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
Which embryological duct becomes the body of the tubes, uterus, cervix and upper 1/3 of the vagina?
Paramesonephric ducts (aka Mullerian ducts)
26
What happens when the Mullerian ducts fuse at around 10 weeks?
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
What are some paramesonephric duct anomalies?
Mullerian hypoplasia/agenesis (cervical agenesis) Unicornuate uterus = single horned, hemiuterus Didelphys (double) uterus Bicornuate uterus (heart shaped) Septate = most common anomaly
28
How does a longitudinal vaginal septum present?
- difficulty inserting tampons - dyspareunia - accumulation of menstrual blood - emergency w/severe dysmenorrhoea and palpable abdominal mass
29
What is MRKH syndrome?
Congenital disorder of genital tract, typically presenting w/primary amenorrhoea w/normal secondary sexual characteristics Characterised by uterine and vaginal hypoplasia
30
How is MRKH syndrome diagnosed?
Clinical diagnosis EXAMINATION: - normal secondary sexual characteristics, normal hormone profile, genital examination shows absent or blind vagina IMAGING: USS/MRI confirms diagnosis
31
How is MRKH syndrome managed?
Focus on congenital impact and psychological impact - dilators + psychological therapy Surgery not usually indicated but high success rate Transplant
32
How may imperforate hymen or transverse vaginal septum present?
Vagina becomes distended, usually painless Results in haematocolpos - cyclical abdominal pain 'Blue bulge' on examination = imperforate hymen only
33
What is the diagnostic criteria for PCOS?
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
How is PCOS managed?
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
What does PCOS increase the risk of?
- lifetime risk of diabetes - endometrial hyperplasia - endometrial cancer - depression
36
How is subfertility investigated?
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
How is anovulation infertility treated?
Ovulation induction w/clomiphene, gonadotrophins Laparoscopic ovarian drilling
38
How is male factor infertility treated?
IUI if mild Donor insemination
39
How is tubal scarring/failed IUI or ovulation induction infertility treated?
IVF ICSI (intracytoplasmic sperm injection)
40
How is lack of oocytes e.g. POI/Turner's syndrome infertility treated?
Donor egg
41
How is an anatomical abnormality infertility treated?
Surgical management e.g. adhesiolysis, myomectomy
42
How is menopause diagnosed?
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
Generally how should menopause be managed?
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
What is POI?
Women experiencing menopause <40yo w/menopausal sx and absent or infrequent periods.
45
How is POI diagnosed?
2 blood tests for FSH level taken 4-6w apart (>40 IU/l) Bone mineral density
46
What does POI increase the risk of?
Cardiovascular disease, osteoporosis and cognitive impairment
47
How is POI managed?
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
What are symptoms of menopause/POI?
- 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
What are potential causes of POI?
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
What are benefits of HRT?
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
What are known risks of HRT?
- 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
What are indications for transdermal HRT?
- 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
How should vasomotor sx be managed in a women with menopause and history of breast cancer?
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
How is vulvo-vaginal atrophy managed in a women with menopause and history of breast cancer?
1st line = vaginal moisturisers Refractory sx = ultra-low dose topical oestrogen Topical oestrogen should be avoided in presence of aromatase inhibitor
55
How is HRT managed if there is endometrial hyperplasia w/o atypia?
Switch from sequential to continuous If on continuous, increase progestogen component
56
How is HRT managed if there is endometrial hyperplasia w/ atypia?
- recommend hysterectomy (TLH + BSO) due to high risk of progression to endometrial cancer - recommend BSO to reduce future risk of ovarian cancer
57
What is the difference between perimenopause and postmenopause and how is HRT managed differently dependent on these?
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