Gynaecology Flashcards
(227 cards)
Explain the Hypothalamic-Pituitary-Gonadal axis in women
- Hypothalamus releases GnRH (gonadotrophin releasing hormone)
- GnRH stimulates anterior pituitary to release LH and FSH
- LH and FSH stimulate follicle development in ovaries, causing theca granulosa cells to secrete oestrogen, which negatively feeds back to Hypothalamus and AP, reducing LH and FSH levels.
What is oestrogen and what does it stimulate
Steroid sex hormone (17-beta oestradiol is main active version).
- Breast tissue development
- Growth and development of female sex organs (vulva, vagina, uterus) at puberty
- Blood vessel development in uterus
- Development of endometrium
What is progesterone and what does it stimulate
Steroid sex hormone produced by corpus luteum after ovulation. In pregnancy, it is produced by placenta from 10 weeks gestation onwards. Acts on tissues previously stimulated by oestrogen.
- Thickens and maintains endometrium
- Thickens cervical mucus
- Increases body temperature
What age does puberty occur in girls, how long does it last and in what sequence do changes occur? Also why does low weight delay puberty.
What staging is used
- 8-14 years
- 4 years
- Growth spurt/breast buds, pubic hair, menarche
- Aromatase found in adipose tissue helps create oestrogen. More aromatase (fat) = earlier puberty. Low birth weight, chronic disease/ED, athletic hence can cause delays
- Tanner staging (under 10, no pubic hair or breasts = 1)
What are the 2 phases of menstrual cycle
Follicular phase (start of menstruation -> ovulation) - first 14 days
Luteal phase (ovulation -> start of menstruation) - final 14 days
What are ovarian follicles
oocytes are cells that have potential to develop into eggs. These are surrounded by granulosa cells, forming follicles.
Primary follicles are always maturing into primary and secondary follicles. When they reach secondary, they grow FSH receptors, which when stimulated, cause granulosa cells to secrete oestradiol (oestrogen).
Describe the follicular phase
Low oestrogen and progesterone causes endometrium shedding and bleeding.
FSH stimulates secondary follicles, causing them to grow, and for surrounding granulosa cells to secrete oestrogen. This reduces LH and FSH production (negative feedback). Rising oestrogen also causes cervical mucus to become more permeable, allowing sperm to penetrate cervix around ovulation.
One follicle will develop more than the rest (dominant follicle) LH spike causes dominant follicle to release an ovum. Ovulation occurs 14 days before end of cycle.
Overall: FSH stimulates oestrogen, which spikes ~day 12. There is an LH spike right before ovulation causing an ovum to release.
Describe luteal phase
The follicle that released the ovum collapses, becoming the corpus luteum. This secretes progesterone, maintaining the endometrial lining. It also causes the cervical mucus to become thick.
If pregnancy: the syncytiotrophoblast of the embryo secretes Human Chorionic Gonadotrophin (HCG), maintaining the corpus luteum.
Without fertilisation the corpus luteum degenerates and stops producing oestrogen and progesterone. This fall causes breakdown of the endometrium and menstruation. The stromal cells in the endometrium release prostaglandins, causing uterus contractions. The fall in Oestrogen and Progesterone causes an increase in LH and FSH, restarting the cycle.
Menstruation marks day 1 of the menstrual cycle.
What is amenorrhoea? Give primary and secondary causes
Failure to establish menstruation at 15 with normal sexual development and 13 without.
Primary
- Gonadal dysgenesis (e.g. Turners)
- Hypogonadotrophic hypogonadism (deficiency of LH and FSH), Hypergonadotrophic hypogonadism (lack of response to LH and FSH by gonads)
- Pregnancy
Secondary - 3-6 months amenorrhoea when previously normal
- Hypothalamic (secondary stress, excessive exercise)
- PCOS
- Thyroid disease
- Hyperprolactinaemia
What is atrophic vaginitis?
Inflammation and thinning of vulvovaginal tissue due to a decline in oestrogen levels. Most commonly in post-menopausal women.
Oestrogen normally makes epithelium of vagina thick and lubricated. Absence causes it to become thin and dry, making it prone to inflammation and infections, due to alteration of pH and microflora.
Lack of oestrogen can also reduce healthy connective tissue in pelvis, causing pelvic organ prolapse and stress incontinence.
Presentation of atrophic vaginitis
- Thin/Pale vaginal mucosa
- Vaginal dryness/itchiness
- Pain during sex and post-coital bleeding
- Discharge, loss of pubic hair and pH>4.5
Investigations and management of atrophic vaginitis
Clinical exam including speculum.
Discharge should be infection screened.
- Transvaginal USS and Endometrial biopsy necessary to exclude endometrial cancer.
- pH >4.5
Non hormonal:
- Moisturisers and lubricants
Hormonal:
- Systemic HRT (Estriol cream/ estradiol tablets)
What is bacterial vaginosis
Overgrowth of anaerobic organisms (e.g. Gardnerella vaginalis). Leads to a fall in lactobacilli which produce lactic acid, so vaginal pH rises.
Very commonly sexually active women (NOT sexually transmitted infection).
Presents as grey-whiteish watery discharge and fishy offensive smell.
Criteria for BV diagnosis
Amsel’s criteria (3/4 must be present)
- Thin, white, homogenous discharge
- Clue cells (stippled vaginal epithelial cells) on microscopy
- Vaginal pH >4.5
- Positive whiff test (adding potassium hydroxide causes fishy odour)
Management of BV
Not needed if asymptomatic
- Oral metronidazole 5-7 days (could have single oral, 2g metronidazole dose if issues adhering)
What is trichomonas vaginalis and how does it present
Flagellated protozoa parasite (STI)
- Vaginal discharge (offensive, yellow/green, frothy)
- Vulvovaginitis
- Strawberry cervix
- pH>4.5
Investigations and management of trichomonas vaginalis
- Microscopy of a wet mount shows motile trophozoites
- Oral metronidazole 5-7 days/ 2g dose one off
Risk factors for urinary incontinence
- Advancing age
- Pregnancy/childbirth
- High BMI
- Hysterectomy
- Family history
Types of urinary incontinence
Overactive bladder (urge incontinence)
- Caused by detrusor overactivity (Urge to urinate quickly followed by uncontrollable leakage)
Stress incontinence (Leaking small amounts when coughing or laughing)
Overflow incontinence (bladder outlet obstruction e.g. prostate)
Mixed (both stress and urge)
Functional incontinence (not enough time to get to bathroom / physical conditions)
Investigating incontinence
- Bladder diaries/3 days
- Vaginal examination to exclude pelvic organ prolapse and ability to initiate voluntary contraction of pelvic floor muscles
- Urine dipstick and culture
Management of incontinence
- Bladder retraining (6 weeks)
- Enuresis alarm (alarm wakes you up when it senses wetness, trains brain to wake before wetting)
- Bladder stabilising drugs (oxybutinin first line - avoid in frail old women)
If stress incontinence
- Pelvic floor muscle training (8 contractions, 3x a day for 3 months)
- Duloxetine (SSRI/SNRI)
What is menopause? With stages
Cessation of menstruation, average age 51. Clinically diagnosed after 12 months of amenorrhoea.
Peri-menopause - First clinical signs of menopause appear (Vasomotor symptoms/irregular menstrual cycles). Ends 12 months after last period, leading into menopause. (usually start around 40s)
Post menopause - >12 months after last period.
Premature menopause - Menopause before 40 as a result of premature ovarian insufficiency
Early menopause - Ovaries stop functioning between 40-45 years.
Clinical features of perimenopause/menopause
- Hot flushes/night sweats (vasomotor)
- Emotional instability and/or depession
- Irregular, heavier/lighter periods
- Joint pain
- Vaginal dryness/atrophy, sex pain/bleeding
- Reduced libido
- Urinary incontinence, recurrent UTI, dysuria
- Weight gain
Long term consequences of menopause
- Osteoporosis/ fragility fractures - most commonly Colle’s fracture (distal radius), neck of femur and vertebrae.
- Cardiovascular disease
- Urogenital atrophy - causing frequency, urgency, nocturia, incontinence and recurrent UTIs. Vaginal dryness/atrophy symptoms