeding
- what is it
- diagnosis
- management
Most common cause of menorrhagia
Diagnosis of exclusion
Managed with OCPs or prostaglandin inhibitors (mefenamic acid)
Investigations for menorrhagia
Subjective assessment/ pictorial blood loss chart to assess degree of menorrhagia
- Blood tests: FBC, TFT, clotting studies
- Pelvic USS
- Endometrial biopsy
- Cervical smears
- Diagnostic hysteroscopy
- Diagnostic laparaoscopy
Management of menorrhagia
Correct iron deficiency anaemia
Treat systemic disease or focal pathology
First line if needing contraception: mirena IUS
Second line: COCP
Third line: long acting progesterone (eg. depo, implant)
First line if not needing contraception: tranexamic acid (or mefenamic acid, esp if dysmenorrhoea)
Surgical management:
- Hysteroscopy
- Open myomectomy
- Endometrial ablation
- Hysterectomy
Tranexamic acid
- MoA
- Risk
- At which part of the menstrual cycle are these taken?
Antifibrinolytic. Prevents activation of plasminogen into plasmin -> reduces excessive fibrinolysis
Risk of thrombosis
Start taking at the beginning of menses for 4 days
Mefenamic acid
- MoA
- At which part of the menstrual cycle are these taken?
NSAID.
Prostaglandin inhibitor.
Inhibits COX enzymes -> prevents conversion of arachidonic acid into prostaglandins (prostaglandins are vasodilators and they inhibit platelet aggregation)
Taken during menses
Presentation of endometriosis
Growth of ectopic endometrial tissue outside of the uterine cavity
Chronic pelvic pain
Dysmenorrhoea (often starts before menses)
Deep dyspareunia
Subfertility
Urinary symptoms
Dyschezia (painful bowel movements)
Differential diagnoses for endometriosis
PID Pelvic pain syndrome Submucous fibroids Ovarian accident Adhesions
Examination, investigations and management for endometriosis
Examination:
Retroverted fixed uterus, tender vaginal fornices, uterine tenderness
Ix:
- Pelvic USS first as less invasive
- Diagnostic laparoscopy is gold standard (active endometriosis shows powder-burn spots and chocolate cysts)
Mx:
- First line analgesia: paracetamol and/or NSAIDs (mefenamic acid, naproxen, ibuprofen)
- COCP helps symptoms by stopping period
- POP, depot, implant, IUS
Secondary care:
- GnRH analogues can induce pseudo-menopause
- Surgical: laparoscopic diathermy, laser ablation, excision of deposits, total abdominal hysterectomy with bilateral salpingo-oophorectomy
Uterine fibroids presentation
Asymptomatic Menorrhagia (due to increased surface area of endometrium, and production of prostaglandins) Abdominopelvic mass Abdominopelvic pain Subfertility Urinary frequency, urgency, nocturia Rectal pressure and abdo bloating
Risk factors for uterine fibroids
Protective factors
African-caribbean
Later reproductive years
Nulligravidity
Obesity
Protective factors: smoking, COCP, full term pregnancy, post-menopause
Investigations for uterine fibroids
Bimanual examination: fibroids are often palpated, the uterus may feel enlarged firm and irregular
Bloods: FBC, U+E, clotting screen
Pelvic USS is diagnostic to visualise the fibroids
Management of uterine fibroids
Leave alone unless symptomatic, rapidly enlarging or concerned about subfertility
Medical:
Fibroids <3cm: IUS, tranexamic acid, mefenamic acid, COCP
Secondary care:
- GnRH analogues (zoladex) used as surgery adjuncts to reduce fibroid size by reducing oestrogen
- Mifepristone (antiprogesterone) shrinks fibroids over a 6m period
Surgery:
- Myomectomy (hysteroscopic approach for submucosal or pedunculated fibroids, abdominal approach for intramural or subserosal fibroids)
- Uterine artery embolisation (stops blood flow to fibroids)
- Myolysis (diathermy, laser ablation, high intensity focused US)
- Hysterectomy
Primary vs secondary amenorrhoea
Primary: failure to commence menses (absence of menarche)
- 16+ in presence of secondary sexual characteristics
- 14+ in absence of secondary sexual characteristics
Secondary: cessation of periods for more than 6 months after menarche
Causes of amenorrhoea
- hypothalamic
- pituitary
- ovarian
- adrenal glands
- genital tract
Hypothalamic causes (reduced GnRH):
- eating disorders, exercise
- severe chronic conditions (thyroid, sarcoid, psychiatric)
- Kallmann syndrome (x-linked recessive characterised by failure of migration of GnRH cells)
Pituitary causes:
- Prolactinoma (prolactin suppresses GnRH)
- Acromegaly/ cushings syndrome
- Sheehan’s syndrome (post-partum pituitary necrosis secondary to massive obstetric haemorrhage)
- Radiation or autoimmune disease destroying pituitary gland
- Post-contraception amenorrhoea
Ovarian causes:
- PCOS
- Turners (45XO)
- Premature ovarian failure
Adrenal gland causes:
-Late onset/mild congenital adrenal hyperplasia
Genital tract causes:
- Ashermann’s syndrome
- Imperforate hymen or transverse vaginal septum
Androgen insensitivity syndrome
- what is it
- features
- diagnosis
- management
X-linked recessive
End-organ resistance to testosterone causing genotypically male children (46XY) with female phenotype
Features:
- primary amenorrhoea
- undescended testes causing groin swellings
- breast development may occur as a result of conversion of tesosterone to oestradiol
Diagnosis:
Buccal smear or chromosomal analysis to reveal 46XY genotype
Management:
Counselling (raise child as female)
Bilateral orchidectomy
Oestrogen therapy
Causes of oligomenorrhoea
PCOS Contraception/hormonal treatment Perimenopause Thyroid disease DM Eating disorders Excessive exercise Medications (eg. antipsychotics) Antiepileptics
Investigations for oligomenorrhoea and amenorrhoea
- Pregnancy test
- Gonadotrophins (LH and FSH) - reduced levels indicate hypothalamic cause, and increased levels indicate ovarian cause
- Prolactin
- Androgen levels (raised in PCOS)
- Oestradiol (converted from testosterone)
- Thyroid function tests
- 17 hydroxyprogesterone (CAH)
- Karyotype
- Pelvic USS
- Progesterone challenge test to elicit a withdrawal bleed
PCOS presentation and differentials
Presentation:
Subfertility /infertility
Oligo-/Amenorrhoea
Hirsutism and acne (due to hyperandrogenism)
Obesity
Acanthosis nigricans due to insulin resistance
Differentials: Hypothyroidism Cushings syndrome Hyperprolactinaemia Congenital adrenal hyperplasia