Gynaecology Flashcards
Menstruation
Hormones (5)
Cycle controlled by hypothalamic-pituitary-ovarian axis
Gonadotrophin-releasing hormones are produced by the hypothalamus
Stimulates pituitary to produce gonadotrophins: FSH + LH
They stimulate the ovary to produce oestrogen and progesterone
They modulate production of gonadotrophins by negative feedback on the hypothalamus and pituitary
Menstruation
Cycle (8)
At start, FSH levels high, stimulating development of a primary follicle
The follicle produces oestrogen, which stimulates the development of a glandular ‘proliferative’ endometrium and of cervical mucus receptive to sperm
14 days before menstruation the oestrogen level becomes high enough to stimulate surge of LH, stimulating ovulation
Primary follicle forms corpus + produces progesterone
Endometrial lining prepared for implantation, ‘secretory phase’
Cervical mucus becomes hostile to sperm
If ovum not fertilised, corpus luteum breaks down and hormone levels fall
Reduced hormones causes arteries in uterine endothelium to constrict and slough
Hypothalamo-Pituitary Ovarian Axis Feedback
+ve feedback: oestrogen on hypothalamus and anterior pituitary days 12-14
-ve feedback: oestrogen and progesterone on hypothalamus and anterior pituitary for most of cycle, this prevent more than one egg being released
Hormones in the Ovarian Cycle
Oestrogen is present in the follicular phase
Progesterone is released in the luteal phase to prepare the uterus for pregnancy, if no implantation the corpus luteum degenerates
Corpus luteum secretes progesterone
Roles of Main Female Reproductive Hormones
GnRH (from hypothalamus): stimulates LH and FSH secretion from anterior pituitary
LH (from anterior pituitary): maintains dominant follicle and stimulates corpus luteum function
FSH (from anterior pituitary): stimulates follicular recruitment and development
Oestradiol (from granulosa cells): supports secondary sex characteristics, -ve feedback of LH + GnRH
Progesterone (from corpus luteum): maintains secondary endometrium
Primary Amenorrhoea
Definition (1)
Failure to start menstruating before age 16, or 14 if no secondary sexual characteristics
Primary Amenorrhoea
Aetiology (6)
Familial late puberty Heavy exercise/stress/weight loss Pituitary and hypothalamus disease Gonadal dysgenesis (ovaries prematurely depleted of follicles and oocytes) Turner syndrome PCOS
Primary Amenorrhoea
Treatment (4)
Weight gain/less exercise/less stress
If amenorrhoea persists for >12 months, consider osteoporosis prophylaxis
Treat hypothalamic/hypoprolactinaemic causes
HRT or COCP if amenorrhoea >12 months
Secondary Amenorrhoea
Definition (1)
Periods stop for >6 months in the absence of pregnancy
Secondary Amenorrhoea
Aetiology (7)
Hypothalamic-pituitary-ovarian causes are common: stress, weight loss, exercise
Hyperprolactinaemia: may have galactorrhoea
Hypo- and hyper-thyroidism
PCOS
Ovarian insufficiency/failure (premature menopause, secondary to chemo/radio, genetic- Turner’s)
Post-pill amenorrhoea
Asherman’s syndrome (adhesions after D+C)
Secondary Amenorrhoea
Investigations (6)
BhCG to exclude pregnancy
Serum free androgen index (increased in PCOS)
FSH/LH (low if hypothalamic-pituitary cause but may be normal if weight loss/exercise)
Prolactin (increased by stress, hypothyroidism, prolactinomas)
TFTs
Testosterone level (may indicate androgen secreting tumour)
Secondary Amenorrhoea
Treatment (2)
Premature ovarian failure can’t be reversed but hormone replacement is necessary to control symptoms of oestrogen deficiency and protect against osteoporosis
For hypothalamic-pituitary-ovarian malfunction: weight loss + lifestyle measures, clomifene/gonadotrophin releasing hormone for fertility
Polycystic Ovarian Syndrome
Signs + symptoms (5)
Oligomenorrhoea/amenorrhoea Hirsutism (excess hair) Acne Subfertility Acanthosis nigrans (reflects hyperinsulinaemia)
Polycystic Ovarian Syndrome Rotterdam Criteria (4)
2 out of 3 must be present
Polycystic ovaries (12 or more follicles or ovarian volume >10cm3 on ultrasound)
Oligo-ovulation or anovulation
Hyperandrogenism (clinical or biochemical signs)
Polycystic Ovarian Syndrome
Investigations (6)
TFTs (rule out dysfunction) Prolactin (rule out hyperprolactinaemia) Rule out androgen secreting tumours Rule out Cushing's Testosterone high LH high
Polycystic Ovarian Syndrome
Treatment (6)
Weight loss (high insulin sensitivity)
Metformin (improve insulin sensitivity and improve menstrual disturbance)
Clomifene (induces ovulation)
Ovarian drilling when don’t respond to clomifene (intent is to reduce steroid production)
COCP (control bleeding and reduce risk of unopposed oestrogen)
Anti-androgen (reduce hirsutism)
Polycystic Ovarian Syndrome
Complications (4)
Gestational diabetes
Type 2 diabetes
CV disease
Endometrial cancer
Menorrhagia
Definition (1)
Heavy periods, blood loss >80ml/cycle
Menorrhagia
Aetiology (8)
Dysfunctional uterine bleeding (most common)- heavy and/or irregular bleeding in absence of pelvic pathology Fibroids Endometriosis Adenomyosis Early pregnancy loss Hypothyroidism Coagulation disorders (vWB, platelet abnormalities, warfarin) Endometrial cancer
Menorrhagia
Signs + symptoms (7)
Heavy, prolonged vaginal bleeding, often worse at extremities of reproductive life
Dysmenorrhoea
Symptoms of anaemia
Pallor
If intermenstrual or post coital bleeding check smear history
Enlarged uterus suggests fibroids or adenomyosis
Speculum examination may reveal a cervical polyp
Menorrhagia
Investigations (6)
Exclude pregnancy FBC TSH Cervical smear if due STI screen If <45 no further investigation and start treatment, if >45 with risk factors/failed medical therapy then do transvaginal US and biopsy to look for fibroids, polyps, endometrial thickness
Menorrhagia
Treatment (7)
Mirena IUS 1st line
Antifibrinolytics eg.tranexamic acid during bleeding
NSAIDs eg. mefanamic acid during bleeding, especially if also dysmenorrhoea
COCP
3rd line progestogens IM eg. norethisterone stops heavy bleeding short term
Endometrial ablation
If have fibroids but wish to retain fertility: uterine artery embolisation or myomectomy, otherwise hysterectomy
Menopause Average age (1)
52
Menopause
Pathology (2)
Perimenopause: high number of anovulatory cycles leads to less progesterone and less endometrial secretory changes and irregular menses
Menopause: oestradiol falls due to lack of developing follicles and their granulosa cells, lack of -ve feedback to pituitary causes and increased FSH and LH
Menopause
Signs + symptoms (4)
Menstrual irregularity as cycles become anovulatory, before stopping
Vasomotor disturbance- sweats, palpitations and flushes
Atrophy of oestrogen-dependent tissues (vagina, breasts)- vaginal dryness which my lead to vaginal and urinary infections, stress incontinence and prolapse
Osteoporosis: menopause accelerates bone loss
Menopause
Treatment (3)
Contraception until >1 year amenorrhoea
Oestrogen cream for vaginal dryness
HRT: systemic- tablets/patches (bypasses 1st pass metabolism so reduces VTE risk) or local-creams, no uterus = oestrogen only, uterus = oestrogen + progesterone (oestrogen and cyclical progesterone whilst still having periods, continuous combined HRT in post-menopausal)
Menopause HRT contraindications (6)
Oestrogen-dependent cancer Past PE Undiagnosed PV bleeding High LFTs Pregnancy Breastfeeding
Menopause
Effects of HRT (6)
Fluid retention Bloating Breast tenderness Nausea Headaches Mood swings, depression , acne due to progesterone
Menopause
Alternatives to HRT (3)
SSRIs for vasomotor symptoms
Calcium, vitamin D, bisphosphonates for osteoporosis
Lubricants/vaginal oestrogens if vaginal dryness main symptom
Menopause
Benefits of HRT (4)
Reduction of vasomotor symptoms (usually evident by 4 weeks and maximum effect by 3 months)
Improved genital symptoms and sexual function
Reduced osteoporotic fractures
Reduced risk of colorectal cancer
Menopause
Risks of HRT (3)
Breast cancer (increases risk by 2.3% per year, back to never user after 5 years) Endometrial cancer (unopposed oestrogen only) VTE (doubled risk)
Post Menopausal Bleeding
Differentials (6)
Endometrial cancer Vaginal atrophy Cervical cancer Bleeding related to HRT use Endometrial hyperplasia or polyp Vaginal cancer
Post Menopausal Bleeding
Investigations (3)
TVUSS: endometrial thickness >4mm requires further investigation
Endometrial biopsy
Hysteroscopy
Post-Coital and Intermenstrual Bleeding
Differentials (3)
Upper: pelvic inflammatory disease
Cervical: cervicitis (chlamydia/gonorrhoea), cervical ectropion/erosion, cervical/endometrial polyps, cervical cancer
Vaginal: vaginal atrophy, trauma/sexual abuse, vaginal cancer
Intermenstrual Bleeding Only
Differentials (6)
Pregnancy related
Physiological: ovulation spotting, perimenopausal
Vaginal: vaginitis
Uterine: endometrial cancer, fibroids, adenomyosis, endometritis
Ovary: oestrogen secreting tumours
Iatrogenic: post smear/colposcopy, missed OCPs
Endometriosis Definition (1)
Endometrial tissue outside uterus (oestrogen dependent)
Endometriosis Risk factors (3)
Reproductive age (oestrogen driven)
Family history
Nulliparity
Endometriosis
Signs + symptoms (7)
Pin- may be cyclical due to endometrial tissue responding to menstruation or it amy be constant due to formation of adhesions from chronic inflammation
Severe dysmenorrhoea
Deep dyspareunia
Subfertility
Tender nodules in rectovaginal septum or uterosacral ligaments
Fixed retroverted uterus
Adnexal masses
Endometriosis Investigations (3)
Laparoscopy + biopsy gold standard: chocolate cysts filled with old blood
TVUSS: identifies ovarian endometriotic cysts but poor for other disease parameters
MRI: maps extent of endometriosis, especially good for bowel involvement
Endometriosis Treatment (2)
Medical: COCP, progesterone (POP, Depo, Mirena), GnRH analogues with addback HRT
Surgical: if medical fails, laparoscopy using ablation/excision/coagulation, hysterectomy last resort
Adenomyosis
Definition (1)
Endometrial tissue in or deep to the myometrium
Adenomyosis
Signs + symptoms (2)
Dysmenorrhoea
Menorrhagia
Adenomyosis
Investigations (2)
MRI indicates diagnosis
Laparoscopy/hysteroscopy may be normal but do uterine muscle biopsy
Adenomyosis
Treatment (2)
Mirena
Hysterectomy
Leiomymoma (Fibroids)
Defintion (2)
Benign smooth muscle tumours of the uterus
Submucosal (under endometrium), intramural, subserosal (under the visceral peritoneum)
Leiomymoma (Fibroids) Risk factors (5)
Age Family history Increased weight Afro-Caribbean Enlarge in pregnancy and on combined pill because they are oestrogen dependent (atrophy after menopause)
Leiomymoma (Fibroids)
Signs + symptoms (6)
May be asymptomatic Menorrhagia Fertility problems if submucosal Pain Mass abdominally If large, may cause urinary frequency or obstructed labour
Leiomymoma (Fibroids)
Investigations (3)
TVUSS
Hysteroscopy
Endometrial biopsy
Leiomymoma (Fibroids)
Treatment (5)
GnRH analogues: shrunk fibroids
Selective progesterone receptor modulator (ullipristal acetate) to shrink fibroids and induce amenorrhoea
Myomectomy to retain fertility
Uterine artery embolisation (doesn’t retain fertility)
Hysterectomy only cure
Leiomymoma (Fibroids)
Complications (1)
Red degeneration in pregnancy: capsular vessel thrombosis then venous engorgement causes abdo pain, vomiting and fever
Endometrial Cancer Risk factors (8)
Post-menopausal Unopposed oestrogen Nulliparity (pregnancy = progesterone) Obesity, type 2 diabetes (increased peripheral oestrogen) Anovulatory cycles as PCOS (absence of corpus luteum = absence of progesterone) Early/late menopause Genetic: HNPCC Oestrogen-only HRT
Endometrial Cancer
Pathology (2)
Adenocarcinoma most common
Serous and clear cell carcinoma more aggressive, older women affected
Endometrial Cancer
Sings + symptoms (3)
Post-menopausal bleeding
PV discharge
If pre-menopausal, irregular + heavy periods
Endometrial Cancer
Investigations (4)
TVUSS (endometrial thickness >4mm)
Endometrial biopsy
Hysteroscopy
CT/MRI for staging
Endometrial Cancer
Staging (FIGO) (4)
I- body of uterus only
II- body + cervix
III- advancing beyond uterus but not beyond pelvis
IV- outside pelvis eg. bladder/bowel
Endometrial Cancer
Treatment (3)
Total hysterectomy + bilateral salpingooophorectomy
Also do radiotherapy if advanced
High dose progesterone for palliation
Endometrial Cancer
Survival (2)
Stage I: 85% 5 year survival
Stage IV: 25% 5 year survival
HPV Infection
Epidemiology (2)
Peak prevalence 15-25
Lifetime exposure risk 75%
HPV Infection
Aetiology (2)
6+11 cause genital warts
16+18 cause cervical cancer
HPV Infection
Pathology (2)
Virus enters cell nuclei disrupting the normal cell cycle to cause abnormal cell growth
Most low grade: intraepithelial lesions (LSILs) cleared within 6-12 months but some persist + progress to HSIL
HPV Infection
Vaccination (1)
Girls + boys aged 12
HPV Infection Cervical screening (3)
Women aged 25-64 (3 yearly 25-50, 5 yearly until 64 if normal)
Cells removed from transformation zone (columnar endocervical canal meeting squamous ectocervix- vaginal cervix)
Looking for dyskaryosis, if present then do colposcopy
Cervical Intra-Epithelial Neoplasia
Aetiology (2)
HPV 16+18 cause high grade changes
HPV 6+11 can cause transient low grade changes
Cervical Intra-Epithelial Neoplasia Risk factors (4)
Persistent high-risk HPV infection
Exposure risk increased by having multiple partners
Smoking
Immunocompromised
Cervical Intra-Epithelial Neoplasia
Pathology (4)
Non-invasive squamous cell changes that don’t invade beyond basement membrane
CIN1 (mild): lowest 1/3 epithelium
CIN2 (moderate): 2/3 epithelial thickness, 3-5% progress to cancer
CIN3 (severe): full epithelial thickness, 20-30% progress to cancer
Cervical Intra-Epithelial Neoplasia
Treatment (2)
CIN1: 6-monthly colposcopy if HPV +ve and LLETZ (large loop excision of transformation zone) if persistent
CIN 2/3: LLETZ
Cervical Cancer Risk factors (5)
HPV 16/18 Multiple partners Early first intercourse age Smoking 45-55 years old
Cervical Cancer
Pathology (1)
Squamous carcinoma
Cervical Cancer
Signs + symptoms (5)
Post coital bleeding
Watery, offensive discharge
On speculum: visible tumour that bleeds on contact
On bimanual: roughened + hard cervix, becomes fixed when advances
Advanced disease: heavy vaginal bleeding, ureteric obstruction, weight loss
Cervical Cancer
Investigations (4)
FBC, U&E, LFT
Punch biopsy for histology
Colposcopy
CT/MRI abdo pelvis for staging
Cervical Cancer
Staging (FIGO) (4)
I: confined to cervix (1a microscopic, 1b macroscopic)
II: spread to upper 2/3 vagina
III: spread to lower 1/3 vagina
IV: spread to bladder/rectum
Cervical Cancer
Treatment (4)
Stage 1a <3mm in depth: local excision (fertility sparing) or hysterectomy
Stage 1a-IIa: radical hysterectomy
Stage IIB/IVA/unfit: radical chemoradiation, 24h caesium insertion
Stage IVB: palliative radiotherapy to control bleeding
Pelvic Mass
Differentials (5)
Ovarian: benign cyst, ovarian cancer Fallopian: ectopic, PID Uterine: fibroid, endometrial cancer Colorectal cancer Pelvic lymphadenopathy
Ovarian Cancer Risk factors (5)
Nulliparity Early menarche and/or late menopause BRCA 1+2 HNPCC Age (rare <30)
Ovarian Cancer Protective factors (4)
Pregnancy
Breastfeeding
COCP
Tubal ligation
Ovarian Cancer
Signs + symptoms (10)
Often vague symptoms misinterpreted as IBS/diverticular disease, 75% only present to gynae at stage III Indigestion Bloating Weight loss/gain Early satiety Fatigue Altered bowel habit Pelvic mass Ascites Supraclavicular node enlargement
Ovarian Cancer
Investigations (6)
FBC, U&E, LFT CA125 (although also raised in endometriosis, menstruation, benign ovarian cysts) TVUSS + TAUSS CXR (pleural effusion/lung mets) CT abdo/pelvis Ascitic fluid pathology
Ovarian Cancer
Risk of malignancy index (5)
RMI = U x M x CA125 U= ultrasound features, 1 point each for; multilocular/solid areas/bilateral/ascites/intra-abdominal mets M= menopausal status (1= pre, 3= post) C= CA125 RMI >200 suggestive of malignancy
Ovarian Cancer
Staging (4)
Stage 1- limited to ovary within capsule
Stage 2- one/two ovaries with pelvic extension
Stage 3- one/two ovaries with peritoneal implants outside pelvis/nodes
Stage 4- distant mets
Ovarian Cancer
Treatment (2)
Full staging laparotomy + removal of as much tumour as possible
Chemotherapy
Ovarian Cancer
Screening (3)
Population screening not proven
Screen high risk women (gene mutations/2+ relatives) with pelvic exam, ultrasound CA125 yearly
For high risk women may recommend bilateral salpingoophorectomy