Download Gynaecology Oncology

Obstetrics
Pre-term labour (Linul)
Overview
 delivery < 36 weeks gestation
 most common cause of neonatal mortality in developed world
 5-10% of all births (unimproved over past 30 years)
Risk factors
 preceded by spontaneous ROM in 1/3rd of cases
 therapeutically induced in 1/3rd of cases
 unknown cause in 1/3rd of cases
 large uterus – multiple gestation or polyhydramnios
 pelvic infection and bacterial vaginosis
 cigarette smoking
 drug abuse, teenage pregnancy, underweight mothers
Foetal consequences
 neonatal death due to severe immaturity
 respiratory distress syndrome – underdeveloped lungs and deficient surfactant
 brain and bowel mucosa susceptible to hypoxia
 hypothermia – low body fat, reduced insulation
 hypoglycaemia – immature liver with low glycogen stores
 hyperbilirubinaemia
 kernicterus
 The preterm infant may require:
o ventilation, exogenous surfactant, intravenous glucose, parenteral feeding,
incubation and ultraviolet irradiation
Diagnosis
 medical history
o regular uterine contractions every 10 minutes ± spontaneous ROM
o progressive cervical dilatation
o painless midtrimester foetal loss suggests cervical incompetence
 avoid digital examination
 high vaginal swab to exclude infection
 fibronectin
o <40% positive predictive value for delivery within 14 days
o ≈97% negative predictive value for delivery within 14 days
Management
 aim to prolong pregnancy or administration of corticosteroids
o promotes foetal lung maturation and surfactant production
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o
o
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single course (two betamethasone injections 24 hours apart)
side effects
 foetal growth restriction
 impaired myelination
 insulin resistance
 hyperglycaemia in diabetic mothers
tocolytic agents suppress labour
o indicated for threatened delivery < 32 weeks gestation
o nifedipine drug of choice
Antepartum haemorrhage (Suren)
Def: vaginal bleeding after 20 weeks of gestation and before delivery of the baby.
Causes @ DDx
1) Placenta Previa
a. Def: implantation of the placenta in the lower segment of the uterus.
b. Incidence: 1/200
c. RFx:
i. PHx of CS (risk varies from 1-4% on subsequent pregnancy, risk is > 10%
if more than 4 pregnancies)
ii. IVF
iii. multiparity
iv. age > 35
v. smoking
vi. drugs
d. Types:
i. Type I (marginal)
1. Encroaches on lower segment but doesn’t reach the internal os
(2.5cm from the os).
ii. Type II (minor)
1. Reaches the internal os but doesn’t cover it.
iii. Type III (major)
1. Partially covers the internal os.
iv. Type IV (major)
1. Completely covers the internal os.
e. Clinical presentation:
i. Painless vaginal bleeding that stops spontaneously but may recur.
ii. Associated with uterine contraction or irritability.
f. Pathophys
i. Thinning of the lower part of the uterus
ii. Disrupt placental attachment
g. Ix:
i. U/S – if unstable use transabdominal, if stable can use transabdominal ,
transvaginal or transperineal.
ii. FBE, coags, cross-match 6 units of blood.
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iii. MUST NOT PERFORMED VE UNTIL PP HAS BEEN EXCLUDED BY U/S
h. Mx:
i. Depend on the severity:
1. If M & F unstable
a. Emergency resuscitation and CS
2. M stable, < 37 weeks
a. Conservative medicine, blood transfusion
3. If premature delivery required (< 34 weeks)
a. Corticosteroid (?)
4. If bleeding stops
a. Observation In hospital at least 48 hrs (60% chance to
recur)
2) Placental Abruption
a. Def: uterine bleeding following premature separation of the placenta from the
uterus, total or partial.
b. Incidence: 0.5 – 2.0%, 20% perinatal mortality
c. RFx:
i. Advanced maternal age
ii. Multiparity
iii. Multipregnancy
iv. Smoking
v. Drugs (anti coags)
vi. Maternal HT
vii. PPROM
viii. Chorioamnionitis
ix. Abdominal trauma
x. Maternal thrombophilia
xi. PHx of PA
xii. IUGR, polyhydramnios
xiii. Low SES
d. Clinical presentation
i. Sx:
1. Abdominal pain (tender tense uterus)
2. Vaginal bleeding (dark, non-clotting)
3. Uterine contraction
4. Usually close to term
5. Nausea, faintness and restlessness
Minor
Major
Mild VB
Sever VB
With or w/o contraction
Bleeding from venupuncture sites
normal Fetal HR
Bruising (DIC)
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ii. Sg:
1. Tachycardia, hypotension, signs of peripheral vasoconstriction
2. ‘woody hard’ uterus on palpation, maybe larger than gestation
suggests
3. Difficult to palpate fetus
iii. Types:
1. Revealed haemorrhage
a. VB, pain not significant
2. Concealed haemorrhage
a. Slight bleeding, tense uterus, ?pain (due to
retroplacental clot)
3. Mixed haemorrhage
a. Some VB, some passage of clots, build up of clots behind
placenta
4. Large haemorrhage
a. Bruised uterus (blood forced into muscle layers)
b. IUF demise
iv. Dx:
1. Exam placenta after delivery (?send to laboratory for biopsy)
2. U/S – if negative, it doesn’t exclude PA.
v. Mx:
Minor
Major
Emergency CS (stop DIC)
Conservative or CS
Investigate coags on M (APTT, PT, fibrinogen,
D-Dimer) but if results are abnormal consult
with haematologist for transfusion
Baby is monitored in NICU
3) Vasa Previa
a. Def: umbilical vessels run in the membrane close to the internal os instead of
the placenta
b. Clinical presentataion:
i. Small VB at the time of rupture
c. Mx:
i. CS (because it can cause fetal blood loss)
4) Bleeding from LGT
a. Cuases:
i. Post coital
ii. Cervical condition (ectropion and polyps, carcinoma)
iii. Infection (candida, trichomonas)
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Gynaecology
Menopause (PQ)
Definitions:
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Menopause: cessation of menstruation due to the demise of ovarian function, which
usually occurs between the ages of 45-57 years (average 51).
Premature menopause: menopause occurring under the age of 40 years (2% of
women).
Climacteric: consists of o Perimenopause: menstrual irregularity and fluctuating menopausal
symptoms, for up to 4 years before and 1 year after final period.
o Postmenopause: all symptoms and sequelae of ovarian senescence (may be
life-long).
Symptoms – experienced by up to 80% of women; most commonly experienced around late
perimenopause and early postmenopause.
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Vasomotor: hot flushes, night sweats and palpitations.
Psychological: depression, anxiety, unloved feelings, irritability, mood changes, less
sexual feelings, sleeplessness, and unusual tiredness.
Locomotor: muscle/joint pain and backache.
Urogenital: dry vagina, uncomfortable intercourse, and urinary frequency and
urgency.
Others: light-headed feelings, headaches, new facial hair, dry skin and crawling
feelings, and crawling feelings under the skin.
Work up:
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History: medical, drug, menstrual, family, sexual, psychosocial issues, attitudes to
menopause and possible therapies, and misconceptions.
Examination: breast, pelvic examination including Pap smear.
Investigations (when indicated): FBE, serum lipids, triglyceride levels, TFTs, BSLs,
bone density scan, and thrombophilia screen.
Management:

Nonhormonal therapies:
o Lifestyle advice: weight control through diet and exercise (30 minutes weightbearing exercise per day), avoid excessive caffeine and alcohol, and stop
smoking.
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o Vasomotor symptoms: venlafaxine, gabapentin, clonidine.
o Psychological symptoms: antidepressants, anxiolytics or NSAIDs.
o Vaginal symptoms: lubricants.
o Urinary symptoms: antispasmodic agents
Hormonal therapies:
o Regimens:
 Perimenopausal: continuous oestrogen + cyclical progestogen.
 Postmenopausal: continuous oestrogen + continuous progestogen.
 After hysterectomy: continuous oestrogen.
 Testosterone therapy: lack of evidence, may improve libido and
energy levels.
 Tibolone: stimulates oestrogen, progestogen and testosterone
receptors – ‘all-in-one’ postmenopausal therapy.
o Routes of administration:
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o
o
o
Oral.
Transdermal.
Gel.
Intranasal spray.
Pessaries or creams (vaginal symptoms).
Indications:
 Relief of menopausal symptoms.
 Prevention and treatment of osteoporosis.
 ? Primary cardioprotective role.
 ? Neuroprotective role (e.g. dementia, depression).
Risks:
 VTEs.
 ? Cardiovascular disease.
 ? Breast cancer.
 Increased gallbladder disease.
 Early adverse effects: breast tenderness, uterine bleeding, bloating,
premenstrual-like symptoms.
Length of therapy: as long as women perceive an improved quality of life from
the alleviation of menopausal symptoms. Yearly review is appropriate.
Osteoporosis:
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Loss of bone density occurs rapidly initially (15% loss in first 5 years), then continues at a
slower rate
Diagnosis: bone densitometry at sites such as hip, spine, and wrist. Osteoporosis is
defined as bone densities more than 2.5 standard deviation units below young normal
mean.
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Treatment is recommended for young postmenopausal women with scores of 1.5-2.5,
older women with scores >2.5 or who have had an osteoporotic fracture.
o Bisphosphonate, e.g. alendronate, risedronate: used in women with CV risk
factors, recent low-trauma fracture but few menopausal symptoms.
o Selective oestrogen receptor modulator, e.g. raloxifene: used in women with an
osteoporotic fracture, breast cacner concerns or fear of uterine bleeding.
o HT: in younger women.
o Others: PTH, strontium ranaleate, calcium, vitamin D, hip protectors and weight
bearing exercise.
Abnormal bleeding
Hx
 Age of menarche?
 Typical bleeding pattern of teenage
years
 Typical bleeding pattern on combined
OCP
 Commencement of abnormalities
 Progression
 Relation to body weight
Ex
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Clots, flooding, tampons, towels
Menstrual calendar
Fatigue/dyspnoea from anaemia
Irregular, intermenstrual or post coital
bleeding
 Dysparaeunia, pelvic pain, or
premenstrual pain
 Abnormal bleeding at other sites
 Pallor
 Pelvi-abdo mass (fibroids)
 Vulval, vaginal, cervical lesion
Menorrhagia
 Abnormally heavy menstrual bleeding (HMB)
 >80ml per period
 Increases with increasing age
 Commonest cause of iron deficiency anaemia
Classified into idiopathic (DUB, where no anatomical causes can be found) or secondary to
an organic cause.
Organic causes:
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Fibroids
Endometrial or endocervical polyps
Endometrial hyperplasia
Adenomyosis
Hypothyroidism
Coagulopathy
Presence of IUD
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 Endometrial or endocervical carcinoma
 Bleeding in pregnancy
Dysfunctional Uterine Bleeding
 Idiopathic menorrhagia, implies a subtle hormone dysfunction
 Ovulatory DUB presenting as regular HMB
o Disordered prostaglandin production
o Abnormalities of endometrial vascular development
 Anovulatory DUB presenting as irregular vaginal bleeding
o In adolescents soon after menarche due to low oestrogen concentrations
o In PCOS due to unopposed oestrogen stimulation – women tend to have
infrequent periods then long periods with heavy bleeding and develop Swiss
cheese endometrium – cystic hyperplasia
o In the first few years before menopause due to a sharp raise and fall of
oestrogen concentrations
Intermenstrual bleeding : endometrial pathology
 Called breakthrough bleeding if woman on combined OCP
Post-coital bleeding: cervical carcinoma or be due to cervical ectopy
Investigations
Exclude pregnancy!
Irregular bleeding: Hysteroscopy and endometrial biopsy
 FBE
 Coagulopathy, TFT if indicated
If women fail to respond to treatment after 3/12
 Trans-vaginal pelvic U/S for women at high risk of endometrial pathology: >45yo, wt
>90kg, nulliparous, Hx of infertility, F.H. of endometrial or colon Ca
 Trans-vaginal sonohysterogram distinguishes endometrial polyps from submucous fibroids
 Endometrial Bx if endometrial thickness is 12mm or greater, or Pipelle sapling
+/- Hysteroscopy (gold standard for endometrial pathology) if TVUS is abnormal.
Treatment for menorrhagia
Medical
 Iron replacement for anaemia
 Antifibrinolytic - Tranexamic acid 1 g QID
Mean reduction in blood loss (MBL) 50ml, theoretical increased risk of VTE
 NSAID – Mefenamic acid 500mg TDS
MBL 35ml
 Cyclical oral progestogens e.g. Medroxyprogesterone acetate or norethisterone
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 Long course oral progestogen treatment (3 out of 4 weeks) but has high incidence of side
effects
 COCP
Mean reduction in MBL of 50%
 Synthetic androgen - Danazol
MBL 100ml. Many androgenic side effects, incompatible with conception but not licensed
as a contraceptive
 Levo-norgestrel intrauterine system (LNG-IUS) releases progestogen locally.
Mean reduction in MBL of 95%. Needs to be replaced every 5 years. 30% women become
amenorrhoeic
If the woman wants
Contraception? – COCP or LNG-IUS
To conceive? – Tranexamic acid or NSAID
Treat dysmenorrhoea? LNG-IUS or NSAID
Surgical
Ablation
This includes methods under hysteroscopic guidance: Transcervical resection of the
endometrium (TCRE), Roller Ablation, Endometrial Laser Ablation (ELA), diathermy and
methods without hysteroscopic guidance: Thermal balloon ablation, Microwave endometrial
ablation (MEA), Heated saline
Ablations successful in 4 out of 5 women, 1 of whom will become amenorrhoeic.
Hysterectomy
For fibroids, a myomectomy can be done if fertility is to be preserved
GnRH analogs can shrink fibroids before hysterectomy, allowing a vaginal rather than abd
hysterectomy
Post-menopausal bleeding (Lin)
Definition
 Any per vaginal bleeding that occurs in a woman > 12 months after last period
**In post-menopausal women not on HRT, any bleeding is abnormal.
** Women on combined HRT may have bleeds in progesterone free period (Bleeds
abnormal if they occur at an unscheduled timing or are abnormal in amount)
Causes
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Endometrial carcinoma (TPO. 10% of patients)
Atrophic vaginitis (most common) and atrophy of endometrium
Cancer of cervix or vulva
Endometrial or cervical polyps
Endometrial hyperplasia
o Can be simple (non-malignant) or atypical hyperplasia (40% progress to
adenocarcinoma. Responsive to P therapy or hysterectomy)
Submucosal fibroids
Oestrogen withdrawal (HRT or ovarian tumour)
Foreign bodies e.g. pessaries
Disease in adjacent organs
Hx taking – Full Hx
More specific questions to ask:
 When did the bleeding start?
 Were there precipitating factors, such as trauma?
 What is the nature of the bleeding (temporal pattern, duration, postcoital, quantity)?
 Are there any associated symptoms such as pain, fever, or changes in bladder or bowel
function?
 What is the medical history and are any medications being taken (eg, hormones,
anticoagulants)?
 Ask risk factors of gynaecological cancer e.g. past or current use of unopposed E,
tamoxifen therapy for breast cancer treatment or prevention, PCOS, syndrome X,
nulliparity, abnormal pap smear, previous gynae malignancy, FHx of cancer
Ex
 Thorough examination of external and internal genital tract.
 Determine any bleeding site, note suspicious lesions, lacerations or foreign bodies.
 Full pelvic and bimanual examination
 General Ex to look for signs of systemic illness e.g. hepatitis, renal disease, splenomegaly
Ix
 Cervical smear
 Transvaginal ultrasound
 Endometrial biopsy +/- hysteroscopy
o Required if:
 Endometrial lining is thicker than 4mm (if on HRT, >5mm)
 Endometrium shows diffuse or focal  echogenicity (heterogeneity)
 Endometrium is not adequately visualised
 Woman has persistent bleeding (can be a sign of endometrial Ca even when
endometrial thickness is <4-5mm since a thin or indistinct endometrial stripe
does not reliably exclude type 2 endometrial cancer)
Mx
 In postmenopausal women, uterine bleeding is usually light and self-limited.
 If atrophic vaginitis – may be treated with topical oestrogen
 Exclusion of cancer is the main objective; therefore, treatment is usually unnecessary once
cancer (or premalignant histology) has been excluded.
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Pre-menstrual syndrome
Definition & Incidence
 PMS is characterized by the presence of both physical and behavioral symptoms that
occur repetitively in the second half of the menstrual cycle & are relieved immediately
when menstrual flow begins. The sx’s must be severe enough to impact on lifestyle,
relationships or work, and not part of another psychiatric disorder.
 Affects up to 95% percent of women of reproductive age. 5% of women are severely
incapacitated by these symptoms.
 Typical age of presentation is 30-40 years
Pathophysiology:
 Hormonal theory:
o Rapidly declining levels of progesterone late in the luteal phase (day 26-27)
 Other contributing factors
o Increased renin-angiotensin-aldosterone activity
o Changing prostaglandin levels
o Vitamin deficiency
o Excess prolactin secretion
o Endogenous endorphin depletion
 Psychosocial factors:
o Negative anticipation of menstruation
o Underlying predisposing personality
o Stereotypic expectation of PMS
o General stress
Sx
 More than 150 symptoms have been ascribed to PMS
 Most common physical manifestations of PMS are
o Breast tenderness
o Fluid retention and weight gain
o Headaches
o Aching joints
 Most common psychological symptom of PMS is
o Affective labile mood – tearfulness, irritability, anger (occurring in >80%)
o Anxiety or tension
o Depression
o Loss of interest, difficulty concentrating, loss of energy, sleep disturbance, appetite
disturbance
 Other common Sx: acne, oversensitivity to environmental stimuli, anger, easy crying, and
gastrointestinal upset. Hot flashes, heart palpitations, and dizziness occur in 15 to 20
percent of patients
Dx
 Specific symptoms should be characteristic of PMS
 The timing with this these symptoms occur.i.e. Should occur in the luteal phase
 The severity of the symptoms i.e. should impair some facet of the woman’s life
 Absence of hormone or drug ingestion and the exclusion of other diagnoses
o Physical Ex to exclude gynaecological, endocrine or other systemic disease; breast Ex,
vaginal Ex & pap smear
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o
Ix: TFT, U&E, serum P and oestradiol in mid-luteal phase, PRL (if galactorrhoea or
oligomenorrhoea present)
DDx
Menopause syndrome, Mastalgia, other causes of fluid retention (renal or adrenal, hyper or
hypo thyroid), PCOS (PMS may be a feature of E excess), Psychiatric disorders (depression,
mania)
Rx
 Mild to moderate Sx
o Pyridoxine (Vitamin B6) 100 mg daily; if ineffective after 3 cycles, try
o Evening primrose oil capsules (gamma lineoleic acid) 1000 mg bd with food (day 12
to first day of next cycle)
o A progestogen may be tried after or with evening primrose oil 4 e.g. Dydrogesterone
5 mg bd days 12-25; after 2 months increase to 10 mg bd
 Severe Sx
o SSRI: Fluoxetine 20 mg daily for 10-14 days before menstruation, or 10-20 mg daily
continuously 11 OR
o Non-SSRI: Clomipramine 25 mg (o) nocte for 2 cycles, increasing if necessary
 Specific treatments
o Spironolactone for fluid retention
o Bromocriptine or evening primrose oil for breast tenderness
o Mefanamic acid for dysmenorrhoea
EBM (ie. RCT evidence)
 SSRI’s (PMS)
 Spironolactone (fluid
retention)
 Bromocriptine OR
 Evening primrose oil
○
○
○
○
Mixed evidence
COCP & POP
Pyridoxine (Vit B6)
NSAIDs
Ca2+ or Mg2+
Worth Trying
 Exercise
 Homeopathy & herbal
remedies
 Relaxation therapy eg.
massage
(breast tenderness)
Prolapse (Kat)
Definition

Utero-vaginal prolapse – abnormal descent of the uterus and/or vagina
o First degree – cervix stays in vagina
o Second degree – protrudes from introitus (especially when stand or strain)
o Third degree (procidentia) – uterus protrudes beyond introitus
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Cystocoele – prolapse of the anterior vaginal wall
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Urethrocoele – prolapse of lower anterior wall
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Rectocoele – prolapse of the posterior vaginal wall
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Enterocele – prolapse of the vaginal vault
Epidemiology
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Common condition which increases in prevalence with age
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Risk Factors / Causes
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Parity
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Increased birth weight
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Age
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Post-menopause
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Increased abdominal pressure
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Inherited connective tissue disorders
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Pelvic surgery
History
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Vaginal
o Dragging or bearing down sensation in vagina
o Appearance of lump or bulge at vaginal entrance
o Difficulty inserting tampons
o Ulceration of prolapsed epithelium may  discharge, bleeding
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Bowel/Bladder
o Difficulties with bladder or bowel emptying or urinary or faecal incontinence
o Hydronephrosis (ureteric kinking) – severe cases
o Urinary retention – descent of bladder base below urethra
o Rectal prolapse and haemorrhoids sometimes associated
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Other
o Low back pain (often reported – may or may not be related)
o Decreased libido
Examination
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Abdominal exam
o Exclude organomegaly or mass (causing raised pressure)
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Pelvic exam
o Look for prolapse, ulceration, atrophy
o Assess anterior and posterior vaginal walls and cervical descent with patient
straining using Sims’ speculum in L lateral position
o Combined VE and PR exam can help differentiate enterocele from rectocele
Investigations
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Prolapse is essentially diagnosed on history/examination
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May wish to investigate urinary or bowel symptoms further
Management
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Options are tailored to the individual
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Multi-disciplinary team often required if complex
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Reassure patient that the condition is not life threatening or particularly dangerous
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Type
Options
General
measures
Address reversible
risk factors
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Manage obesity, constipation, chronic cough (smoking, asthma, CF),
oestrogen deficiency
Pelvic floor exercises
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Shown to improve Sxs of prolapse and incontinence
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Unlikely to reduce prolapse that has extended beyond introitus
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Poor long term compliance
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Consider physiotherapy or nurse adviser
Intra-vaginal
oestrogen
supplementation
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May enhance effect of pelvic floor exercises if post-menopausal
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With ↑ use of oestrogen consider DVT prophylaxis if other risk factors
e.g. immobility
Vaginal packing
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To manage chafing/ulceration of externalised epithelium – should
respond in 2-3wks (can then undertake definitive Rx)
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Pack cotton gauze smeared with oestrogen cream into vagina to reduce
prolapse (replace daily)
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Rubber rings that are fitted into vagina to reduce prolapse
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Lower part sits in posterior fornix, upper part near symphysis
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Also come as ‘shelf’ pessaries (rarely used unless rings not retained)
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Remove, wash and re-insert regularly (every 3-6 months)
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May increase physiological discharge and rates of anaerobic infection
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Should not affect enjoyment of intercourse
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Aim to correct anatomical defect, maintain sexual function and treat
associated urinary or bowel dysfunction
Medical
Vaginal pessaries
Surgical
Corrective surgery
(see below)
Details
Prolapse Surgery
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Traditionally involves vaginal hysterectomy, midline suturing of vaginal fascia and
excision of redundant vaginal epithelium with
o Newer operations exist but are not well evaluated
o Synthetic mesh or slings sometimes used if woman’s own tissue is
inadequate
o Non-absorbable synthetic materials are potentially more durable but ↑risk
of chronic infection or rejection
o Some procedures to obliterate vaginal cavity (e.g. Le Fort) can be performed
relatively quickly under LA in selected cases
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Re-operation common (up to 30%)
o Decreasing time intervals between each successive repair
o Multiple surgeries associated with progressive scarring, loss of vaginal
length and calibre and deterioration in sexual, bladder and bowel function
o Surgery may exacerbate pelvic neuropathy by direct trauma to nerves
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Surgical repair will not necessarily improve sexual enjoyment
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o
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Also consider low libido, relationship problems, inflammatory conditions of
vaginal or vulva, psychological influences
Pelvic floor surgery may be adversely affected by subsequent pregnancy
Prolapse
Surgery
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Anterior colporrhaphy most commonly performed
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Vaginal wall incision made and defect allowing herniation closed
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Redundant vaginal epithelium excised and incision closed
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Avoid anterior repair if concurrent stress incontinence
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Posterior colporrhaphy (as for anterior, but on opposite side)
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Surgery on posterior vaginal wall may cause dyspareunia
Enterocele
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Similar to ant/post repair, but peritoneal sac containing small bowel
should be excised and pouch of Douglas closed
Uterovaginal
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Vaginal hysterectomy with adequate support of vault to utero-sacral
ligaments
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If uterine conservation required can do Manchester operation or
sacrohysteropexy (abdominal approach)
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Sacrocolpoplexy – vault attached to sacrum using mesh, POD closed
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Sacrospinous ligament fixation – vaginal procedure where vault
sutured to ligament(s)
Cystocoele
Rectocoele
Vault
Gynaecology Oncology
Case 05- Ovarian oncology and cysts (Alan)
Physiological cysts
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Follicular cyst
o Most common benign ovarian tumour
o Diameter up to 10cm, smaller cysts do not need intervention
o Can be caused by ovulation induction and gestational trophoblastic disease
due to gonadotropin overstimulation
o Pelvic ultrasound should be repeated in 4-6 weeks time
o If symptomatic or not resolved in 8-16 weeks, treat with
 wait until half way through pregnancy before removing the cyst
laparoscopically (lower chance of miscarriage)
 Symptoms are menstrual disturbances, endometrial hyperplasia
Luteal cyst
o More common on the right side, <3cm = corpora lutea
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o
o
o
o
Can rupture causing intraperitoneal bleeding on days 20-26 of menstrual
cycle
Sometimes, it fills with fluid or blood, creating a cyst that can grow to 6cm
across.
can rupture causing hemoperitoneum, hypotension, and peritonitis
 haemorrhagic corpus luteal cysts are usually seen in the first
trimester, with most resolving by 12 weeks' gestation
Treatment is laparoscopy if ruptured or torsion
Germ cell tumours
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Happens more commonly in <30 years old
All three germ layers are present
Benign
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Dermoid cyst (25% of all ovarian tumours)
o Bilateral in 11%, 60% are asymptomatic
 3.5-10% can have torsion
 1-4% can rupture, risk is higher in
pregnancy and labour
o Unilocular cyst <15 cm in diameter, has predominantly ectodermal
structures
 Skin, teeth, hair, nervous tissue, thyroid, bronchus, intestine
 Mesodermal structures can be present too: bone, cartilage, muscle
Mature solid teratoma
o Rare, less cystic than dermoid cyst
Malignant
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Dysgerminoma (2-5% of ovarian malignancy)
o <30 yo, 10% bilateral
o Mean diameter 15cm, spread via lymphatics
o Can coexist with choriocarcinoma, endodermal tumour or teratoma (10%)
 Do beta hCG
o Pure dysgerminoma is mostly Stage 1=good prognosis
Choriocarcinoma
o Secretes beta hCG, usually diagnosis is done when haematological spread
has occurred
Yolk sac (endodermal)
o Usually in <40 yo
o Can rupture causing pain, aggressive and fast growing
 Diagnosed late, with extensive metastases
o Areas of necrosis, haemorrhage
o Often makes AFP, can be measured to monitor treatment
Teratoma
o about 20% of all malignant tumors, mainly in <20 yo
16
o
gliomatosis peritonei, caused by rupture. Seeding of neural tissue in the
peritoneum
 if the metastases are immature, it indicates a poorer prognosis
Epithelial tumours (60 to 80% of ovarian tumors)

Most ovarian neoplasia are of this category, they are mesothelial in nature
Benign (more in <40 yo)





Serous cystadenoma
o Bilateral in 10%, inner surface is cuboidal or columnar and maybe ciliated
o Usually smaller than mucinous cystadenoma
o Sometimes psamoma bodies (round collections of calcium) are present
Mucinous cystadenoma (10-15% of all ovarian tumours)
o Large unilateral, multilocular cysts
 Has columnar mucin secreting cells, produces thick glutinous
o pseudomyxoma peritonei is a rare complication, this follows preoperative
rupture and spreading of tumour cells
 mucin in the peritoneum can cause bowel obstruction
 50% 5 year survival, 18% 10 year survival
 Treatment is surgically debulking the metastases and abdominal
chemotherapy
Endometrioid cystadenoma (5%)
o Most are malignant, edges are badly defined
o Looks like and can co-exist with endometriosis
Brenner tumours
o Wolffian metaplasia, usually benign and <2cm in diameter
o between 2 to 3 cm, solid, well circumscribed and may be calcified
o 75% occur in >40 yo
Clear cell (mesonephroid tumour)
o Rarely benign, almost all are malignant
Malignant



Serous carcinoma
o Commonest malignant ovarian tumor (33% of ovarian tumours)
o Presents with ascites due to metastases
o Often bilateral
o Psamoma bodies often are seen
Mucinous carcinoma
o Multilocular, large like its benign counterpart but contains solid areas
 25cm cyst is not uncommon
o Pseudomyxoma peritonei
Endometrioid carcinoma
o Most are malignant, edges are badly defined
17
o
o


Looks like and can co-exist with endometriosis
15% can have endometrial carcinoma, where both are separate primary
tumours (not metastasis)
Clear cell carcinoma
o Cannot be distinguished from the other surface epithelial tumors by their
gross appearances. They are partially cystic but may be entirely solid.
Necrosis and haemorrhage may be seen in the solid areas.
o May be a variant of endometrioid tumour, as they frequently co-exist
o Strong association with endometriosis
Borderline epithelial tumour
o Most are confined in the ovary, usually serous or mucinuous
o Good prognosis even if metastases are found, they often regress when
primary lesion is removed
Sex cord stromal tumours (3% of all ovarian tumor)
Benign



Theca cell tumour
o Almost all are benign, incidence is high in 60yo
 5-10 cm
o Has systemic effects
 Precocious puberty, postmenopausal bleed, endometrial
hyperplasia and cancer
Fibroma
o ~50yo
o commonest ovarian stromal tumor
o Meig’s syndrome is rare (1%): ascites and pleural effusion
 40% of fibroma> 6cm
Sertoli-leydig cell tumour
o ~30yo
o Rare, <0.2% of all ovarian tumours
o 75% make androgen, many non-functional, some make oestrogen
Malignant




Granulosa cell tumour
o Usually solid, but can develop cysts
o 75% of pure granulosa cell tumors are functional and makes estrogen
Fibrosarcoma
o Very rare
Sertoli-leydig cell tumour (rare)
o 50% makes male hormones
Gynandroblastoma
o producing both ovarian (granulosa and/or theca) and testicular (Sertoli
and/or Leydig) cells or tissue
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Natural history of Ovarian Cancers







2/3 present with cancer spread beyond the pelvis because of insidious and nonspecific symptoms or fast growing tumour
Metastases commonly happen via
o Direct (peritoneum, omentum, peritoneal surface of bowels)
o Lymphatic (pelvic and para-aortic nodes)
o Haematological (brain, lungs)
Risk factors
o Nulligravida
o Obesity (>30 BMI)
o Tubal ligation (protective)
o Clomiphene citrate for infertility treatment
o HRT
o Family history (BRCA 1 and 2)
o History of breast cancer
HOPC
o Abdominal pain or discomfort
o Abdominal distension or lump (77%)
o Bowel changes (70%), urinary frequency (34%), weight loss, menstrual
changes
Examination findings
o Pelvic mass +/- enlarged lymph nodes (groin, neck)
o Hormonal changes
Investigations
o FBE, EUC
o ultrasound pelvis + CA 125 can combine to give an estimate on the risk of
malignancy
o definitive diagnosis is made using laparotomy
Treatment
o Laparotomy with vertical incision
 Objective is to remove all macroscopically visible neoplastic tissues
 Usually involves total hysterectomy, bilateral salpingooophorectomy and infracolic omentectomy if the cancer has
spread extensively
 If the tumour is unilateral and low stage (no spread):
unilateral salpingo-oophrectomy will suffice
 Do sampling of peritoneal fluids or saline washing
o Interval bulking
 For unresectable disease, it is possible to laparotomy after an initial
chemotherapy. Chemotherapy is then resumed as soon as possible
after surgery
o Any ovarian cancers with Stage >1c should have adjuvant therapy
 Chemotherapy
 5-6 cycles at 3-4 weekly intervals
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


Platinum based chemo drugs are best
o Caboplatin, paclitaxel (Taxol, usually in combination
with carboplatin as first line regime and is not
platinum based)
Radiotherapy
 Experimental, not usually used in practice
 occasionally used for women with ovarian cancer, especially
if it is confined to the pelvic cavity
Prognosis
o
The 5-year survival rates are as follows: Stage I - 73%, Stage II - 45%, Stage III
- 21%, Stage IV - Less than 5%
Characteristics
Benign
Germ cell tumours


<30 years old
2-3% malignant, but 33%
for <20 yo


Dermoid cyst
Mature teratoma
Epithelial tumours

Most ovarian cancers are in
this category





Serous cystadenoma
Mucinous cystadenoma
Endometrioid cystadenoma
Brenner tumours
Clear cell
Sex cord stromal tumours

Most common ones are
granulosa and theca
tumours, produces steroid
hormones (usually
oestrogen)
In general, have better
prognosis compared to
other ovarian tumours




Granulosa cell tumour
Theca cell tumour
Fibroma
Sertoli-leydig cell tumour

Malignant














Dysgerminoma
Choriocarcinoma
Yolk sac (endodermal)
Teratoma
Serous carcinoma
Mucinous carcinoma
Endometrioid carcinoma
Clear cell carcinoma
Borderline epithelial
tumour
Granulosa cell tumour
Theca cell tumour
Fibrosarcoma
Sertoli-leydig cell tumour
Gynandroblastoma
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References
http://atlasgeneticsoncology.org/Tumors/OvarSexCordStromID5223.html
http://www.babycenter.com.au/pregnancy/complications/ovariancystexpert/
http://www.med-ed.virginia.edu/courses/path/gyn/ovary3.cfm#germ
http://www.cancer.org/cancer/ovariancancer/detailedguide/ovarian-cancer-risk-factors
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ENDOMETRIAL CANCER (Dan)
EPIDEMIOLOGY
 Most common gynaecological malignancy in Australia (1400 new cases and >250
deaths each year)
 1 in 80 lifetime risk of an Australian woman developing endometrial cancer
 Median age of diagnosis is 60-65 years; 10-20% of cases are found in premenopausal
women; rare below the age of 40
 Risk factors: age, anovulation, obesity, hypertension, diabetes and insulin resistance,
past or family history of endometrial, breast (especially if treated with tamoxifen) or
ovarian cancer, HNPCC syndrome, and inappropriate endogenous or exogenous
oestrogen unopposed by progestogens (e.g. PCOS, anovulation, oestrogen-only HRT)
 Protective factors: oral contraceptive pill, parity, combined oestrogen/progestogen HRT
Hx:
 Abnormal vaginal bleeding – postmenopausal bleeding, menorrhagia or intermenstrual
loss
 Endometrial cancer cells incidentally found on cervical (Pap) smear
 Incidental finding on ultrasound examination (abnormally thick endometrium >4mm in
postmenopausal woman)
Ix:
 All women >40yrs and all women with risk factors who have abnormal vaginal
bleeding must have endometrial cancer excluded as the cause of bleeding
 Gold standard: Hysteroscopically directed curettage → histology
o Alternative: Pipelle endometrial sampling
 Staging: surgical + CXR (disseminated disease)
STAGING
Stage Extent of cancer
I
Confined to the uterine body
A. No myometrial invasion
B. Invasion of <50% myometrium
C. Invasion of >50% myometrium
II
Extending to cervix
A. No cervical stromal invasion
B. Cervical stromal invasion
III
Outside the uterus
A. Extension through uterine serosa or positive peritoneal cytology
B. Involvement of adnexal structures
C. Involvement of pelvic or para-aortic lymph glands
IV
At distant site
A. Invasion of bladder or bowel mucosa
B. Distant metastases or involvement of inguinal nodes
Rx:
SURGICAL
 Total hysterectomy and bilateral salpingo-oophorectomy (radical hysterectomy) ±
pelvic/para-aortic lymphadenectomy
 Adjuvant radiotherapy: for disease that has spread beyond the uterus
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MEDICAL
 High-dose progestogen therapy: produces a clinical response in 30% of women, few
side effects
 Chemotherapy: for symptomatic disseminated or recurrent disease
o Most effective agents: carboplatin, Taxol, Adriamycin
PROGNOSIS
 80% of women with endometrial cancer present with localised disease
o 5-year survival in women with localised disease >90%
 Prognosis is poorer in the presence of metastatic nodal disease
Cervical Cancer



Second most common cancer in women worldwide (most in developing countries)
Aus: 6.9 per 100 000.
Two main types:
o Squamous cell carcinoma – usually preceded by a pre-malignant phase of about
10y. Screening has reduced incidence, more for SCC than Adenocarcinoma.
o Adenocarcinoma (~15%) – less known about these lesions.
Presentation
 Abnormal vaginal bleeding – usually post-coital, may be irregular
or postmenopausal.
 More advanced disease – discharge, weight-loss, mets
Patho-physiology


Main Risk Factors
 HPV (types 16, 18, -in 70%
case)
 Smoking (doubles risk)
 Immune suppression
 Multiple sexual partners
 Early age of coitarche
 Multiparity
Normal metaplasia in the transformation zone disrupted –
dysplasia - HPV implicated (but not sufficient)
Dysplasitic epithelium:
o Lack normal maturation – nuclei larger, variable in shape and size, more actively
dividing
o CIN1 – affects deepest third CIN2 – affects deepest 2/3rd CIN3 – full thickness
o Bethesda system: Low grade (CIN1) vs High grade (CIN2, CIN3)
Studies have indicated that at the ages of
greatest sexual activity, the prevalence of HPV
can be as high as 40% in the female population
(6). Around 90% of these infections will
spontaneously resolve (6) and many women may
not even know that they were infected.
It is in the smaller subgroup of women who have
the persistent infection that there is a chance
that Cervical Intraepithelial Neoplasia (CIN)-also
known as ‘lesions’-will develop.
In the clinical setting, LSIL is followed up quite
conservatively as it may disappear in time.
Spontaneous regression from it has been
23
reported to be around 50% (3), to as high as 70 – 90% (8). LSIL, however, can convert to
HSIL, which poses the greater risk of leading to invasive carcinoma, and is sometimes known
as the ‘precursor to cervical cancer’. It should be understood that dysplasia does not always
begin as LSIL and progress to HSIL and that HPV infection, in some cases, can directly result
in HSIL
Screening – Pap Smear
Recommended Australian Cervical Screening
 Start at age 18-20 or 1-2 years after first intercourse
 Repeat every 2 years until 70 if had two normal smears in past 5 years
Sensitivity 66% (hence may get false negative – regular smears important)
Specificity 92%
Results of Pap Smear – 10% of smears abnormal – vast majority will not have cancer
Negative smear
Repeat in 2 years
LSIL
Repeat in 6 months, if abnormality persists, refer for colposcopy
HSIL
Refer for colposcopy
Inconclusive for HSIL
Has some features of high grade epithelial abnormality
Unsatisfactory
Repeat 6-12 weeks later (don’t take in the presence of
blood/infection)
Colposcopy
 Allows visual examination of the cervix to check for CIN
 Inspect – apply Lugol’s iodine – low and high grade lesions will show glycogen depletion
 Paint with dilute acetic acid – abnormal cells turn white (have high density of optically
dense chromatin)
 Green filter – used to visualize neovascularisation – shows up as thin lines or tiny red
spots
 Biopsies can then be taken.
Management of CIN –
Surgical: Remove abnormal tissue by destroying or cutting out tissue
Radiotherapy: Used more for later stages
Excisional: large loop excisin, cold knife, etc.
Large-loop excision of transformation zone –
 Most popular, area of suspected CIN of depth 10mm removed
 Cheap, quick, easy to perform and gives tissue for examination.
 Cx: haemorrhage, 1% incidence of cervical stenosis, and cervical incompetence
Ablative: laser ablation, cryotherapy, cold coagulatin
Prognosis
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