Gynae presentations - 1) Amenorrhoea Flashcards
(37 cards)
1
Q
What is primary and secondary amenorrhoea?
A
-
Primary: absence of menarche
- (girls aged 16+ with secondary sexual characteristics;
- aged 14+ without)
- Secondary: cessation of periods for ≥6 months after menarche (excluding pregnancy)
2
Q
What are the main causes of amenorrhoea?
A
- hypothalamic
- pituitary
- ovarian
- adrenal
- genital tract abnormalities
3
Q
What are the hypothalamic causes of amenorrhoea?
A
- Eating disorders (suppress GnRH),
- Hypo/hyperthyroidism,
- Kallmann syndrome
4
Q
What are the pituitary causes of amenorrhoea?
A
- Prolactinomas (negative feedback on GnRH),
- Other pituitary tumours (mass effect),
- Sheehan’s syndrome,
- Post-contraception amenorrhoea (Depot causes downregulation of pituitary hormones)
5
Q
What are the ovarian causes of amenorrhoea?
A
- Turner’s syndrome,
- Gonadal dysgenesis
- PCOS,
- Premature ovarian insufficiency/menopause
6
Q
What are the adrenal causes of amenorrhoea?
A
- Mild CAH
7
Q
What are the genital tract abnormalities causes of amenorrhoea?
A
-
Congenital obstruction to normal menses flow e.g.,
- vaginal septum,
- imperforate hymen,
- Rokintansky syndrome,
-
Iatrogenic obstruction to menses flow e.g.,
- cervical stenosis
- Asherman’s syndrome
8
Q
What is oligomenorrhoea?
A
Oligomenorrhoea:
- irregular periods
- with cycle length >35d
- and/or <9 periods/year
9
Q
What must be looked for on examination in a woman presenting with amenorrhoea?
A
-
BMI
- (high ~ = PCOS, low ~ = eating disorder)
-
Assess for features of:
- Cushing’s syndrome (striae, buffalo hump, significant central obesity, easy bruising, hypertension, and proximal muscle weakness)
- Hypo-/hyperthyroidism
-
Excess androgens (hirsutism, acne) + features of virilization (hirsutism, acne, deep voice, temporal balding, increase in muscle bulk, breast atrophy, and clitoromegaly)
- (~ = PCOS, CAH, androgen-producing tumour of the ovaries, adrenals, pituitary, etc.)
-
Decreased endogenous oestrogen (reddened or thin vaginal mucosa)
- (~ = premature ovarian insufficiency, etc.)
-
Hyperprolactinaemia (galactorrhoea)
- (~ = prolactinoma, hypothyroidism, etc.)
-
Visual field assessment
- (~ = pituitary tumour)
-
Bimanual examination
- (~ = genital tract abnormalities e.g., vaginal septum, imperforate hymen, etc.)
10
Q
What are the Ix in a woman presenting with amenorrhoea?
A
- Pregnancy test
-
Bloods:
- TFTs,
- Prolactin,
- LH, FSH,
- Testosterone, oestrogen, 17-hydroxyprogesterone
- Progesterone challenge to elicit a withdrawal bleed (no bleed suggests low oestrogen/outflow obstruction)
- Karyotyping
- USS (malformations, Turner’s, PCOS)
- Hysteroscopy
11
Q
Suggest what might be seen on FSH and LH in different causes of amenorrhoea
A
- High FSH and LH levels on two occasions suggest premature ovarian insufficiency (in women younger than 40 years of age)
- Normal or low FSH levels and normal or low LH levels suggest hypothalamic causes (weight loss, excessive exercise, stress, or rarely, a hypothalamic or pituitary tumour)
- Normal FSH levels and normal or moderately increased LH levels may be found in PCOS
12
Q
Suggest what might be seen on testosterone in different causes of amenorrhoea
A
- High levels of total testosterone (5.0 nanomol/L or greater) warrant investigation to exclude other causes, such as Cushing’s syndrome, late-onset congenital adrenal hyperplasia, or an androgen-secreting tumour
- A moderately increased testosterone level (2.5–5.0 nanomol/L) may be seen in PCOS.
13
Q
What must be seen on transvaginal/transabdominal USS to diagnose PCOS?
A
Polycystic ovaries on US =
- presence of ≥12 follicles (measuring 2–9 mm in diameter) in one or both ovaries
- and/or increased ovarian volume (greater than 10 cm3)
14
Q
What is the cause of PCOS?
A
The 2 main hormonal abnormalities are:
-
Insulin resistance
- Leads to high insulin levels
- Insulin promotes androgen production (possibly directly or through LH) and suppresses hepatic SHBG production (leading to higher levels of free circulating androgens)
-
Excess LH
- Due to increased GnRH pulse frequency (which may be due to excess insulin)
- Stimulates ovarian androgen production
- LH is increased relative to FSH
- Despite high LH levels, the LH surge is suppressed (due to increased androgens) → anvovulation
- Follicles develop within the ovary but are arrested at an early stage remain visible as cysts
15
Q
What are the RFs for PCOS?
A
- FHx,
- premature adrenarche,
- obesity (exacerbates severity),
- DM
16
Q
What are the signs & symptoms of PCOS?
A
- Oligomenorrhoea or amenorrhoea (75%)
- 40% have anovulatory cycles
- Subfertility (75%)
- Obesity (40%)
- Hirsutism
- Acne
- Acanthosis nigricans
- HTN
17
Q
What are the criteria for diagnosing PCOS?
A
- Rotterdam criteria for diagnosis (2 of the following):
- Oligo- or anovulation
- Clinical and/or biochemical signs of hyperandrogenism
- Polycystic ovaries on imaging
18
Q
What are the Ix for PCOS?
A
- Bloods:
- To aid diagnosis:
-
Serum total and free testosterone, and serum dehydroepiandrosterone sulfate (DHEAS)
- Raised
-
LH & FSH
- Raised LH, raised LH:FSH ratio → >3:1
- Now not essential for diagnosis
- Day 21 progesterone (low – suggests anovulation)
- SHBG (low)
-
Serum total and free testosterone, and serum dehydroepiandrosterone sulfate (DHEAS)
- To exclude other causes (PCOS is largely a diagnosis of exclusion)
- TFTs, prolactin, 17-hydroxyprogesterone
- To aid diagnosis:
- OGTT and fasting lipid panel
-
TVUSS
- ≥12 follicles in each ovary, 2-9mm in diameter, and/or increased ovarian volume (>10ml)
19
Q
What is the Mx of PCOS?
A
Tailored to the symptoms and need for fertility
Lifestyle advice (for all patients)
- Weight management → having normal BMI can reduce symptoms/trigger menstruation
- Promote healthy diet and exercise
- Hair removal (e.g. laser hair removal, hair removal cream)
- Also treat underlying conditions (DM, HTN)
Treatment of oligo/amenorrhoea:
- Need to induce bleeds because unopposed oestrogen (without progesterone) can cause endometrial hyperplasia
-
COCP (2nd line after weight loss)
- Also increases SHBG → helps to reduce androgenic symptoms
-
Metformin (3rd line)
- Insulin sensitiser; improves menstrual irregularity and restores ovulation; improves insulin sensitivity
- Also improves hyperandrogenic symptoms by decreasing testosterone and increasing SHBG
-
Cyclic oral progestogen (4th line)
- If COCP is contra-indicated, or in refractory cases
Treatment of hyperandrogenic features (hirsutism, acne):
- COCP (1st line)
- Metformin (adjunct)
-
Anti-androgen (e.g. spironolactone, finasteride)
- Avoid in pregnancy (cause ambiguous genitalia)
Treatment of infertility (if desiring fertility):
-
Metformin
- Weight loss should be tried first; metformin added if no response
- Lower live birth rate than clomifene but no increased risk of multiple pregnancy
-
Clomifene (1st esp in normal weight women)
- Anti-oestrogen → blocks oestrogen receptors in hypothalamus/pituitary → increased FSH and LH
- Given on days 2-6; stepwise dose increase induces follicular maturation and ovulation
- 10% risk of multiple pregnancy, risk of ovarian hyperstimulation syndrome
- Metformin can be added if not responsive
-
Gonadotrophins (2nd line)
- Used if clomifene has failed
- Daily SC injections
- Risk of multiple pregnancies and ovarian hyperstimulation syndrome
-
IVF or laparoscopic ovarian drilling (3rd line)
- Laparoscopic ovarian drilling uses laser to reduce the amount of functional ovarian tissue to reduce androgen and inhibin production restores FSH levels and ovulation
20
Q
What are the complications and prognosis of PCOS?
A
Complications:
- T2DM later in life (50%) and GDM (30%)
- Increased risk of endometrial cancer (due to unopposed oestrogen)
There is no cure for PCOS so treatment should be continued through reproductive years
- Improves after menopause
21
Q
What is Ashmerman’s sydrome?
A
Rare condition in which scar tissue or adhesions partially or completely occlude the uterine cavity
22
Q
Aetiology of Ashmerman’s sydrome?
A
Due to damage of the basal layer of endometrium
- Basal layer does not regenerate → fibrosis and adhesion formation inside uterine cavity
- Occurs after trauma (from instrumentation, e.g. D&C, ERPC, myomectomy), or infection (endometritis)
23
Q
What are the signs and symptoms of Asherman’s syndrome?
A
- Amenorrhoea or reduced menstrual bleeding
- Dysmenorrhoea or cyclical abdominal pain
- Subfertility
24
Q
What are the Ix for ?Asherman’s syndrome?
A
- Ix for subfertility
- Hysteroscopy (gold standard)
- Other:
- Hysterosalpingogram (HSG): dye injected into cervix; X-rays visualise uterine cavity defects
- Saline hysterosonography (TVUSS with saline in uterus)
25
What is the Mx of Asherman's syndrome?
**Treatment is not needed if not planning to conceive & asymptomatic**
**Hysteroscopic adhesionolysis**
* To manually break down adhesions
* Risks further trauma → scarring may recur
* Reduce risk of adhesion recurrence with **copper IUD** and **PO oestrogens** (induce endometrial proliferation)
* Reassess cavity 2-3 months later
**Fertility treatment may be needed**
26
What are the complications and prognosis of Asherman's syndrome?
Complications:
* Subfertility
* If patient does conceive, increased risk of miscarriage, placenta praevia and placenta increta
Menstrual disturbance often improves after treatment; post-treatment pregnancy rates are 50%
27
What is menopause?
Permanent cessation of menstruation, defined as **12 months after the final period**
28
What is difference between:
* perimenopause
* early menopause
* premature ovarian insufficiency?
**Perimenopause**: time from the beginning of the first features of menopause, until 12 months after the last period
**Early menopause**: menopause in a woman aged *40-45yo*
**Premature ovarian insufficiency**: menopause in a woman *\<40yo*
29
What is the aetiology of menopause? Which other symptoms may be seen and why?
Hormonal changes:
* Decreased follicular activity (due to reduced quality and quantity of eggs) causes reduced oestrogen secretion from ovaries
* LH and FSH rise due to low oestrogen and inhibin (so removal of negative feedback)
* Irregular bleeding occurs → some bleeds are menstruation from ovulatory cycles; others are anovulatory cycles which can occur up to every fortnight
Symptoms are due to hormonal changes
* **Vasomotor symptoms**: due to pulsatile LH influencing temperature control
* **Urogenital symptoms**: uterus, vagina, bladder and urethra are maintained by circulating oestrogen → decreased oestrogen causes atrophy of vagina/bladder/urethra and thinning of myometrium
* **Bone density**: oestrogen reduces osteoclast activity → drop causes increase bone resorption
* **Ischaemic heart disease**: oestrogen is protective by reducing LDL and raising HDL
30
Aetiology of premature ovarian insufficiency?
* In most women no cause is found, but causes can include:
* **Primary POI:** chromosomal abnormalities (Turner’s), autoimmune diseases (hypothyroid, Addison’s, myasthenia gravis), enzyme deficiencies (CAH)
* **Secondary POI**: surgical following bilateral oophorectomy, chemo/radiotherapy, infections
* It can be reversible, so is not termed an early menopause
* May experience unpredictable spontaneous ovarian activity → irregular vaginal bleeding and small risk/chance of pregnancy
31
What are the signs and symptoms of menopause/early menopause/POI?
* **Persistent amenorrhoea**
* Often initial oligomenorrhoea or irregular/shortened cycles
* **Vasomotor symptoms**: hot flushes, night sweats, palpitations, headaches
* **Urogenital symptoms**: vaginal dryness, dyspareunia, frequency, dysuria, recurrent UTIs
* **Psychological symptoms**: poor concentration, lethargy, mood disturbance, reduced libido
* Usually the first to present
32
What are the Ix for menopause/early menopause/POI?
* **Largely clinical diagnosis**
* **Pregnancy test (for everyone)**
* **Bloods**:
* In women \<45yo; not recommended in \>45yo
* **FSH**: \>30Iu/L is high → indicated menopause
* Increased levels suggest fewer oocytes remaining in the ovaries
* Varies throughout the cycle → best measured between days 2-5
* **Oestradiol**: low
* **Anti-Mullerian hormone (AMH):** low
* Direct measurement of ovarian reserve; stable throughout menstrual cycle
* **Exclude other causes of symptoms**: TFTs, catecholamines and 5-hydroxyindolacetic acid (phaeo and carcinoid syndrome), progesterone (low indicates anovulation), prolactin
* **TVUSS**
* Only if uncertainty
* **DEXA scan**
* If RFs for osteoporosis (early menopause, low BMI, FHx, corticosteroids etc.)
33
What is the Mx for menopause/early menopause/POI?
**Conservative measures:**
* Stop smoking, regular exercise, healthy eating, avoid alcohol and caffeine
* To improve symptoms and address long-term health
* Some women try alternative therapies (acupuncture, evening primrose oil)
* May be sufficient for some women
**Hormone replacement therapy (HRT):**
* **_For women who cannot tolerate the symptoms; and in POI until 50yo_**
* Regimens:
* _Women with a uterus_: **oestrogen + progestogen**
* Unopposed oestrogen increases risk of endometrial hyperplasia and carcinoma (progesterone is given to counteract this)
* Usually given as norethisterone/oestradiol transdermal patch; changed twice weekly
* May be given orally; oestrogens are sometimes given as implant; progestogens are sometimes given as IUS
* Perimenopausal women are given cyclic therapy (continue to bleed); postmenopausal women are given continuous therapy
* _Women without a uterus_ (or IUS fitted in last 5yrs): **oestrogen** (as above)
* _For urogenital atrophy_ (without other symptoms): **topical** oestrogen
* Progesterone is not needed (don’t increase systemic oestrogen)
* Cream, ring, pessary
* _For reduced libido_: **methyltestosterone**
* Patch or subcutaneous implant
* Not successful in all women → other factors may be involved
* NB tibolone is sometimes used as an alternative → oestrogenic, progestogenic and androgenic actions
**POI**:
* **HRT** until 50yo
* **Oocyte donation** for fertility treatment
* Supportive care and counselling
34
What are the risks and benefits of HRT?
Benefits of HRT:
* Menopausal symptoms: reduces hot flushes and urogenital symptoms
* Libido may be improved by oestrogen alone or may need testosterone in addition
* Reduces risk of osteoporosis
* Reduces risk of colorectal cancer and may slightly reduce risk of CVD
Risks of HRT:
* Breast cancer: combined HRT (but not oestrogen alone) increases risk
* Effect is not seen in women who start oestrogen early for premature ovarian insufficiency (not seen below 50yrs) suggests lifetime exposure is relevant
* Endometrial cancer: unopposed oestrogen increases risk
* Venous thromboembolism: oral HRT increases risk 2x
* Gallbladder disease: risk increased by oral HRT
35
What is the duration of therapy for different types of ‘menopause’?
* **Menopausal symptoms**: 5yrs then stop to assess whether still needed
* **Premature menopause/POI until 50yo**: continue until 50yo
* **Osteoporosis**: treatment may need to be lifelong
36
What are some other Mx options for types of ‘menopause’?
Other management options (considered if HRT contraindicated or insufficient):
* SSRIs may be effective for hot flushes
* Lubricants and moisturisers for vaginal atrophy
* Osteoporosis treatments, e.g. vitamin D/calcium, bisphosphonates
37
What are the complications and prognosis of menopause?
Complications:
* CVD → same risk as men after menopause
* Osteoporosis
* Depression increases during perimenopausal period
Troublesome symptoms usually decrease after 5 years; may persist (esp vaginal dryness
