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Phase 3a > Gynaecology > Flashcards

Gynaecology Flashcards

1
Q

Define Subfertility

A

When a couple have not conceived after a year of regular unprotected intercourse (15% affected)

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2
Q

What is ‘primary’ and ‘secondary’ failure to conceive?

A

Primary- the female has never conceived.

Secondary- the female has previously conceived (even if the pregnancy ended in miscarriage or termination).

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3
Q

What are the 4 basic conditions required for pregnancy?

A
  1. An egg must be produced. (Failure is anovulation).
  2. Adequate sperm must be released. (Failure is ‘male factor’ problems).
  3. The sperm must reach the egg.
  4. The fertilised egg (embryo) must implant.
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4
Q

What are the 6 contributors to subfertility?

A
  1. Ovulatory Problems (30%)
  2. Male Problems (25%)
  3. Tubal Problems (25%)
  4. Coital Problems (5%)
  5. Cervical Problems (<5%)
  6. Unexplained (30%)
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5
Q

Briefly summarise the process of ovulation:

A
  1. Low oestrogen levels –> hypothalamic GnRH stimulates anterior pituitary to produce FSH + LH
  2. This causes maturation of follicles in the ovary –> follicles produce oestradiol which suppresses LH + FSH when at intermediate amount–> one follicle survives
  3. Follicle matures –> more oestradiol –> high levels cause positive feedback so LH + FSH levels increase rapidly –> LH peak causes ripe follicle to rupture (ovulation)
  4. Follicle is now corpus luteum –> releases oestrogen + progesterone to maintain secretory endothelium for implantation. If this does not occur then the corpus luteum involutes + hormone levels fall –> menstruation
  5. If implantation does occur –> hCG produced by trophoblast tissue acts on corpus luteum to maintain oestrogen and progesterone production until the feto-placental unit takes over around 8-10 weeks
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6
Q

How is ovulation detected?

A
  1. History (regular cycles, vaginal spotting + pelvic pain/discharge around time of ovulation
  2. Examination (temperature changes during cycle- temperature chart)
  3. Investigations (elevated serum progesterone levels in mid-luteal phase, USS to monitor follicular growth, urine predictor kits for LH surge)
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7
Q

What are the causes of anovulation?

A
  1. PCOS
  2. Hypothalamic Hypogonadism
  3. Hyperprolactinaemia
  4. Thyroid Disease
  5. Premature Ovarian Failure
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8
Q

What criteria is needed for PCOS diagnosis?

A

2 out of the following 3:

  1. Polycystic Ovary on USS
  2. Irregular Periods (>35 days apart)
  3. Hirsutism (Clinical (acne/excess body hair) and/or biochemical (raised serum testosterone))
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9
Q

What is the characteristic transvaginal USS appearance of polycystic ovary?

A

Multiple (12+) small (2-8mm) follicles in an enlarged ovary.

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10
Q

How does PCOS present clinically?

A
  1. Nothing
  2. Subfertility
  3. Oligomenorrhoea/ amenorrhoea
  4. Obesity
  5. Miscarriage
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11
Q

How is PCOS investigated? (4 things)

A
  1. Exclude alternative causes for symptoms
  2. Transvaginal ultrasound scan
  3. Bloods (FSH (normal), Prolactin, TSH, LH, Testosterone (raised))
  4. Fasting lipids + glucose to screen for complications
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12
Q

What are the 2 complications of PCOS?

A
  1. Type 2 diabetes

2. Endometrial Cancer

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13
Q

How are PCOS symptoms treated (not including infertility)?

A
  1. Advice about diet and exercise (weight loss)
  2. COCP to regulate menstruation (or mirena IUS) + treat hirsutism (if fertility not required)
  3. Antiandrogens (cyproterone acetate or spironolactone) for hirsutism
  4. Metformin to reduce insulin (therefore reduce androgens + hirsutism)
  5. Eflornithine (topical antiandrogen for facial hirsutism)
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14
Q

What can cause hypothalamic hypogonadism and how is it managed?

A
  1. Anorexia nervosa
  2. Dieting, athletes, stress

Restore body weight to restore hypothalamic function. Gonadotrophins if weight normal

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15
Q

What causes hyperprolactinaemia and how is it managed?

A

Causes: benign tumours (adenomas), hyperplasia of pituitary cells, PCOS, hypothyroidism, psychotropic drugs

Management: dopamine agonist (cabergoline/bromocriptine) will inhibit prolactin release

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16
Q

How is ovulation induced in PCOS?

A
  1. Weight loss + Lifestyle changes. Then…
  2. Clomifene (antioestrogen- first line) . If it fails add…
  3. Metformin, gonadotrophins, ovarian diathermy.
  4. If no success then IVF
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17
Q

What are the side effects of ovulation induction?

A
  1. Multiple pregnancy
  2. Ovarian hyperstimulation syndrome (OHSS)
  3. Ovarian + Breast Carcinoma
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18
Q

Briefly outline physiology of sperm production:

A
  1. Spermatogenesis dependent on pituitary LH + FSH (LH acts largely via testosterone production in the Leydig cells of the testis
  2. FSH + testosterone control Sertoli cells –> involved in synthesis + transport of sperm
  3. Testosterone + other steroids inhibit LH release
  4. It takes 70 days for sperm to develop fully
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19
Q

How is sperm production detected?

A

Semen Analysis

If normal result- virtually excludes male cause for infertility

If abnormal- do again in 12 weeks

If persistently abnormal- examination + investigations follow

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20
Q

What are the common causes of abnormal/absent sperm release

A
  1. Idiopathic oligospermia/ asthenozoospermia (common)
  2. Drug exposure (alcohol, smoking, drugs, exposure to industrial chemicals)
  3. Varicocoele
  4. Genetic abnormalities
  5. Anti-sperm antibodies
  6. Other (infections, mumps orchitis, testicular abnormalities, obstruction to delivery etc.)
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21
Q

How is male factor investigated and treated?

A

Semen analysis (if abnormal then repeat and examine scrotum and optimise lifestyle factors).

If oligospermic: intrauterine insemination

If moderate to severe oligospermia: IVF +/- ICSI

If azoospermic: examine for presence of vas deferens (CF). Check karyotype, CF, hormone profile. Surgical sperm retrieval then IVF + ICSI or donor insemination

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22
Q

Briefly describe the physiology of fertilisation:

A
  1. At ovulation, the fallopian tubes move so that fimbrial end collects the oocyte from ovary.
  2. Peristaltic contractions and cilia in the tube help sweep the oocyte toward the sperm (blockage or ciliary damage will prevent this).
  3. At ejaculation, millions of sperm enter vagina. The cervical mucus helps them get through the cervix.
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23
Q

What causes failure to fertilise?

A
  1. Tubal Damage (infection (PID), endometriosis, previous surgery/sterilisation)
  2. Cervical Problems (antibody production, infection, cone biopsy)
  3. Sexual Problems (impotence etc.)
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24
Q

How is tubal damage detected?

A
  1. Laparoscopy + Dye Test (with hysteroscopy done first)

2. Hystersalpingogram (HSG)- preferred as less invasive + safer

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25
Q

What are the different types of assisted conception?

A
  1. Intrauterine Insemination

2. IVF (potentially also involves ICSI, oocyte donation, preimplantation genetic diagnosis, and surrogacy)

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26
Q

What are the 3 complications of assisted conception?

A
  1. Superovulation
  2. Difficult egg collection
  3. Pregnancy complications (chromosome/gene abnormalities)
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27
Q

What is the pathology./aetiology of PCOS?

A

PCO is genetic

Peripheral insulin resistance –> raised fasting insulin (made worse by obesity)

Increased LH secretion

Increased androgen production –> hirsutism/acne

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28
Q

Define vaginal prolapse:

A

Descent of the uterus and/or vaginal walls beyond normal anatomical confines

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29
Q

What are the different types of vaginal prolapse?

A
  1. Urethrocoele: prolapse of lower anterior vaginal wall (urethra only)
  2. Cystocoele: prolapse of the upper anterior vaginal wall (bladder only)
  3. Cystourethrocoele: both bladder + uterus
  4. Apical Prolapse: prolapse of the uterus, cervix, upper vagina (vaginal vault prolapse after hysterectomy)
  5. Enterocoele: prolapse of upper posterior vaginal wall (pouch of Douglas)
  6. Rectocoele: prolapse of the lower posterior vaginal wall
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30
Q

Give 5 causes of uterovaginal prolapse:

A
  1. Vaginal delivery + pregnancy
  2. Congenital factors (Ehler-Danlos syndrome)
  3. Menopause
  4. Chronic disposing factors
  5. Iatrogenic factors
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31
Q

What are the symptoms of prolapse?

A

Often asymptomatic

General Symptoms: dragging sensation, vaginal lump

Cystourethrocoele: urinary frequency, incontinence

Rectocoele: occasional difficulty in defecating.

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32
Q

How is uterovaginal prolapse prevented?

A
  1. Pelvic floor exercises

2. Improved management of labour (avoid excessively long second stage).

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33
Q

How is uterovaginal prolapse treated?

A
  1. General: lose weight, treat chest problems for cough (stop smoking etc.)
  2. Pessaries (medical): ring or shelf. Change 6-9 monthly
  3. Surgery
    Hysteropexy/ vaginal hysterectomy for uterine prolapse.
    Anterior repair for cystocoele, posterior repair for rectocoele
    Sacrospinous fixation or sacrocolpopexy for vault prolapse
    Consider surgery for stress incontinence
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34
Q

What is the function of the cervix?

A
  1. Connects the uterus + vagina: allowing sperm in and menstrual flow out
  2. In pregnancy it holds the foetus in the uterus and then dilates in labour to allow delivery
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35
Q

How does the histology of the cervix leave it prone to neoplastic change?

A
  1. The squamocolumnar junction is where the columnar epithelium meets the squamous epithelium in the cervix.
  2. During puberty + pregnancy eversion of the cervix occurs. The lower pH of the vagina causes the exposed columnar epithelium to undergo metaplasia to squamous epithelium (the transformation zone)
  3. Cells undergoing metaplasia are vulnerable to agents that induce neoplastic change (HPV), this is where cervical cancer commonly originates.
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36
Q

List some benign conditions of the cervix:

A
  1. Cervical ectropion
  2. Acute cervicitis
  3. Chronic cervicitis
  4. Cervical polyps
  5. Nabothian follicles
  6. Congenital malformations
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37
Q

What is CIN and how is it graded?

A

CIN: presence of atypical cells within the squamous epithelium

CIN I (mild): atypical cells in the lower 1/3 of epithelium

CIN II (moderate): atypical cells in the lower 2/3 of epithelium

CIN III (severe): atypical cells occupy the full thickness of epithelium (malignancy happens if these abnormal cells invade the BM)

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38
Q

What causes CIN/cervical cancer?

A
  1. HPV (types 16, 18, 31, 33)
  2. Oral contraceptive usage
  3. Smoking
  4. Immunocompromise (HIV, long term steroid use)
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39
Q

How often should cervical smears done?

A

25-49: every 3 years

50-64: every 5 years

65: only if not been screened since 50 or had recent abnormal result

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40
Q

How are different smear results managed further?

A
  1. Normal result: repeat every 3/5 years as normal
  2. Borderline/mild dyskaryosis: if HPV negative- back to routine recall
  3. Moderate dyskaryosis: colposcopy
  4. Severe dyskaryosis: urgent colposcopy
  5. CGIN: colposcopy- if abnormality not found then hysteroscopy
41
Q

How is CIN treated?

A

If CIN I: observe

If CIN II/III: Large loop excision of transformation zone (LLETZ)

42
Q

Epidemiology of cervical cancer:

A
  1. Can occur at any age after first intercourse, but peaks during 30s + 80s
  2. Majority of cases occur in women aged 25-49
43
Q

What is the main cell type involved in cervical cancer?

A
  1. Squamous cell carcinoma (90%)

other 10% is adenocarcinoma originating from the columnar epithelium

44
Q

What are the symptoms of cervical cancer?

A
  1. PCB, offensive vaginal discharge, IMB/PMB.

2. Later symptoms (uraemia, haematuria, rectal bleeding, pain)

45
Q

What is seen on examination of cervical cancer?

A

Often normal in early disease

An ulcer then mass may be visible or palpable on the cervix

46
Q

How is cervical cancer investigated?

A
  1. Biopsy confirms diagnosis

2. Vaginal + rectal examination, cystoscopy, MRI to stage disease

47
Q

How is cervical cancer treated?

A
  1. Microinvasive disease: treated with cone biopsy/simple hysterectomy
  2. Other stage 1 and 2a: surgery + chemo-radiotherapy if lymph node involvement
  3. Stage 2b+ (or positive lymph nodes): treated with radiotherapy + chemotherapy
  4. Recurrent tumours: chemo-radiotherapy if not used before, pelvic exenteration if it has.
48
Q

Define puberty:

A

The onset of sexual maturity, marked by the development of secondary sexual characteristics.

49
Q

What are the secondary sexual characteristics and at what age do they begin?

A
  1. Thelarche (development of breasts): 9-11 years
  2. Adrenarche (pubic hair growth): 11-12 years
  3. Menarche (menstruation): 13 years (final stage)
50
Q

Describe the Menstruation phase of the menstrual cycle:

A

Days 1-4

Start of the menstrual cycle –> the endometrium is shed as its hormonal support is withdrawn.

Myometrial contraction also occurs (can be painful)

51
Q

Describe the Proliferative phase of the menstrual cycle:

A

Days 5-13

  1. GnRH pulses from hypothalamus –> LH + FSH release –> follicular growth –> follicles produce oestradiol + inhibin –> suppresses FSH secretion –> one follicle + oocyte matures
  2. Oestradiol levels rise + reach maximum –> positive feedback on hypothalamus + pituitary –> LH levels rise sharply –> ovulation follows 36 hours later
  3. Oestradiol causes endometrium to reform + proliferate (it thickens as the stromal cells proliferate + the glands elongate)
52
Q

Describe the Luteal/Secretory phase of the menstrual cycle

A

Days 14-28

  1. The follicle from which the egg was released becomes the corpus luteum (still produces oestradiol, but relatively more progesterone) –> progesterone levels peak around a week later (day 21) –> induces secretory changes in the endometrium (stromal cells enlarge, the glands swell, and the blood supple increases)
  2. Towards the end of the luteal phase, the corpus luteum starts to fail if the egg is not fertilised –> progesterone + oestrogen levels fall –> hormonal support withdrawn –> endometrium breaks down, menstruation follows, and the cycle restarts
53
Q

Define menorrhagia:

A

Excessive bleeding in an otherwise normal menstrual cycle (subjective) that interferes with the woman’s physical, emotional, social, and material quality of life, which can occur alone or in combination with other symptoms.

54
Q

What are the causes of menorrhagia?

A
  1. Majority have no histological abnormality
  2. Uterine fibroids (30%)
  3. Uterine Polyps (10%)
  4. Chronic pelvic infection
  5. Ovarian tumours,
  6. Endometrial carcinoma, cervical carcinoma,
  7. Adenomyosis
  8. Rarer causes (thyroid disease, haemostatic disorders, anticoagulant therapy)
55
Q

How is menorrhagia investigated?

A
  1. Check haemoglobin (assess blood loss- FBC)
  2. Exclude systemic causes: (check thyroid function + coagulation if history suggests problem)
  3. Exclude local organic causes: transvaginal USS of pelvis (assess endometrial thickness, excludes fibroid/mass, detects large polyps)
  4. Endometrial biopsy (at hysteroscopy/with pipelle): if endometrial thickness >10mm or polyp suspected, or if the woman is over 40 and with recent onset menorrhagia, has IMB, or has not responded to treatment.
  5. Hysteroscopy: allows inspection of uterine cavity, and therefore detects polyps + submucous fibroids that could be resected
56
Q

How is menorrhagia managed?

A

(remember it depends on if woman wishes to conceive + must exclude systemic pathology first)

Medically:
1st line- IUS
2nd line- antifibrinolytics (transexamic acid), NSAIDs (mefanamic acid), COCP
3rd line- progestogens, GnRH analogues

Surgically:
Hysteroscopic techniques
Radical (myomectomy, hysterectomy, uterine artery embolisation)

57
Q

What is the epidemiology of irregular menstruation + IMB?

A
  1. May coexist with HMB

2. More common at extremes of reproductive age

58
Q

What are the causes of irregular menstruation + IMB?

A
  1. Anovulatory cycles (early + late reproductive years)
  2. Fibroids, uterine/cervical polyps, adenomyosis, ovarian cysts, chronic pelvic infection
  3. Ovarian/cervical/endometrial (particularly endometrial)
59
Q

How is irregular menstruation + IMB investigated?

A

Same as for menorrhagia + cervical smear

60
Q

How is irregular menstruation + IMB managed?

A
  1. Treat systemic disease

Medical:
To reduce volume: IUS, COCP, transexamic acid, mefanamic acid, COCP
To regulate timing: IUS, COCP, cyclical/continuous progestogens

Surgical:
Hysteroscopic surgery; resection or ablation; hysterectomy occasionally; myomectomy/embolisation if fibroids

61
Q

Define amenorrhoea (primary/secondary) + oligomenorrhoea:

A

Absence of menstruation

Primary amenorrhoea: menstruation has not started by the age of 16

Secondary amenorrhoea: when previously normal menstruation ceases for 6 months or more

Oligomenorrhoea: menstruation occurs every 35 days to 6 months

62
Q

What are the causes of amenorrhoea/oligomenorrhoea?

A
  1. Physiological amenorrhoea (pregnancy, menopause, lactation, constitutional delay)
  2. Hypothalamus (hypothalamic hypogonadism)
  3. Pituitary (hyperprolactinaemia)
  4. Adrenal or thyroid gland (hypothyroidism, hyperthyroidism, congenital adrenal hyperplasia)
  5. Ovary (PCOS, Turner’s syndrome)
  6. Outflow tract problems
63
Q

What are the causes of postcoital bleeding?

A
  1. Cervical ectropion
  2. Benign polyps
  3. Invasive cervical cancer
64
Q

How is postcoital bleeding managed?

A

Inspect cervix + take smear

If polyp evident- avulse and send for histology

If smear normal- ectropion can be frozen with cryotherapy

If normal abnormal- colposcopy to exclude malignancy

65
Q

What are the causes of dysmenorrhoea?

A

Primary dysmenorrhoea: no organic cause- usually coincides with start of menstruation + is common

Secondary dysmenorrhoea: fibroids, adenomyosis, endometriosis, PID, ovarian tumours

66
Q

Define fibroids:

A

Benign tumours of the myometrium

67
Q

What is the epidemiology of fibroids?

A
  1. Occur in 25% of women
  2. Most common near menopause, in Afro-Caribbean women, and with a FH
  3. Less common in parous women, and those who have taken COCP or injectable progestogens
68
Q

What is the cause of fibroids?

A

Oestrogen + progesterone dependent

Monoclonal origin

Fibroids regress after menopause due to reduced circulating oestrogen

69
Q

What are the clinical features of fibroids?

A
  1. 50% asymptomatic
  2. Menstrual problems (menorrhagia, IMB)
  3. Dysmenorrhoea (rarely cause pain unless torsion etc.)
  4. Other (frequency, urinary retention, hydronephrosis, subfertility)
  5. On examination (solid mass palpable, multiple small fibroids cause irregular ‘knobbly’ enlargement)
70
Q

How are fibroids investigated?

A
  1. FBC (haemoglobin)
  2. Hysteroscopy/ hysterosalpingogram
  3. Transvaginal USS
  4. MRI/laparoscopy if diagnosis unsure
71
Q

What are the complications of fibroids?

A
  1. Torsion of pedunculated fibroid
  2. Degeneration (red or hyaline)
  3. Sarcomatous change
  4. Complicates pregnancy
72
Q

How are fibroids managed?

A
  1. Observation (if asymptomatic/small/slow-growing)
  2. Medical Treatment-
    Transexamic acid/NSAIDs/progestogens
    GnRH agonists
3. Surgical Treatment-
Hysteroscopic surgery (intrauterine)
Myomectomy (preserves fertility)
Radical hysterectomy
Embolisation/ablation
73
Q

Define adenomyosis:

A

Presence of endometrium and its underlying stroma within the myometrium

74
Q

What is the epidemiology of adenomyosis?

A
  1. Most common around 40
  2. Associated with endometriosis + fibroids
  3. Symptoms stop after menopause
75
Q

What is the pathology of adenomyosis?

A

Endometrium grows into the myometrium to form adenomyosis

76
Q

What are the clinical features of adenomyosis:

A
  1. Symptoms may be absent
  2. Painful, regular, heavy menstruation
  3. Examination- uterus mildly enlarged + tender
77
Q

How is adenomyosis investigated?

A

Transvaginal USS or MRI

78
Q

How is adenomyosis managed?

A

Medical:

  1. IUS / COCP +/- NSAIDs
  2. GnRH analogues

Surgical:
1. Hysterectomy often required

79
Q

Briefly summarise endometritis:

A

Inflammation of endometrium

Causes: secondary to STIs; complication of surgery; foreign tissue and retained products of conception

Management: antibiotics + ERPC

80
Q

Define intrauterine polyps:

A

Small benign tumours that grow into uterine cavity

81
Q

What is the epidemiology of intrauterine polyps?

A
  1. Common in ages 40-50 + when oestrogen levels are high

2. In postmenopausal women- found in patients on tamoxifen for breast cancer

82
Q

What are the symptoms are intrauterine polyps?

A
  1. Sometimes asymptomatic
  2. Menorrhagia + IMB
  3. Occasionally prolapse through cervix
83
Q

How are intrauterine polyps investigated?

A

Normally diagnosed at USS or when hysteroscopy is done for abnormal bleeding

84
Q

How are intrauterine polyps managed?

A

Resection of polyp with cutting diathermy or avulsion

85
Q

What is the epidemiology of endometrial cancer?

A
  1. Most common genital tract cancer

2. Prevalence highest at 60 years (only 15% premenopausal)

86
Q

What is the pathology of endometrial cancer?

A
  1. Adenocarcinoma of columnar endometrial gland cells (>90%)

2. Of the rest, most common is adenosquamous carcinoma (poorer prognosis)

87
Q

What causes endometrial cancer?

A
  1. High ratio of oestrogen to progestogen

Risk Factors:

  1. Exogenous oestrogen without progestogen
  2. Obesity
  3. PCOS
  4. Nulliparity
  5. Late menopause
  6. Tamoxifen

COCP is protective

88
Q

What are the clinical features of endometrial cancer?

A

Postmenopausal: PMB (most common presentation)

Premenopausal: irregular or intermenstrual bleeding, or occasionally recent-onset menorrhagia

89
Q

How is endometrial cancer investigated?

A
  1. USS and/or endometrial biopsy with a pipelle or hysteroscopy
  2. Staging possible following hysterectomy
  3. MRI/CXR to assess spread
  4. Assess patient’s fitness for surgery (FBC, renal function, glucose, ECG)
90
Q

How is endometrial cancer managed?

A

Hysterectomy + bilateral salpingo-oophorectomy (unless disseminated disease/unfit)

Radiotherapy: patients with high risk of lymph node involvement

Chemotherapy possibly

91
Q

What 3 ‘ovarian cyst accidents’ can occur?

A
  1. RUPTURE of the contents of an ovarian cyst into the peritoneal cavity
  2. HAEMORRHAGE into a cyst or the peritoneum
  3. TORSION of the pedicle (causes infarction of the ovary +/- tube and severe pain)
92
Q

What are the three main groups of ovarian tumours?

A
  1. Epithelial tumours
  2. Germ cell tumours
  3. Sex cord tumours

(also thecomas + fibromas)

93
Q

What is the prognosis of ovarian cancer?

A

Poor due to silent nature- 5 year survival is below 35%

94
Q

What is the pathology of ovarian cancer?

A

90% are epithelial carcinomas

In women under 30, it is most likely to be a germ cell tumour

95
Q

What are the causes of ovarian cancer?

A

The risk factors relate to number of ovulations

Increases Risk: early menarche, late menopause, nulliparity

Decreases Risk: pregnancy, lactation, use of the pill

5% of cases are familial

96
Q

What are the clinical features of ovarian cancer?

history + examination

A

(70% of patients present with stage 3-4)

  1. Persistent abdominal bloating, feeling full and/or loss of appetite
  2. Pelvic/abdominal pain
  3. Increased urinary urgency/frequency
  4. Symptoms similar to IBS
  5. Examination: cachexia; abdominal/pelvic mass; ascites
97
Q

How is ovarian cancer investigated?

A
  1. CA125 (in women over 50 with abdominal symptoms). USS if it is raised
  2. alpha-fetoprotein + hCG: to identify non-epithelial ovarian cancer
  3. Risk of malignancy index (RMI): calculated using USS score, menopausal status, and serum CA125 level
  4. CT of pelvis + abdomen: establish extent of disease
98
Q

How is ovarian cancer managed?

A

Surgery: total abdominal hysterectomy, bilateral salpingo-oohorectomy, omentectomy, at staging laparotomy. Lymph node biopsy/ removal.

Possible laparoscopy + oophorectomy alone for women wanting fertility (w/ very close monitoring

Then chemo unless borderline or low risk stage 1a/1b

Phase 3a (7 decks)

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