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Gynaecology Flashcards

1
Q

Average blood loss in a menstrual cycle

A

37-43ml

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2
Q

Normal menstrual cycle

A

Days 1-4: menses

Days 5-13:

  • Follicular phase ovarian cycle: follicles develop, one follicle becomes dominant
  • Proliferative phase uterine cycle: endometrial proliferation

Day 14: ovulation

Days 15-28:

  • Luteal phase ovarian cycle: formation of corpus luteum
  • Secretory phase uterine cycle: endometrial changes to secretory lining under the influence of progesterone
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3
Q

Hormones involved in the menstrual cycle and at which points

A

Days 5-13: rise in FSH -> development of follicles -> secretion of oestrogen

Day 14: when there is sufficient oestrogen, this causes a surge of LH to be released -> ovulation

Days 15-28: progesterone secreted by corpus luteum. if fertilisation does not occur then the corpus luteum will degenerate and progesterone levels fall. Oestrogen levels rise during this period.

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4
Q

Differential diagnoses for IMB and PCB

A

Cervical bleeding: ectropion, polyps, malignancy, cervicitis

Intra-uterine: polyps, submucous fibroids, endometrial hyperplasia, endometrial malignancy, endometriosis

Hormonal: breakthrough bleeding

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5
Q

Investigations for PCB and IMB

A 
High vaginal swab and endocervical swabs (STIs)
Cervical smear (CIN, cancer)
Pelvic USS (polyps, fibroids)
Hysteroscopy and endometrial biopsy
Laparoscopy
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6
Q

How much blood defines menorrhagia?

Signs/symptoms

Causes of menorrhagia

A

> 80ml/cycle
60-70% get anaemia
May have menstrual pain, lethargy, breathlessness, affects QoL

Causes:

  • Systemic: thyroid disease, clotting disorders
  • Iatrogenic: IUD, IUS, POP, implant, depo, anticoag
  • Local pathology: dysfunctional uterine bleeding, fibroids, endometrial polyps, endometrial carcinoma, endometriosis, PID
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7
Q

Dysfunctional uterine bleeding

  • what is it
  • diagnosis
  • management
A

Most common cause of menorrhagia
Diagnosis of exclusion
Managed with OCPs or prostaglandin inhibitors (mefenamic acid)

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8
Q

Investigations for menorrhagia

A

Subjective assessment/ pictorial blood loss chart to assess degree of menorrhagia

  • Blood tests: FBC, TFT, clotting studies
  • Pelvic USS
  • Endometrial biopsy
  • Cervical smears
  • Diagnostic hysteroscopy
  • Diagnostic laparaoscopy
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9
Q

Management of menorrhagia

A

Correct iron deficiency anaemia
Treat systemic disease or focal pathology

First line if needing contraception: mirena IUS
Second line: COCP
Third line: long acting progesterone (eg. depo, implant)

First line if not needing contraception: tranexamic acid (or mefenamic acid, esp if dysmenorrhoea)

Surgical management:

  • Hysteroscopy
  • Open myomectomy
  • Endometrial ablation
  • Hysterectomy
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10
Q

Tranexamic acid

  • MoA
  • Risk
  • At which part of the menstrual cycle are these taken?
A

Antifibrinolytic. Prevents activation of plasminogen into plasmin -> reduces excessive fibrinolysis

Risk of thrombosis

Start taking at the beginning of menses for 4 days

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11
Q

Mefenamic acid

  • MoA
  • At which part of the menstrual cycle are these taken?
A

NSAID.
Prostaglandin inhibitor.
Inhibits COX enzymes -> prevents conversion of arachidonic acid into prostaglandins (prostaglandins are vasodilators and they inhibit platelet aggregation)

Taken during menses

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12
Q

Presentation of endometriosis

A

Growth of ectopic endometrial tissue outside of the uterine cavity
Chronic pelvic pain
Dysmenorrhoea (often starts before menses)
Deep dyspareunia
Subfertility
Urinary symptoms
Dyschezia (painful bowel movements)

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13
Q

Differential diagnoses for endometriosis

A 
PID
Pelvic pain syndrome
Submucous fibroids
Ovarian accident
Adhesions
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14
Q

Examination, investigations and management for endometriosis

A

Examination:
Retroverted fixed uterus, tender vaginal fornices, uterine tenderness

Ix:

  • Pelvic USS first as less invasive
  • Diagnostic laparoscopy is gold standard (active endometriosis shows powder-burn spots and chocolate cysts)

Mx:

  • First line analgesia: paracetamol and/or NSAIDs (mefenamic acid, naproxen, ibuprofen)
  • COCP helps symptoms by stopping period
  • POP, depot, implant, IUS

Secondary care:

  • GnRH analogues can induce pseudo-menopause
  • Surgical: laparoscopic diathermy, laser ablation, excision of deposits, total abdominal hysterectomy with bilateral salpingo-oophorectomy
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15
Q

Uterine fibroids presentation

A 
Asymptomatic
Menorrhagia (due to increased surface area of endometrium, and production of prostaglandins)
Abdominopelvic mass
Abdominopelvic pain
Subfertility
Urinary frequency, urgency, nocturia
Rectal pressure and abdo bloating
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16
Q

Risk factors for uterine fibroids

Protective factors

A

African-caribbean
Later reproductive years
Nulligravidity
Obesity

Protective factors: smoking, COCP, full term pregnancy, post-menopause

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17
Q

Investigations for uterine fibroids

A

Bimanual examination: fibroids are often palpated, the uterus may feel enlarged firm and irregular

Bloods: FBC, U+E, clotting screen

Pelvic USS is diagnostic to visualise the fibroids

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18
Q

Management of uterine fibroids

A

Leave alone unless symptomatic, rapidly enlarging or concerned about subfertility

Medical:
Fibroids <3cm: IUS, tranexamic acid, mefenamic acid, COCP

Secondary care:

  • GnRH analogues (zoladex) used as surgery adjuncts to reduce fibroid size by reducing oestrogen
  • Mifepristone (antiprogesterone) shrinks fibroids over a 6m period

Surgery:

  • Myomectomy (hysteroscopic approach for submucosal or pedunculated fibroids, abdominal approach for intramural or subserosal fibroids)
  • Uterine artery embolisation (stops blood flow to fibroids)
  • Myolysis (diathermy, laser ablation, high intensity focused US)
  • Hysterectomy
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19
Q

Primary vs secondary amenorrhoea

A

Primary: failure to commence menses (absence of menarche)

  • 16+ in presence of secondary sexual characteristics
  • 14+ in absence of secondary sexual characteristics

Secondary: cessation of periods for more than 6 months after menarche

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20
Q

Causes of amenorrhoea

  • hypothalamic
  • pituitary
  • ovarian
  • adrenal glands
  • genital tract
A

Hypothalamic causes (reduced GnRH):

  • eating disorders, exercise
  • severe chronic conditions (thyroid, sarcoid, psychiatric)
  • Kallmann syndrome (x-linked recessive characterised by failure of migration of GnRH cells)

Pituitary causes:

  • Prolactinoma (prolactin suppresses GnRH)
  • Acromegaly/ cushings syndrome
  • Sheehan’s syndrome (post-partum pituitary necrosis secondary to massive obstetric haemorrhage)
  • Radiation or autoimmune disease destroying pituitary gland
  • Post-contraception amenorrhoea

Ovarian causes:

  • PCOS
  • Turners (45XO)
  • Premature ovarian failure

Adrenal gland causes:
-Late onset/mild congenital adrenal hyperplasia

Genital tract causes:

  • Ashermann’s syndrome
  • Imperforate hymen or transverse vaginal septum
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21
Q

Androgen insensitivity syndrome

  • what is it
  • features
  • diagnosis
  • management
A

X-linked recessive
End-organ resistance to testosterone causing genotypically male children (46XY) with female phenotype

Features:

  • primary amenorrhoea
  • undescended testes causing groin swellings
  • breast development may occur as a result of conversion of tesosterone to oestradiol

Diagnosis:
Buccal smear or chromosomal analysis to reveal 46XY genotype

Management:
Counselling (raise child as female)
Bilateral orchidectomy
Oestrogen therapy

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22
Q

Causes of oligomenorrhoea

A 
PCOS
Contraception/hormonal treatment
Perimenopause
Thyroid disease
DM
Eating disorders
Excessive exercise
Medications (eg. antipsychotics)
Antiepileptics
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23
Q

Investigations for oligomenorrhoea and amenorrhoea

A
  • Pregnancy test
  • Gonadotrophins (LH and FSH) - reduced levels indicate hypothalamic cause, and increased levels indicate ovarian cause
  • Prolactin
  • Androgen levels (raised in PCOS)
  • Oestradiol (converted from testosterone)
  • Thyroid function tests
  • 17 hydroxyprogesterone (CAH)
  • Karyotype
  • Pelvic USS
  • Progesterone challenge test to elicit a withdrawal bleed
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24
Q

PCOS presentation and differentials

A

Presentation:
Subfertility /infertility
Oligo-/Amenorrhoea
Hirsutism and acne (due to hyperandrogenism)
Obesity
Acanthosis nigricans due to insulin resistance

Differentials:
Hypothyroidism
Cushings syndrome
Hyperprolactinaemia
Congenital adrenal hyperplasia
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25
Q

PCOS investigations and management

A

Ix:

  • Bloods: FSH, LH, prolactin, TSH, testosterone
  • Pelvic USS (multiple cysts on ovaries)

Raised LH/FSH ratio
Raised free androgen index (ratio of testosterone/sex-hormone binding globulin)
Prolactin normal or raised

Management if normal weight and desiring fertility:

  1. Clomifene (+/- metformin, +/- dexamethasone)
  2. Gonadotrophins

Management if overweight and desiring fertility:
1. Weight loss +/- metformin

Management if not desiring fertility:
1. COCP +/- metformin
2. Anti-androgen (spironolactone, finasteride)
Weight loss

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26
Q

Premature overian failure

  • what is it
  • causes
  • symptoms
A

Onset of menopause and increased gonadotrophins before the age of 40

Causes: idiopathic, chemo, autoimmune, radiation

Symptoms: perimenopause symptoms, infertility, secondary amenorrhoea, raised FSH and LH

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27
Q

Diagnosis of menopause

A

> 45 with symptoms = clinical diagnosis
40-45 = FSH and LH blood tests, or clinical diagnosis
<40 = FSH and LH tests

Menopause = no period + FSH levels >40 on at least 2 occasions (4-6wks apart)

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28
Q

Symptoms of perimenopause

A

Change in period cycle length, dysfunctional uterine bleeding

Hot flushes, night sweats

Vaginal dryness, atrophy, urinary frequency

Anxiety, depression, short-term memory impairment

Osteoporosis, increased risk of IHD

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29
Q

Combined HRT

  • Who to give it to
  • Who to give cyclical combined HRT to
  • Risks
A

Give combined HRT to women with a uterus (=oestrogen + progesterone)

Give cyclical combined HRT to perimenopausal women who have menopausal symptoms

Risks:
VTE (risk if given orally)
IHD (no risk if started <60y)
Breast cancer (risk reduces when stopped)
Ovarian cancer
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30
Q

Unopposed oestrogen HRT

  • who to give it to
  • risks
A

Give to women with no uterus
If given to women with a uterus it could cause endometrial proliferation and cancer (they need combined which includes progesterone to prevent overproliferation and cancer)

Risks:
VTE (risk if given orally)
Stroke (if oral)
Endometrial cancer (if they have a uterus)
Ovarian cancer
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31
Q

Contraindications to HRT

Benefits of HRT

A

CI: current/past breast cancer, oestrogen-sensitive cancer, undiagnosed vaginal bleeding, untreated endometrial hyperplasia

Benefits: prevents osteoporosis, reduces urinary symptoms, reduces risk of UTIs, most effective treatment for menopause

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32
Q

Non-hormonal management of menopause

A

Lifestyle (exercise, good sleep hygiene, weight loss, stress reduction, relaxation)

Vasomotor symptoms: fluoxetine, citalopram, venlafaxine

Vaginal dryness: lubricants

Psychological: self-help groups, CBT, antidepressants

Urogenital symptoms: vaginal oestrogen for atrophic vaginitis, lubricants, moisturisers

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33
Q

Causes of post-menopausal bleeding

  • ovary
  • uterus
  • cervix
  • vagina
  • urethra
  • vulva
A

Ovary: ovarian carcinoma, oestrogen-secreting tumour

Uterine body: submucous fibroid, atrophic changes, polyp, hyperplasia

Cervix: atrophy, squamous cell carcinoma, adenocarcinoma

Vagina: atrophy

Urethra; Urethral caruncle, haematuria

Vulva: vulvitis, dystrophies, malignancy

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34
Q

Investigations for PMB

A 
Pelvic USS (endometrial thickness should be <5mm)
Hysteroscopy
Endometrial biopsy
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35
Q

Atrophic vaginitis features and management

A

Post-menopausal
Vaginal dryness, dyspareunia, occasional spotting
O/E: vagina is pale and dry

Mx: vaginal lubricants and moisturisers, or topical oestrogen cream

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36
Q

Risk factors for urinary incontinence

A 
Advancing age
Previous pregnancy and child birth
High BMI
Hysterectomy/ previous pelvic surgery
Family history
Smoking -> chronic cough -> worsens incontinence
Neurological history
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37
Q

Different types of pelvic organ prolapses

A

Cystocele= bladder bulges into the anterior vaginal wall

Rectocele= rectum bulges into the posterior vaginal wall

Uterine prolapse- uterus hangs down into vagina, and may protrude outside of the body if severe

Enterocele= pouch of douglas bulges into posterior vaginal wall

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38
Q

Risk factor for prolapse

A 
Increasing age
Multiparity
Obesity
Spina bifida
Constipation
Persistent chronic cough
Prolonged heavy lifting
Hysterectomy/ pelvic surgery
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39
Q

Management of prolapse

A

Conservative: weight loss, pelvic floor exercises, stop smoking, avoid constipation, avoid heavy lifting, avoid high-impact exercise

Vaginal oestrogen

Pessary: more beneficial for anterior and uterine prolapse

Surgery:

  • Pelvic floor repair
  • Sacrocolpopexy or supraspinous fixation
  • Vaginal hysterectomy
  • Colpocleisis (close the vagina)
40
Q

Causes of chronic pelvic pain

A

Adenomyosis, endometriosis, adhesions (gynae operations, PID, appendicitis), gynae malignancy, GI pathology (diverticulosis, IBD)

41
Q

Causes of acute pelvic pain

A 
Ectopic pregnancy
Miscarriage
Ovarian torsion
PID
Ovarian cysts
UTI
Appendicitis
42
Q

Presentation and investigations for ovarian cysts

A

Presentation: asymptomatic, or chronic pain, acute pain, PV bleed, bloating, change in bowel habit, change in urinary frequency, weight loss, IBS

Ix: transvaginal pelvic USS

43
Q

Non-neoplastic ovarian cysts

A

Functional:

  • Follicular cysts: most common, <3cm. Developing follicle.
  • Corpus luteal cysts: <5mm. Luteal phase.

Pathological:

  • Endometrioma (chocolate cyst)
  • Polycystic ovaries (ring of pearls on US)
  • Theca lutein cyst (raised hCG, eg. molar pregnancy)
44
Q

Benign neoplastic cysts

A

Epithelial tumours:

  • Serous cystadenoma: most common. 30% bilateral
  • Mucinous cystadenoma: unilateral
  • Brenner tumour: unilateral. grey/yellow

Benign germ cell tumours:
-Dermoid cyst: hair, skin, teeth, bone

Sex cord stromal tumours:
-Fibroma: most common

45
Q

Management of ovarian cysts

A

Premenopause:

  • Measure LDH, AFP, hCG
  • Simple cyst <5cm -> rescan in 8-12wks. If persistent -> monitor with USS and CA-125 3-6monthly
  • If >5cm -> laparoscopic cystectomy or oophorectomy

Postmenopause:

  • Low malignant risk: monitor with USS and CA-125 for 1 yr
  • Moderate risk: bilateral oophorectomy, if malignancy is found then stage it
  • High risk: staging and laparotomy
46
Q

Pelvic inflammatory disease risk factors and causes

A 
History of STIs
Young age of onset of first sexual activity
Unprotected sex
Multiple sexual partners
IUD
History of PID

Causes: chlamydia trachomatis (most common), Neisseria gonorrhoea, Mycoplasma genitalium, Mycoplasma hominia

47
Q

Presentation of PID

A 
Lower abdo pain
Fever
Deep dyspareunia
Dysuria and menstrual irregularities
Vaginal or cervical discharge
Cervical excitation

Chandelier sign: patient reaches out to the ceiling during vaginal examination due to pain

Perihepatitis: Fitz-Hugh-Curtis syndrome. RUQ pain, often confused with cholecystitis

48
Q

Investigations for PID

A 
Pregnancy test
High vaginal swab
Endocervical swabs
Blood tests (FBC, CRP, ESR, blood cultures)
MSU
Transvaginal USS
49
Q

Complications of PID

A

Low threshold for empirical treatment due to the risk of infertility and long-term morbidity

Complications if untreated: pelvic abscess, sepsis, infertility, ectopic, chronic pelvic pain, dyspareunia, menstrual disturbance, psychological effects

50
Q

Management of PID

A

6months contact tracing and management

Empirical IM ceftriaxone 500mg stat + oral doxycycline 100mg BD + oral metronidazole 400mg BD for 14 days

Pain relief with paracetamol and ibuprofen

Consider removing IUS or IUD

Avoid sexual intercourse until treatment is complete

51
Q

Ovarian torsion

  • risk factors
  • presentation
  • investigations
  • management
A

Risk factors: ovarian cysts, ovarian enlargement, pregnancy, fertility treatment, prior tubal ligation

Presentation: sudden onset deep seated colicky lower abdo pain, unilateral, vomiting, distress, fever
Vaginal examination may reveal adnexal tenderness

Exclude pregnancy

Investigations: pelvic USS may show free fluid, laparoscopy is diagnostic and therapeutic

Mx: pain relief, laparoscopy (untwist ovary)

52
Q

Ectopic pregnancy risk factors

A 
Damage to tubes (salpingitis, PID, previous surgery)
Previous ectopic
Endometriosis
IUD
POP
IVF
53
Q

Ectopic pregnancy presentation and differential diagnoses

A

Presentation:

  • Constant unilateral lower abdo pain (tubal spasm)
  • Vaginal bleeding
  • History of recent amenorrhoea (6-8wks)
  • Shoulder tip pain and pain on defaecation/urination if peritoneal bleeding

DDx:
Ovarian cyst, ovarian torsion, PID, appendicitis, bowel obstruction, IBS, UTI, cervical ectropion/cervicitis, miscarriage, molar pregnancy

54
Q

Examination, investigations and management of ectopic pregnancy

A

O/E: abdo tenderness, cervical excitation. Do not palpate for adnexal mass due to risk of rupture

Ix:
Pregnancy test positive
Pelvic USS is diagnostic
MRI is secondline

Repeat transvaginal scans and serial hCG levels to monitor

Management:
- Size <30mm, no pain, not ruptured, no heartbeat, bhCG <200 and reducing: monitor for 48 hours

  • Size <35mm, not ruptured, no significant pain, no heartbeat, bhCG<1500: methotrexate injection (surgery if bhCG 1500-5000)
  • Size >35mm, ruptured, severe pain, heartbeat, bhCG>1500: salpingectomy or salpingotomy
55
Q

Causes of sporadic miscarriage

A 
Foetal abnormality
Infection (ToRCH, TB, malaria, salmonella, listeria)
BV
Materan age 
Abnormal uterine cavity
Maternal illness
Interventions
56
Q

Causes of recurrent miscarriages

A 
Antiphospholipid syndrome
Endocrine (poorly controlled DM, thyroid disorders, PCOS)
Uterine abnormalities
Cervical weakness
Parental chromocomal abnormalities
Smoking
57
Q

Types of miscarriages and their presenting features

A

Threatened miscarriage: closed cervical os, painless PV bleeding <24wks gestation (typically 6-9wks), complication of pregnancy not an actual miscarriage

Missed miscarriage: closed cervical os, gestational sac contains dead foetus <20wks gestation without symptoms of expulsion, there may be light PV bleeding, usually painless, normal pregnancy symptoms may disappear

Inevitable miscarriage: open cervical os, heavy PV bleeding, clots, pain

Incomplete miscarriage: open cervical os, pain and PV bleeding, not all products of conception have been expelled

58
Q

Investigations for miscarriage

A

Serial pelvic ultrasounds
Serum b-hCG measurements

Laparoscopy if ectopic likely

59
Q

Management of miscarriage

A

Uterus usually expels the products on its own (may take weeks)

Expectant Mx: first line. Wait 7-14 days for miscarriage to complete spontaneously. Take pregnancy test at 3 weeks, return if positive.

Medical Mx: done if expectant hasnt worked or not appropriate.
Vaginal or oral misoprostol (synthetic prostglandin analogue) stimulates uterine expulsion
Take pregnancy test 3 weeks later and return if positive

Surgical Mx: done if products still remain despite medical management or if patient still has symptoms 14 days after expectant, or patient unstable.
Manual vacuum aspiration under LA, or surgical intervention under GA.
Rh-ve women need anti-D.
Syntocinon may be given to encourage uterine contraction and reduce blood loss
Send products of conception for histology.

60
Q

Investigations for recurrent miscarriages

A

Karyotype both partners and the products of conception
Pelvic USS
High vaginal swab
Antiphospholipid antibodies assay on two occasions at least 6 weeks apart

61
Q

Molar pregnancy

  • what are they
  • risk factors
  • presentation
  • Ix
  • Mx
A

Hydatidiform moles are chromosomally abnormal pregnancies that have the potential to become malignant

Risk factors: extremes of maternal age, previous gestational trophoblastic disease

Presentation: usually presents in first trimester, PV bleeding, unusually large uterus for gestational age, hyperemesis gravidarum

Ix:
Serum bhCG >100,000
USS shows snow storm appearance in uterine cavity
Histological examination of products of conception

Mx:
Dilation and evacuation

Hysterectomy if no intention on becoming pregnant again

62
Q

Adenomyosis

  • what is it
  • at risk group
  • investigations
  • management
A

Growth of endometrial tissue in the myometrium

Multiparous women towards the menopause

TVUS or MRI

Tranexamic acid or mefenamic acid
COCP, POP or IUS
GnRH analogues
Uterine artery embolisation
Hysterectomy
63
Q

Criteria for PCOS

A

Rotterdam criteria: at least 2 of the 3 for diagnosis

  1. Oligomenorrhoea/ anovulation
  2. Clinical/ biochemical hyperandrogenism
  3. Multiple cysts on USS (>= 12 follicles on 1 ovary)
64
Q

What is infertility and what is primary vs secondary infertility

A

Infertility = failure to conceive after regular unprotected sexual intercourse for at least 1 year

Primary: never been able to conceive.
Secondary: has conceived before but now unable to

65
Q

Causes of female infertility

A

Ovulatory dysfunction: chronic systemic illness, eating disorders, PCOS, hyperprolactinaemia, hypo/hyperthyroidism, cannabis, NSAIDs, congenital adrenal hyperplasia

Tubal damage: PID, previous tubal surgery, previous ectopic, endometriosis

Uterine dysfunction: fibroids, uterine septae, congenital anomaly, ashermann’s syndrome (Adhesions following curettage or TOP)

Coital dysfunction: vaginismus, dyspareunia

66
Q

Causes of male infertility

A

Semen: lack of semen, sperm that arent moving properly, abnormal sperm

Testicles: infection, testicular cancer, testicular surgery, congenital defect, undescended testes, trauma

Sterilisation
Ejaculation disorders
Hypogonadism

Drugs; Sulfasalazine, anabolic steroids, chemo, marijuana, cocaine

67
Q

Investigations for female infertility

A
  • Mid-luteal phase progesterone levels (7 days before the end of a cycle, eg. day 21 of a 28 day cycle)
  • STI screen
  • FSH and LH levels
  • TFTs
  • Prolactin levels
  • Test for tubal patency: diagnostic laparoscopy and dye, or hysterosalpingography
  • Consider: Pelvic USS, hysteroscopy, testosterone levels/ sex hormone binding globulin
68
Q

Investigations for male infertility

A 
Semen analysis
Chlamydia screen (/STI screen)
69
Q

Semen analysis (what is normal?)

  • sperm count
  • motility
  • vitality
  • morphology
  • volume
  • fructose
  • pH
A 
Sperm count (conc): >15million/ml 
Motility: 50%
Vitality (healthy living sperm): 60%
Morphology: >4% should have normal morphology
Vol: 1.5-5.0ml
Fructose: >13micromoles/sample
pH: 7.2-7.8
70
Q

Management of infertility

A

Conservative: stress management, stop smoking, aim for BMI 19-25, occupational risks, reduce alcohol consumption, medication review

Medical treatment:

  • Clomifene citrate (anti-oestrogen): raises FSH and LH levels
  • Gonadotrophins: offerend to clomifene-resistant women
  • Pulsatile GnRH and dopamine agonists can induce ovulation

Surgical treatment:

  • Tubal microsurgery
  • Surgical ablation or resection of endometriosis

Assisted conception:

  • Intrauterine insemination (sperm is placed into the utuerus during ovulation)
  • In-vitro fertilisation: fertilisation in a petri dish and then implant
  • Intracytoplasmic sperm injection: inject sperms into the egg
  • Donor insemination of sperm
  • Oocyte donation
  • Embry donation
71
Q

Side effects of clomifene citrate

A 
Multiple pregnancy
Reversible ovarian enlargement
Double vision
Headache
Hot flushes
Abnormal uterine bleeding
Breast tenderness
72
Q

Cervical screening programme

A

Offered every 3 years for women aged 25-49, and every 5 years to women aged 50-64

Women >65 only need a smear if they have recently had abnormal tests

73
Q

Cervical screening results interpretation

A

Inadequate: insufficient/ unsuitable sample. Repeat after 3 months. If 3 consecutive inadequate sample -> colposcopy within 6 weeks.

Negative (normal)

Borderline: abnormal nuclei but cant say for certain that it is dyskaryosis. Test HPV, if positive then colposcopy <6wks, if negative then return to normal screening programme

Mild dyskaryosis: usually cervical intraepithelial neoplasia grade 1 (CIN1) on biopsy. Test HPV, if positive colposcopy within 6 weeks, if negative return to normal screening programme.

Moderate dyskaryosis: CIN grade II. considered pre-cancerous with intermediate risk of developing into cancer. Colposcopy within 2 weeks.

Severe dyskaryosis: CIN grad III, high risk developing into cancer. Colposcopy within 2 weeks.

74
Q

What happens during colposcopy?

A

Examines the cervix to look for any abnormalities suggesting precancerous/cancerous changes.

If acetic acid is applied to the cervix, abnormal areas (such as CIN) tend to turn white (sometimes referred to as acetowhite).

If an iodine solution is applied, normal tissue (on the outside of the cervix) stains dark brown. Pre-cancerous abnormalities may not stain with iodine. The cells on the inner part of the cervix do not stain brown.

May take a biopsy to confirm the diagnosis.
Loop excision
Needle excision
Cone biopsy

75
Q

Risk factors for cervical cancer

A 
HPV 16 and 18
Early age of first intercourse
High number of sexual partners
Low socioeconomic group
Smoking
Partner with prostatic or penile cancer
Premenopausal age
76
Q

Presentation and types of cervical cancer

A

90% are squamous cell carcinomas and 10% are adenocarcinomas

Presentation: may be asymptomatic.
PCB, discharge, IMB, ulcer/ mass

77
Q

Investigations for cervical cancer

A

Borderline or mild dyskaryosis at smear: HPV test -> if positive then colposcopy clinic in 6 weeks, if negative then return to normal screening programme

Moderate or severe dyskaryosis: colposcopy within 2 weeks

Colposcopy investigations: staining with acetic acid or iodine, and a biopsy (loop, needle, cone biopsy)

Following diagnosis -> MRI/CT examination to check for mets and staging

Blood tests and CXR may also be done

78
Q

Management and staging of cervical cancer

A

Staging:
0 - carcinoma in situ
1 - confined to cervix
2 - beyond the cervix
3 - spread to the pelvic side wall, or affecting ureter or lower third of vagina
4 - involves rectal or bladder mucosa, or beyond true pelvis

Management:

  • If a large loop excision has been done and the lesion has been completely removed then no further Mx is necessary
  • Surgery, chemo, radiotherapy are all options depending on patient circumstances
79
Q

Endometrial cancer risk factors

Endometrial cancer protective factors

A 
Postmenopausal
Unopposed oestrogen (exogenous, obesity, PCOS, nulliparity, late menopause, tamoxifen)

Protective factors: COCP, combined HRT

80
Q

Features and presentation of endometrial cancer

A

Most are adenocarcinomas

Presentation: PMB, irregular bleeding, IMB, normal examination

81
Q

Endometrial hyperplasia

A

Premalignant condition

Simple hyperplasia and complex hyperplasia - treated with progesterone to encourage regression

Atypical hyperplasia has a high chance of developing into cancer so hysterectomy is advised

82
Q

Investigations for endometrial cancer

A

Gold standard: hysteroscopy and biopsy
Pelvic USS (measure endometrial thickness)
Endometrial sampling (pipelle biopsy)
MRI/CT for staging

Post menopausal women should have an endometrial thickness of <5mm due to their low oestrogen levels, endometrial cancer causes increased oestrogen which thickens the endometrium

83
Q

Staging and prognosis of endometrial cancer

A

Stage 1: body of the uterus (85% 5yr)
Stage 2: extends to cervix (60% 5yr)
Stage 3: adnexae, or +ve peritoneal cytology (40% 5yr)
Stage 4: involves bladder or bowel mucosa (10% 5yr)

84
Q

Management of endometrial cancer

A

Total abdominal hysterectomy and bilateral salpingo-oophorectomy = mainstay of treatment

Stage 3 requires surgical debulking before radiotherapy
Stage 4 requires a mixture of surgery, radiation and palliation

85
Q

Risk factors for ovarian cancer

Protective factors for ovarian cancer

A 
Age (60-64 peak incidence)
FHx
BRCA 1/2
Lynch II syndrome
Nulliparity
Early menache and late menopause
Smoking
Obesity

Protective: pregnancy, breast feeding, exercise (due to less ovulation)

86
Q

Features and presentation of ovarian cancer

A

Epithelial, germ cell, sex-cord stromal, secondary malignant

Presentation: often a silent killer. Abdo distension, bloating, abdo pain, abdo mass, urinary frequency, PMB, loss of appetite

87
Q

Investigations for ovarian cancer

A

Pelvic USS
CA125 tumour marker
CT abdo pelvis (+/- chest)

Suspected patients under 40 should have AFP, b-hCG and CA125 levels

88
Q

Staging and prognosis for ovarian cancer

A

Stage 1: localised to ovary/ovaries (80% 5yr)
Stage 2: peritoneal deposits in pelvis (60% 5yr)
Stage 3: peritoneal deposits outside of pelvis (25% 5yr)
Stage 4: distant mets (5-10% 5yr)

89
Q

Management of ovarian cancer

A

Surgery: total abdominal hysterectomy and bilateral salpingo-oophorectomy and omentectomy (plus peritoneal washings)

Chemotherapy may be required post-op in stage 2 and 3

Surgery is usually for palliation in stage 4

90
Q

Risk factors for vulval cancer

A 
Age >60
History of CIN, VIN or HPV
HIV/ SLE/ immunosuppression
Iatrogenic immunosuppression
Smoking
91
Q

Features and presentation of vulval cancer

A

Most are squamous cell

Presentation is often late.
Pruritis, bleeding, discharge, ulcer, mass, inguinal nodes

92
Q

Staging for vulval cancer

A

1 - confined to vulva, <2cm diameter, no inguinal nodes
2 - confined to vulva, >2cm diameter, no inguinal nodes
3 - confined to vulva and suspicious nodes, or beyond vulva and no suspicious nodes
4 - obvious inguinal nodes, or involving rectum, bladder, urethra, or bone, or pelvic or distant mets

93
Q

Investigations and management of vulval cancer

A

Biopsy, thorough examination, CT/MRI, staging

Management:
Wide local excision
Radical vulvectomy,
Bilateral groin lymphadenectomy +/- radiotherapy

94
Q

Types of female genital mutilation

A

1: partial/total removal of clitoris and/or prepuce
2: partial/total removal of clitoris and labia minora +/- excision of labia majora
3: narrowing of vaginal orifice with creation of a covering seal (apositioning of labia)
4: all other harmful procedures for non-medical reasons

95
Q

Cervical ectropion

  • what is it
  • presentation
  • investigations
  • management
A

High oestrogen causes the stratified squamous epithelium of the ectocervix to undergo metaplastic change into columnar epithelium with releases mucus

Presentation: asymptomatic, discharge, IMB, PCB

Ix: clinical diagnosis, pregnancy test, triple swabs, cervical smear

Mx: leave alone if asymptomatic, stop oestrogen medications, ablation (cryotherapy, or electrocautery)

96
Q

Cervical polyps

  • what are they
  • presentaiton
  • ix
  • mx
A

Benign growths protruding form inner surface of cervix

Asymptomatic, abnormal vaginal bleeding (menorrhagia, IMB, PCB, PMB), vaginal discahrge

Histological exam after removal, triple swabs, cervical smear

Mx:
Small polyps -> grab and twist with forceps -> falls off
Large polyps -> remove with diathermy

Send polyps for histology

Obs and Gynae (3 decks)

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