Gynae Flashcards

1
Q

What are the branches of the internal iliac artery?

A

Posterior branch:
- iliolumbar
- lateral sacral(s)
- superior gluteal

Anterior branch
- umbilical (to superior vesical)
- obturator
- vaginal
- uterine
- middle rectal
- inferior gluteal
- internal pudendal

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2
Q

What is the most common cause of vaginal discharge in prepubertal girls?

A

Vulvovaginitis (often non-specific secondary to poor hygiene)

Also vulval dermatoses and foreign bodies

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3
Q

Management of vulvovaginitis in prepubertal girls?

A

Hygiene measures (avoid irritants, loose clothing, cotton underwear, wiping front to back), emollients and barrier creams.
Penicillin / erythro for GAS.

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4
Q

Definition of precocious puberty

A

Onset of pubertal development < 8years
Onset of menarche before 9 years

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5
Q

Causes of precocious puberty?

A

Central (80%) - idiopathic 75%, brain tumour/cyst/hydroceph
Brain trauma/malformations

Peripheral (pseudo) 20% - Hormone producing tumour, CAH, hypothyroid, exogenous estrogen, McCune Albright

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6
Q

Management of central precocious puberty

A

Only treat if young with rapid progression (shortened predicted height)
- GnRH analogues, eg zoladex Q3monthly
- monitor 3-6m with pubertal staging, annual bone age XR

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7
Q

Definition of delayed puberty

A

Absence of sexual characteristics by age 13

No menstruation by 15

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8
Q

Causes of hypogonadotrophic hypogonadism (for delayed puberty)

A

Constitutional delay
Chronic illness / suppression of the HPO axis (anorexia, exercise etc)
Kallman’s syndrome
Hydrocephalus, CNS tumours, adenoma
Panhypopituitarism

Can treat with pulsatile GnRH via pump

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9
Q

Causes of hypergonadotrophic hypogonadism (for delayed puberty)

A

Abnormal gonadal development
Turners or Swyers syndrome
Premature ovarian failure
Chemo/radiation
Autoimmune
Infections

Management: Administer small doses of oestradiol and increase 6m until BTB, then add progesterone

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10
Q

What is Swyers syndrome?

A

46 XY with genetic mutation in SRY gene in 10%
- phenotypically female
- failure of testes to develop, therefore no testosterone or AMH (tubes + uterus present)
- 30% risk of gonadal malignancy

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11
Q

Classical features of Turners syndrome
- appearance
- associated conditions

A

Short, low hairline, neck folds, widely spaced nipples, elbow deformity, naevi, lymphoedema

Aortic coarctation, renal anomalies, rudimentary ovaries and poor breast development (delayed puberty).
Insulin resistance, hypothyroidism

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12
Q

Management of Turners syndrome

A

Growth hormone to improve height
Induction of puberty with oestradiol + progesterone once bleeding
Long term HRT
Childbearing possible with ovum donation
Gonadectomy if any Y material

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13
Q

What is the Rotterdam Criteria?

A

For PCOS - 2 out of 3 of:
1. Oligo or anovulation (<21 to >35 days, or less than 8 cycles per year)
2. Clinical and/or biochemical signs of hyperandrogenism (acne/hirsutism, elevated free and total testosterone)
3. PCO morphology on USS (>20 follicles 2-9mm per ovary and/or ovarian volume >10ml)
4. Exclusion of thyroid disease, hyperprolactinaemia, non-classic CAH, and androgen secreting tumours

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14
Q

Biochemical findings in PCOS

A

Increased free testosterone
DHEAS/androstenedione may be elevated
Decreased SHBG
Increased LH to FSH ratio
Mildly increased prolactin
Increased oestrogen and decreased progesterone.

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15
Q

Goals of management for PCOS (4)

A
  1. Correct hyperandrogenism
  2. Correct cycles
  3. Manage fertility problems
  4. Improve long term health - risk of depression/anxiety, diabetes, CVD, and endometrial hyperplasia
    +/- cosmetic symptoms
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16
Q

Causes of hypergonadotrophic hypogonadism (for male infertility)

A

High FSH, low/normal testosterone

Congenital:
- Androgen insensitivity
- Klinefelters (XXY)
- Y chromosome microdeletions

Acquired:
- Infection (mumps)
- Trauma / torsion
- Chemoradiation
- Drugs, lifestyle + exposure to heat

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17
Q

Normal semen analysis (6)

A

Volume >1.5ml
Count > 40 million
Concentration >16mill/ml
Motility >40%
Normal morphology >4%
pH > 7.2

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18
Q

Investigations for male infertility

A

Semen analysis

If semen analysis abnormal - FSH/testosterone +/- karyotype.
Post-ejaculatory urine sample (retrograde ejaculation), TSH/prolactin.

Hep B, C and HIV screening if contemplating IVF

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19
Q

What are the absolute and relative contraindications for MHT?

A

Absolute:
1. Breast, endometrial or other hormone dependent cancer (past or present)
2. Undiagnosed abnormal vaginal bleeding
3. Current / untreated VTE

Relative:
1. Established CVD / high risk CVD
2. Previous VTE
3. Active liver disease or active SLE
4. Untreated HTN
5. Possibly migraine with aura

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20
Q

What is a T score?

A

How your BMD compares to your expected BMD (for age/ethnicity/gender) - reported as no. of SD from the mean
-1 to +1 is normal
-2.5 to -1 is osteopenia
Less than -2.5 is osteoporosis

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21
Q

What is Stage 1a endometrial cancer?

A

Tumour confined to corpus, no or less than 1/2 myometrial invasion

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22
Q

What is Stage 1b endometrial cancer?

A

Tumour confined to corpus, equal or more than 1/2 myometrium involved.

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23
Q

What is Stage II endometrial cancer?

A

Tumour invades the cervical stroma but not beyond the uterus

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24
Q

What is Stage III endometrial cancer?

A

Local and/or regional spread of the tumour
IIIa = Invades serosa and/or the adnexa
IIIb = Vaginal involvement and/or parametrial involvement
IIIc = Positive nodes

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25
Q

What is Stage IVa Endometrial cancer

A

Invasion of the bladder or bowel

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26
Q

Radiological staging for Endometrial cancer?

A

MRI pelvis + CXR for grade 1-2 endometrioid

CT CAP or PET scan for high grade

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27
Q

What is the adjuvant therapy recommended for Endometrial Ca with intermediate/high risk factors (e.g stage 1b)

A

Adjuvant vaginal brachytherapy - excellent vaginal control without impacting QoL

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28
Q

Definition of endometrial hyperplasia

A

Disordered proliferation of endometrial glands with increased gland to stromal ratio

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29
Q

What are the risks of co-existent Ca and risk of progression with hyperplasia with and without atypia?

A

Hyperplasia without atypia: <1% risk of co-existent Ca, <5% risk of progression over 20 years

Hyperplasia with atypia: ~40% of coexistent Ca, ~30% risk of progression

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30
Q

Management of endometrial hyperplasia without atypia?

A

Mirena 1st line (resolution in 89-96%)
Oral progestins

Resample in 6m intervals
Discharge after 2x consecutive normal samples

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31
Q

What are the indications for hysterectomy in the management of endo hyperplasia without atypia?

A

No resolution after 12m
Relapse of hyperplasia
Non-resolution of bleeding
Non-compliance with treatment and/or sampling

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32
Q

What is the management of endometrial hyperplasia with atypia?

A

Hysterectomy

If post-menopausal: TLH + BSO
If pre-menopausal: TLH + BS

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33
Q

What are the fertility sparing options for managing endometrial hyperplasia with atypia?

A

Rule out cancer (Hysteroscopy D+C, MRI, + consider Ca125)
Thorough counselling about risks

Mirena 1st line, or high dose progestins (Provera 100-600mg daily)
3m sampling until 2x consecutive are negative
Then sample 6-12m until hysterectomy

Surgery indicated when:
1. Patient request / fertility no longer required
2. Progression to cancer
3. Persistence at 12 months

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34
Q

Types of germ cell tumours (4)

A
  1. Dysgerminoma
    - exquisitely sensitive to chemo, equivalent to serminoma in testicular cancer)
  2. Teratoma (mature vs immature)
  3. Yolk sac / endodermal sinus tumour
    - secretes AFP, aggressive
  4. Choriocarcinoma - secrete HCG

All are highly sensitive to chemo and so conservative surgery (USO) is standard

35
Q

What are two types of sex cord stromal cells tumours of the ovary?

What is their management?

A

Granulosa - secrete oestrogen and inhibin
- can be Juvenile or Adult

Sertoli-Leydig - secrete testosterone

Treatment is USO unless post-menopausal

36
Q

What is Stage 1a Ovarian cancer?

A

One ovary with capsule intact

37
Q

What is Stage 1b ovarian cancer?

A

Both ovaries involved, with capsules intact

38
Q

What is Stage 1c ovarian cancer?
- 1c1
- 1c2
- 1c3

A

One or both ovaries affected
1c1 = surgical spill
1c2 = capsule ruptured pre-surgery or tumour on surface
1c3 = malignant cells in ascites or washings

39
Q

What is stage II ovarian cancer?

A

Involves one or both ovaries / tubes with pelvic extension (below pelvic brim) or peritoneal cancer

IIa = Extension and/or implants on uterus and/or tubes and/or ovaries

IIb = Extension to other pelvic intraperitoneal tissues

40
Q

What is Stage III ovarian cancer?

A

Involves one or both ovaries or tubes (or primary peritoneal ca) with spread to peritoneum outside the pelvis +/- mets to retroperitoneal LNs

41
Q

What is Stage IIIb ovarian cancer?

A

Macroscopic peritoneal mets beyond the pelvis up to 2cm. With or without retroperitoneal lymph nodes.

42
Q

What is Stage IIIc ovarian cancer?

A

Macroscopic peritoneal mets beyond the pelvis >2cm diameter, with or without mets to retroperitoneal LNs

43
Q

What is Stage IVa ovarian cancer?

A

Stage IV = Distant mets

Stage IVa = Pleural effusion with positive cytology

44
Q

What is Stage IVb ovarian cancer

A

Parenchymal mets, and mets to extra-abdominal organs (including inguinal lymph nodes, and lymph nodes outside the abdominal cavity)

45
Q

When is adjuvant chemo recommended for ovarian Ca?

A

Stage 1c and above

46
Q

What are the types of cervical cancer?

A

Squamous cell carcinoma 70-80%
Adenocarcinoma 15-20%
Rare = Melanoma, sarcoma, lymphoma, small cell carcinoma

47
Q

What is Stage Ia1 cervical cancer?

A

Strictly confined to cervix

Microscopic with deepest invasion <3mm invasion and <7mm wide

48
Q

Stage Ia2 cervical cancer?

A

Strictly confined to cervix

Microscopic 3-5mm invasion and <7mm wide

49
Q

What is Stage 1b cervical cancer?

A

Strictly confined to cervix
Clinically visible or pre-clinical lesion larger than Ia

Ib1 = <2cm wide
Ib2 = 2-4cm wide
Ib3 = >4cm wide

50
Q

What is stage II cervical cancer?

A

Invades beyond the cervix but not to the pelvic wall or lower 1/3rd of the vagina

51
Q

What is stage IIa1 and IIa2 cervical cancer?

A

Stage IIa = No parametrial invasion

IIa1 = Clinically visible lesion <4cm diameter

IIa2 = Clinically visible >4cm diameter

52
Q

What is Stage IIb cervical cancer?

A

Obvious parametrial invasion

53
Q

What is Stage III cervical cancer?

A

Extends to the pelvic side wall and/or involves the lower 1/3 of the vagina and/or is causing hydronephrosis

IIIa = Lower third of vagina
IIIb = Pelvic side walls or hydronephosis
IIIc = Lymph nodes (pelvic then para-aortic)

54
Q

What is Stage IV cervical cancer?

A

Spread beyond the true pelvis and/or involves the mucosa of the bladder or bowel (biopsy proven)

55
Q

Treatment of Stage Ia1 cervical cancer

A

Lletz or Cone with adequate margins
Consider simple hysterectomy if no desire for ongoing fertility

56
Q

Treatment of Stage Ia2 and Ib1 cervical cancer

A

Modified simple hysterectomy + PLND or SNLB
If fertility desired consider large cone vs trachelectomy + lap PLND

57
Q

Treatment of Ib2 and IIa1 cervical cancer

A

Radical hysterectomy + PLND

58
Q

Treatment of Ib3, IIa2 (and above) cervical cancer

A

Surgery is feasible but not encouraged due to size of lesions and likelihood of needing adjuvant chemorad (surgery + chemorad increases morbidity)
Recommend primary chemorad

59
Q

What is the management of glandular abnormalities on smear (AGC or AIS) / cervical biopsy?

A

Refer straight to colposcopy
Type 3 excision (Cone) + Hysteroscopy D&C recommended

60
Q

Management of AIS on Type 3 excision?

A

Depends on age and fertility expectations + status of excisional margins.

Once family complete -> Hysterectomy
- recurrence after cone is high (up to 20%)
- difficult reliable cytology f/u as disease is often multi-focal

61
Q

What is the transformation zone?

A

The area between mature squamous epithelium distally and columnar epithelium proximally
- the site of active squamous metaplasia

62
Q

What are abnormal findings you might see at colposcopy?

A
  1. Mosaicism (abnormal vessel pattern)
    - CIN1 = fine, CIN2-3 = coarse
  2. Punctation (abnormal dilated blood vessels)
    - CIN1 = fine, CIN 2-3 = coarse, large
  3. Abnormal branching of vessels - suggests microinvasion
63
Q

Describe high grade changes on colposcopy (4)

A

Oyster grey, rapid change with acetic acid
Relatively small, smooth and flat
In upper TZ or near the new SCJ
Border: Straight, raised or rolled and prominent

(c.f low grade changes: large ad geographic throughout ectocervix, slow to change with acetic acid, irregular and indistinct border)

64
Q

What is the risk of progression to malignancy with uVIN?

A

4-6%
Causes 20% of SCC of the vulva
22% also have high grade CIN

65
Q

What is the risk of progression to malignancy with dVIN?

A

60%, and shorter time to progression
Causes 80% of SCC of the vulva

Higher risk of recurrence - excision is the treatment of choice

66
Q

What is the risk of recurrence of VIN after CO2 ablation?

A

40% risk recurrence

67
Q

What is the risk of recurrence of VIN after topical immune modulator therapy (imiquimod 5%)?

A

50% short term recurrence

68
Q

What is Stage Ia vulvar cancer

A

Site <2cm and stromal invasion </=1mm

Treat with WLE
- no lymph node dissection needed
Aim surgical margins of 2cm, pathological margins of 8mm

69
Q

What is Stage Ib vulvar cancer

A

> 2cm or >1mm invasion

Treat with vulvectomy + LND

70
Q

What is Stage II vulvar cancer

A

Any size, with extension to the lower 1/3rd of the urethra, vagina or anus, with negative nodes

Resection with adjuvant CCRT, vs Definitive CCRT

71
Q

When is adjuvant radiotherapy required after excision of vulvar cancer?

A

If extra-capsular spread
2+ positive groin nodes
<5mm pathological margins (and unable to re-excise)

72
Q

What is the risk of ovarian cancer with BRCA1?

A

2-3% by age 40, 10-20% by age 50
Overall risk of 44% (by age 80)

73
Q

What is the risk of ovarian cancer with BRCA 2?

A

<3% by age 50, 17% by age 80

74
Q

What are the lifestyle modifications possible for management of urinary incontinence (5)?

And management of underlying health conditions? (5)

A

Weight loss
Decrease fluid intake to 1-1.5L per day
Decrease caffeine intake
Avoid ETOH
Smoking cessation

Manage diabetes, constipation, sleep apnoea, chronic cough
- Review medications e.g diuretics, ACEIs

75
Q

What are the different medical management options for Urge urinary incontinence?

A

Topical oestrogens

Anticholinergics
- Solifenacin (Vesicare) 5mg daily, increase to 10mg if required
- Oxybutynin 5mg TDS

Intra-vesical botox injection
- risk of urinary retention

76
Q

Management of vesicovaginal fistula if not recognised with 48hrs from injury?

A

Delay 6-12 weeks, IDC in situ for this time.
- allow reduction in granulation tissue, infection and necrosis

Surgical repair - vaginal or abdominal
- tension-free, closure in 4 layers, excision of all scar tissue

77
Q

What is the most common generalised cause of male infertility?

What are 4 congenital and 4 acquired causes of this?

A

Hypergonadotrophic hypogonadism (primary testicular failure)
- no predisposing factors in 50% of cases

Congenital = Klinefelters (XXY), androgen insensitivity, Y chromosome microdeletions and undescended testes

Acquired = Infection (mumps), trauma / torsion, cancer / chemorad, drugs and lifestyle / environmental

78
Q

What are the long term health risks with PCOS (5)?

A

T2DM
Heart disease
Hypercholesterolaemia / hyperlidipiaemia
Anxiety / depression
Endometrial hyperplasia and cancer

79
Q

Differentials for irregular periods / secondary amenorrhoea (8)

A

Rule out pregnancy

PCOS

Prolactinaemia - check prolactin
Thyroid disease - check TFTs
Ovarian failure or hypothalamic amenorrhoea - check FSH and oestradiol
Late onset / non-classical CAH - check 17-OHP
Androgen secreting tumour - check DHEAS
Ovarian androgen secreting tumour - check androstenedione
Cushings - consider 24hr urinary cortisol

80
Q

Classical biochemical findings with PCOS?

A

Elevated free and total testosterone
Elevated LH to FSH ratio
Decreased SHBG
Oestradiol may be increased
May have mildly increased DHEAS
Prolactin may be mildly increased

81
Q

What is vaginismus?

A

Psychological conditioned reflex in the pelvic musculature with muscle spasm occurring during attempts at vaginal penetration
- may be triggered by an early painful sexual experience or by childhood sexual abuse

82
Q

Treatment options for vaginismus?

A

MDT with sex therapist, physiotherapist and psychologist +/- vaginal dilatos

Psychodynamic / psychotherapeutic vs physical with dilators

83
Q

Possible causes / triggers for Vaginismus?

A

Early painful encounter
Previous sexual abuse
Endometriosis
Vaginitis
Can be related to previous childbirth / epis / tear