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YEAR 5 SPECIALTIES KEY INFO > GYNAE 1: Ovarian pathology, Amenorrhoea and Subfertility, Menopause/POI/HRT > Flashcards

GYNAE 1: Ovarian pathology, Amenorrhoea and Subfertility, Menopause/POI/HRT Flashcards

1
Q

What is a tubo-ovarian abscess?

A

Complex infectious mass of adnexa that forms as a sequela of PID

Causative organisms:
- 30-40% polymicrobial
- STIs
- Related to FB (coil) = actinomyces israelli

Sx = abdominal pain, fever, often PV discharge (not always)

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2
Q

What are long term consequences of tubo ovarian abscess?

A

infertility, increased risk of ectopic pregnancy and chronic pelvic pain

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3
Q

How is a tubo ovarian abscess managed?

A

USS = cogwheel sign may see pyosalpinx

Mx = antibiotic therapy +/- surgical intervention

Resus as appropriate to clinical condition

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4
Q

What is ovarian torsion and how does it present?

A

Obstruction of blood supply - may be adnexal, ovarian or rarely tubal torsion only

Sx = severe abdominal pain, vomiting, history of ovarian cyst

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5
Q

How is ovarian torsion diagnosed?

A

CLINICAL DIAGNOSIS

USS - oedematous ovary, peripheral distribution of follicles, whirlpool sign

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6
Q

How is ovarian torsion managed?

A

Laparoscopic detorsion +/- cystectomy

Necrotic and falling apart = oophorectomy

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7
Q

What is ovulation pain/ovarian cyst accident?

A

Sx = sharp, unilateral pain around ovulation

Most often simple, haemorrhagic cysts, less often dermoids/endometriomas (thick-walled)

USS = free fluid/blood in POD, probe tenderness, may see collapsing cyst

Mx = conservative

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8
Q

What are some epithelial ovarian tumours/cysts?

A

BENIGN = serous cystadenoma, mucinous cystadenoma

BORDERLINE = serous BOT, mucinous BOT, seromucinous BOT

MALIGNANT = serous carcinoma, mucinous carcinoma, clear cell carcinoma, endometrioid carcinoma

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9
Q

What are some germ cell ovarian tumours?

A

BENIGN = teratoma, dermoid

MALIGNANT = dysgerminoma, immature teratoma, yolk sac tumour, embryonal carcinoma, choriocarcinoma

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10
Q

What are some sex cord stromal ovarian tumours?

A

PURE STROMAL = fibroma, thecoma (benign)

PURE SEX CORD = adult/juvenile granulosa cell tumour (malignant)

MIXED SEX CORD-STROMAL = sertoli-leydig cell tumours (benign or malignant)

These tend to produce hormones e.g. oestrogens, steroids, androgens

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11
Q

What is a krukenberg tumour?

A

Metastatic adenocarcinoma of the ovary characterised by mucin-rich, signet-ring cells, originating from a GI primary in 70% of cases, but also involving the colon, breast, appendix, and biliary tract.

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12
Q

When should a woman be referred to 2ww ovarian cancer pathway from primary care?

A

2WW:
- ascites and/or a pelvic or abdominal mass (clear it’s not fibroids)

PRIMARY CARE TESTS if following sx 1 or more times a month:
- persistent abdo distension i.e. bloating
- early satiety or loss of appetite
- pelvic or abdo pain
- increased urinary urgency or frequency
- unexplained weight loss, fatigue, change in bowel habit

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13
Q

How should ovarian cancer be investigated in primary care?

A

Serum Ca125
- If serum Ca125 >35 IU/ml arrange an USS AP

If USS suggests ovarian cancer, refer woman urgently for further investigation

Risk of malignancy index - if >250 refer to gynae-onc team

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14
Q

How is risk of malignancy index calculated?

A

ultrasound score x menopausal score x Ca125

US features = multilocular cyst, solid areas, bilateral lesions, ascites, intra-abdominal metastases (0 = none, 1 = 1 abnormality, 3 = 2 or more abnormalities)

Pre-menopausal score = 1
Post-menopausal = 3

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15
Q

How is ovarian cancer investigated in secondary care?

A

Ca125 +/- AFP/hcg (<40yo to identify those w/non-epithelial ovarian cancer)

USS abdo and pelvis

CT CAP (can offer MRI if nature of mass remains indeterminate)

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16
Q

How is ovarian cancer managed?

A

CONSERVATIVE

MEDICAL:
- chemotherapy first line usually paclitaxel + platinum based e.g. cisplatin/carboplatin
- bevacizumab (avastin) only for advanced

SURGICAL:
- usually ultra-radical surgery
- primary or interval debulking

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17
Q

Roughly what are the stages of ovarian cancer?

A

Stage 1 = cancer in one or both ovaries

Stage 2 = spread within pelvis to fallopian tubes, uterus etc.

Stage 3 = spread within abdomen to nearby lymph nodes, diaphragm, intestines or liver

Stage 4 = spread beyond abdomen e.g. to lungs or spleen

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18
Q

What does a PC of primary amenorrhoea combined with a transabdominal USS showing absence of uterus w/a pelvic kidney suggest?

A

Mayer-Rokitansky-Kuster-Hauser (MRKH) syndrome

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19
Q

When should primary amenorrhoea be suspected?

A
  • girls who haven’t established menstruation by 13yo w/no secondary sexual characteristics e.g. breast development
  • girls who haven’t established menstruation by 15yo and normal secondary sexual characteristics

NOTE: normal age of puberty from 8yrs old in girls

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20
Q

What are causes of amenorrhoea?

A
  1. Hypothalamic hypogonadism
  2. Pituitary hypogonadism
  3. Ovarian pathology
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21
Q

What are causes of amenorrhoea caused by hypothalamic hypogonadism?

A

Kallman’s syndrome
Tumours
Low BMI
Exercise
Stress
Hyper or hypothyroidism
CAH
Virilising tumours

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22
Q

What are causes of amenorrhoea caused by pituitary hypogonadism?

A

Sheehan’s syndrome
Pituitary tumours
Prolactinoma

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23
Q

What are causes of amenorrhoea caused by ovarian pathology?

A

POI
Menopause
Turner’s syndrome
Gonadal dysgenesis
Androgen insensitivity

24
Q

What are structural causes of amenorrhoea?

A

Imperforate hymen
Rokitansky syndrome
Asherman’s syndrome
Cervical stenosis

25
Q

Which embryological duct becomes the body of the tubes, uterus, cervix and upper 1/3 of the vagina?

A

Paramesonephric ducts (aka Mullerian ducts)

26
Q

What happens when the Mullerian ducts fuse at around 10 weeks?

A

Merge to form mesonephric ducts aka Wolffian ducts

(uterine septum temporarily in midline, where edges of 2 paramesonephric ducts meet, cranial ends remain open, where caudal ends meet urogenital sinus, the vaginal plate forms)

27
Q

What are some paramesonephric duct anomalies?

A

Mullerian hypoplasia/agenesis (cervical agenesis)

Unicornuate uterus = single horned, hemiuterus

Didelphys (double) uterus

Bicornuate uterus (heart shaped)

Septate = most common anomaly

28
Q

How does a longitudinal vaginal septum present?

A
  • difficulty inserting tampons
  • dyspareunia
  • accumulation of menstrual blood
  • emergency w/severe dysmenorrhoea and palpable abdominal mass
29
Q

What is MRKH syndrome?

A

Congenital disorder of genital tract, typically presenting w/primary amenorrhoea w/normal secondary sexual characteristics

Characterised by uterine and vaginal hypoplasia

30
Q

How is MRKH syndrome diagnosed?

A

Clinical diagnosis

EXAMINATION:
- normal secondary sexual characteristics, normal hormone profile, genital examination shows absent or blind vagina

IMAGING: USS/MRI confirms diagnosis

31
Q

How is MRKH syndrome managed?

A

Focus on congenital impact and psychological impact
- dilators + psychological therapy

Surgery not usually indicated but high success rate

Transplant

32
Q

How may imperforate hymen or transverse vaginal septum present?

A

Vagina becomes distended, usually painless

Results in haematocolpos - cyclical abdominal pain

‘Blue bulge’ on examination = imperforate hymen only

33
Q

What is the diagnostic criteria for PCOS?

A

Rotterdam criteria
- oligo/anovulation (>2yrs)
- clinical or biochemical features of hyperandrogenism
- polycystic ovaries on USS (>12 in one ovary measuring 2-9mm in diameter)

Hyperoestrogenic state = conversion to androgens
- assoc. w/insulin resistance

Shouldn’t be diagnosed within 8yrs of menarche

34
Q

How is PCOS managed?

A

CONSERVATIVE = weight loss

MEDICAL =
- Dianette COCP (androgenic sx) - contains cyproterone acetate (anti-androgenic)
- Metformin

SX management e.g. laser therapy for excessive hair

If desiring pregnancy:
1. weight loss
2. ovulation induction = clomiphene (SERM)/gonadotrophin +/- metformin
3. laparoscopic ovarian drilling
4. IVF

35
Q

What does PCOS increase the risk of?

A
  • lifetime risk of diabetes
  • endometrial hyperplasia
  • endometrial cancer
  • depression
36
Q

How is subfertility investigated?

A

Blood hormones = day 2-3 FSH, LH and oestradiol. AMH demonstrates ovarian reserve

STI screening

TVUSS, antral follicle count

Tubal assessment (hysterosalpingogram or lap+dye)

Semen analysis

37
Q

How is anovulation infertility treated?

A

Ovulation induction w/clomiphene, gonadotrophins
Laparoscopic ovarian drilling

38
Q

How is male factor infertility treated?

A

IUI if mild
Donor insemination

39
Q

How is tubal scarring/failed IUI or ovulation induction infertility treated?

A

IVF
ICSI (intracytoplasmic sperm injection)

40
Q

How is lack of oocytes e.g. POI/Turner’s syndrome infertility treated?

A

Donor egg

41
Q

How is an anatomical abnormality infertility treated?

A

Surgical management e.g. adhesiolysis, myomectomy

42
Q

How is menopause diagnosed?

A

In women >45yo w/menopausal sx, diagnosis of perimenopause or menopause should be considered based on their symptoms alone, w/o confirmatory blood tests unless uncertainty about diagnosis.

Average age = 51

Menopause = a retrospective diagnosis, absence of menses for 12 months

43
Q

Generally how should menopause be managed?

A

IMPORTANT: cannot give oestrogen w/o progesterone if a woman has a uterus in situ

Unopposed oestrogen can cause endometrial hyperplasia which can cause cancer

All women should be offered HRT for menopausal sx first-line

Women w/GU sx should be offered vaginal oestrogen rx

44
Q

What is POI?

A

Women experiencing menopause <40yo w/menopausal sx and absent or infrequent periods.

45
Q

How is POI diagnosed?

A

2 blood tests for FSH level taken 4-6w apart (>40 IU/l)

Bone mineral density

46
Q

What does POI increase the risk of?

A

Cardiovascular disease, osteoporosis and cognitive impairment

47
Q

How is POI managed?

A

Hormone replacement w/HRT or COCP continued at least until average age of menopause (51yrs)

Can have intermittent ovarian activity and have a chance of natural conception estimated to be in region of 5-10%.

48
Q

What are symptoms of menopause/POI?

A
  • vasomotor sx
  • cognitive sx and mood disorders
  • sleep disturbances
  • fatigue, tiredness and low energy levels
  • loss of libido
  • joint and muscle pains
  • headaches
  • GU sx
49
Q

What are potential causes of POI?

A

Exact causes unknown

GENETICS e.g. fragile X, Turner’s

TOXIC CAUSES e.g. chemotherapy, radiotherapy

SURGERY

AUTOIMMUNE causes e.g. adrenal or thyroid gland problems

50
Q

What are benefits of HRT?

A

PROVEN =
- control of menopausal sx
- maintenance of bone mineral density, reduced osteoporosis risk

ADDITIONAL POTENTIAL =
- reduced risk of CHD and reduced risk of Alzheimers disease when oestrogen started early
- reduced risk colorectal Ca
- reduced risk T2DM

51
Q

What are known risks of HRT?

A
  • endometrial cancer if oestrogen only given, this is reduced by adding a progestogen continuously
  • DVT/PE: greatest risk in first 12mths, no increase in risk of VTE w/transdermal
  • CHD: possible increase when combined HRT started in women >60yo or pre-existing CHD
  • Stroke: increased risk when oral HRT started in >60yo
  • Breast cancer: increased slightly after min. 5yrs of combined HRT >50yo, risk assoc. w/oestrogen alone much less. Mortality not increased.
52
Q

What are indications for transdermal HRT?

A
  • individual preference
  • poor sx control w/oral
  • GI disorder affecting oral absorption
  • prev. or family hx of VTE
  • BMI >30
  • variable BP control
  • migraine
  • current use of hepatic inducing enzymes medication
  • gallbladder disease
53
Q

How should vasomotor sx be managed in a women with menopause and history of breast cancer?

A

1st line = lifestyle changes and HRT alternatives

Avoid paroxetine and fluoxetine in women taking tamoxifen.

If severe, refractory sx, systemic HRT may be offered but requires informed, documented consent and discussion w/breast ca team

Systemic HRT should not be used in women treated w/an aromatase inhibitor

54
Q

How is vulvo-vaginal atrophy managed in a women with menopause and history of breast cancer?

A

1st line = vaginal moisturisers

Refractory sx = ultra-low dose topical oestrogen

Topical oestrogen should be avoided in presence of aromatase inhibitor

55
Q

How is HRT managed if there is endometrial hyperplasia w/o atypia?

A

Switch from sequential to continuous

If on continuous, increase progestogen component

56
Q

How is HRT managed if there is endometrial hyperplasia w/ atypia?

A
  • recommend hysterectomy (TLH + BSO) due to high risk of progression to endometrial cancer
  • recommend BSO to reduce future risk of ovarian cancer
57
Q

What is the difference between perimenopause and postmenopause and how is HRT managed differently dependent on these?

A

Perimenopause = women w/irregular menstrual cycles + vasomotor sx
- Mx = sequential HRT

Postmenopause = women w/o bleeding for at least 1yr in absence of interventions that may cause amenorrhoea
- Mx = continuous HRT

YEAR 5 SPECIALTIES KEY INFO (16 decks)

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