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Medicine Finals > Gynaecology > Flashcards

Gynaecology Flashcards

Contents: - Menstrual cycle and associated disorders - Sexuality and sexual development disorders - Fertility, contraception and reproductive endocrinology - Gynaecological infectious diseases - Urogynaecology - Neoplastic disorders - Breast disorders

1
Q

The menstrual cycle:

What are the different phases of the menstrual cycle?

A
  • The follicular phase
  • Ovulation
  • The luteal phase (always 14 days)
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2
Q

The menstrual cycle:

How long does a normal menstrual cycle last? When does it begin?

A
  • 24 - 38 days
  • Average is 28 days
  • The first day of menstrual bleeding is counted as day 1
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3
Q

The menstrual cycle:

What occurs during the follicular phase?

A
  • Pulsatile GnRH release from the hypothalamus → LH and FSH
  • Follicles mature → negative feedback inhibits FSH release
  • One follicle becomes dominant, growing while all others regress (due to low FSH)
  • Due to fewer developing follicles oestrogen begins to drop → less inhibition → rapid LH surge → ovulation
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4
Q

The menstrual cycle:

What occurs in the luteal phase?

A
  • After ovulation, the dominant follicle becomes a corpus luteum, secreting progesterone → inhibits LH secretion
  • Falling LH causes the corpus luteum to degrade → decreased oestrogen and progesterone secretion → the endometrium cannot be maintained and is sloughed off → menstruation
  • If no pregnancy occurs, the corpus luteum regresses
  • If pregnancy occurs, β-hCG maintains the corpus luteum allowing further endometrial proliferation
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5
Q

The menstrual cycle:

What are the stages of endometrial growth and development? How long does each last?

A
  • The menstrual phase (lasts 3 - 7 days)
  • The proliferative phase (lasts ∼ 10 days)
  • The secretory phase (lasts 10 - 14 days)
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6
Q

The menstrual cycle:

What are the functions of oestrogen?

A
  • Stimulates endometrial & vaginal epithelial proliferation
  • Thins cervical mucous → facilitates passage of sperm
  • Stimulates development of secondary sexual characteristics (pubic hair, breast development)
  • Inhibits GnRH, LH, and FSH secretion
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7
Q

The menstrual cycle:

What are the functions of progesterone?

A
  • Increases endometrial secretions
  • Inhibits endometrial hyperplasia
  • Thickens cervical mucous
  • Downregulates oestrogen receptors
  • Raises body temperature
  • Inhibits LH and FSH secretion
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8
Q

The menstrual cycle:

Adverse effects of oestrogen?

A
  • Risk factor for malignancy (endometrial and breast)
  • Thrombosis risk
  • Breast hypertrophy and gynaecomastia
  • Weight gain (oedema)
  • Liver toxicity
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9
Q

Menopause:

What is menopause?

A

The time at which a woman permanently stops menstruating (usually between 45 and 55 years)

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10
Q

Menopause:

What is perimenopause?

A
  • The time period lasting from the first onset of menopausal symptoms until one year after menopause (typically lasts around 4 years)
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11
Q

Menopause:

What is premenopause?

A
  • The period between the onset of menopausal symptoms and the final menstrual period
  • Characterised by increasingly infrequent periods
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12
Q

Menopause:

What is postmenopause?

A

The time period beginning 12 months following a woman’s final menstrual period

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13
Q

Menopause:

What is the physiology of menopause?

A
  • Numerical depletion of ovarian follicles occurs with age
  • This causes low oestrogen and progesterone levels → loss of negative feedback to the anterior pituitary
  • Ends up with raised FSH and LH and anovulatory cycles
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14
Q

Menopause:

Features of menopause?

A
  • Oligo- → amenorrhoea
  • Autonomic symptoms: hot flushes, sweating, heat intolerance
  • Mental symptoms: mood swings, impaired sleep, anxiety
  • Atrophic symptoms (due to ↓oestrogen): atrophic vaginitis, osteoporosis
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15
Q

Menopause:

Diagnosis of menopause?

A
  • Diagnosis is usually clinical, but can be helped with blood tests:
  • ↓oestrogen, ↓progesterone, ↓inhibin B, ↑↑FSH
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16
Q

Menopause:

Management?

A

Advise regarding contraception:

  • Women ≥ 50 should use contraception for 12 months following their last menstrual period
  • Women < 50 should use contraception for 24 months following their last menstrual period

Lifestyle management:
- Regular exercise, weight loss, good sleep hygeine, and reducing stress all help

HRT management:

  • Must be combined if the patient has a uterus (mirena coil is sufficient if they already have one in)
  • If the patient has no uterus then oestrogen alone can be used

Non-HRT management:

  • Vaginal dryness = vaginal lubricant/moisturiser
  • Vasomotor symptoms = fluoxetine, citalopram
  • Psychological symptoms = CBT, antidepressants
  • Urogenital symptoms: urogenital atrophy → oestrogen cream
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17
Q

Menopause:

Contraindications for HRT?

A
  • Current or past breast cancer
  • Any oestrogen-sensitive cancer
  • Undiagnosed vaginal bleeding
  • Untreated endometrial hyperplasia
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18
Q

Menopause:

Risks of HRT?

A
  • VTE → slight increase in risk with all oral forms, no increase with transdermal forms
  • Stroke → slightly increased risk with oestrogen
  • Ovarian cancer → increased risk with all forms
  • Breast cancer → increased risk with all forms, but no increased risk of dying from breast ca.
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19
Q

Menopause:

Define premature menopause?

A

Also known as premature ovarian failure or primary ovarian insufficiency, it is defined as the onset of menopausal symptoms with raised gonadotrophin levels before the age of 40

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20
Q

Menopause:

Risk factors for premature menopause?

A
  • Idiopathic (90% of cases)
  • Genetic disorders associated with ovarian hypoplasia (e.g. Turner’s syndrome)
  • Autoimmune disorders (e.g. Addison’s disease)
  • Toxins (smoking is a major risk factor)
  • Iatrogenic (e.g. chemotherapy/radiotherapy)
  • Infectious diseases (e.g. mumps)
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21
Q

Menstrual disorders:

What is primary dysmenorrhoea?

A

Recurrent lower abdominal pain shortly before or during menstruation in the absence of pathology that could explain such symptoms

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22
Q

Menstrual disorders:

Diagnosis of primary dysmenorrhoea?

A

Diagnosis of exclusion; must rule out disorders that cause secondary dysmenorrhoea (e.g. endometriosis)

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23
Q

Menstrual disorders:

Treatment of primary dysmenorrhoea?

A
  • NSAIDs (e.g. mefenamic acid) are effective in 80% of women

- COCP is second line

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24
Q

Menstrual disorders:

What are some causes of secondary dysmenorrhoea?

A
  • Endometriosis
  • Adenomyosis
  • PID
  • Copper coil
  • Fibroids
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25
Q

Menstrual disorders:

Investigation of secondary dysmenorrhoea?

A
  • FBC to check for infection
  • Urinalysis to check for UTI
  • β-hCG to rule out pregnancy
  • Gonococcal/chlamidyal swabs to check for STI/PID
  • Pelvic ultrasound

Treatment depends on the underlying cause

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26
Q

Menstrual disorders:

What is primary amenorrhoea?

A

The failure to establish menstruation by 15 years of age in girls with normal secondary sexual characteristics (such as breast development), or by 13 years of age in girls with no secondary sexual characteristics

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27
Q

Menstrual disorders:

What is secondary amenorrhoea?

A

The cessation of menstruation for 3-6 months in women with previously normal and regular menses, or 6-12 months in women with previous oligomenorrhoea

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28
Q

Menstrual disorders:

Causes of primary amenorrhoea?

A
  • Gonadal hypoplasia (e.g. Turner’s syndrome)
  • Imperforate hymen
  • Congenital adrenal hyperplasia
  • Functional hypothalamic amenorrhoea (e.g. anorexia nervosa)
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29
Q

Menstrual disorders:

Causes of secondary amenorrhoea?

A
  • Hypothalamic amenorrhoea (e.g. excessive exercise, stress)
  • Polycystic ovarian syndrome (PCOS)
  • Hyperprolactinaemia
  • Sheehan’s syndrome
  • Premature ovarian failure
  • Thyrotoxicosis
  • Asherman’s syndrome (intrauterine adhesions)
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30
Q

Menstrual disorders:

Investigation of amenorrhoea?

A
  • β-hCG to rule out pregnancy
  • Full blood count, U&Es, TFTs
  • Gonadotrophins (↓in hypothalamic cause, ↑ovarian causes e.g. premature failure)
  • Prolactin
  • Androgen levels (may be raised in PCOS)
  • Oestradiol
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31
Q

Menstrual disorders:

Management of amenorrhoea?

A

Primary:

  • Identify and treat underlying cause
  • HRT in hypogonadism (e.g. Kallman’s syndrome)

Secondary:

  • Exclude pregnancy, lactation and menopause
  • Treat underlying cause
  • HRT in ovarian failure
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32
Q

Endometriosis:

Pathophysiology?

A

Poorly understood, seems to be associated with:

  • Retrograde menstruation
  • Haematological/lymphatic disssemination
  • Results in disseminated growth of endometrial tissue around the body
  • Endometrial implants → release of inflammatory mediators
  • Can cause adhesions → infertility
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33
Q

Endometriosis:

Commonly affected sites?

A

Pelvic organs:

  • Ovaries (most common, often affected bilaterally)
  • Fallopian tubes
  • Bladder
  • Cervix

Peritoneum;

Less commonly:

  • Lungs
  • Diaphragm
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34
Q

Endometriosis:

Clinical features?

A
  • Chronic pelvic pain that worsens before the onset of menses
  • Uterosacral tenderness and nodularity
  • Pre-/postmenstrual bleeding
  • Subfertility

4 D’s:

  • Dysuria
  • Dyspareunia
  • Dyschezia (pain on defacation)
  • Dysmenorrhoea
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35
Q

Endometriosis:

Diagnosis?

A
  • Laparoscopy is the gold standard investigation
  • Ultrasound of little use (except ruling-out other pathology) - if diagnosis suspected, they should be referred for expert assessment
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36
Q

Endometriosis:

Management?

A

Mild-moderate symptom control:

  • 1st line = NSAIDs and/or paracetamol
  • Danazol (synthetic androgen that ↓FSH and LH secretion)

Severe/non-responsive symptom control:

  • Hormonal treatment e.g. COCP, depot-provera
  • GnRH analogues (e.g. goserelin)

Subfertility:

  • Drug treatments unfortunately do not seem to help
  • Laparoscopic excision and laser ablation of endometrial implants may help
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37
Q

Endometriosis:

Complications?

A
  • Anaemia
  • Increased risk of ectopic pregnancy
  • Adhesions can cause intestinal obstruction (mainly small bowel)
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38
Q

Polycystic ovarian syndrome:

Clinical features?

A
  • Menstrual irregularities: amenorrhoea/oligomenorrhoea; menorrhagia
  • Infertility/subfertility
  • Obesity
  • Hirsutism & acne
  • Insulin resistance → acanthosis nigricans
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39
Q

Polycystic ovarian syndrome:

Diagnosis?

A

Rotterdam Criteria:

  • Oligomenorrhoea/amenorrhoea
  • Hyperandrogenism (e.g. hirsutism)
  • Polycystic ovaries on ultrasound

Lab studies:

  • LH:FSH ratio (typically raised)
  • Confirm hyperandrogenism (↑testosterone)
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40
Q

Polycystic ovarian syndrome:

Management?

A
  • Weight loss (improves symptoms AND fertility)

Patient not wishing to conceive → COCP:

  • Improves menstrual abnormalities
  • Improves acne and hirsutism
  • Reduces risk of endometrial cancer

Patient wishing to conceive:

  • Inducing ovulation: 1st line = letrozole, clomiphene, 2nd line = exogenous gonadotrophins
  • Metformin; combination with clomiphene especially effective in obese women
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41
Q

Ovarian cysts:

Types?

A

Functional:

  • Follicular cyst (commonest cyst in young women) - occurs when dominant follicle fails to release the oocyte, and instead continues to grow
  • Corpus luteum cyst

Non-functional:

  • Chocolate cyst (endometrioid)
  • Dermoid cyst (mature teratomas)
  • Cystadenoma (serous/mucinous)
  • Malignant cysts (e.g. cystadenocarcinoma)
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42
Q

Ovarian cysts:

Clinical features?

A
  • Usually asymptomatic until a complication occurs
  • Adnexal mass may be felt
  • May show signs of underlying cause such as in endometriosis
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43
Q

Ovarian cysts:

Investigation and diagnosis?

A

Any palpable ovarian mass in premenarchal/postmenopausal patients must be investigated for ovarian cancer!

Pelvic ultrasound is investigation of choice

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44
Q

Ovarian cysts:

Mangagement?

A
  • In most patients watchful waiting is recommended

- Surgery may be required in patients with complications, large cysts, or persistent cysts that are painful

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45
Q

Ovarian cysts:

Complications?

A
  • Rupture

- Torsion

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46
Q

Ovarian cysts:

Clinical features of a ruptured cyst?

A
  • Often occurs following vigorous exercise
  • Sudden-onset unilateral, lower abdominal pain
  • Small amount of vaginal bleeding (spotting)
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47
Q

Ovarian cysts:

Diagnosis of a ruptured cyst?

A

Transabdominal/transvaginal ultrasound scan, showing free fluid in the pouch of Douglas

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48
Q

Ovarian cysts:

Management of a ruptured cyst?

A
  • Haemodynamically stable patients: conservative management with analgesia and monitoring
  • Haemodynamically unstable patients: emergency exploratory laparoscopy/laparotomy
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49
Q

Ovarian cysts:

Pathophysiology of ovarian torsion?

A
  • Twisting of the ovary and fallopian tube around the infundibulopelvic ligament and ovarian ligament
  • This causes compression of the venous and lymphatic drainage, causing oedema
  • If this gets bad enough, it can compress the arteries supplying the ovary, causing ischaemia and necrosis, though this is rare as the ovaries receive dual blood supply from the ovarian and uterine arteries
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50
Q

Ovarian cysts:

Clinical features of ovarian torsion?

A
  • Sudden onset, progressive, unilateral lower abdominal/pelvic pain
  • Nausea and vomiting
  • Adnexal mass may be palpable
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51
Q

Ovarian cysts:

Diagnosis of ovarian torsion?

A
  • Transabdominal/transvaginal pelvic ultrasound with Doppler → enlarged, oedematous ovary with reduced blood flow
  • MRI abdomen and pelvis with contrast → “whirlpool sign”
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52
Q

Ovarian cysts:

Management of ovarian torsion?

A

Emergency exploratory laparoscopy in all patients, allowing adnexal detorsion and preservation of ovarian function

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53
Q

Anomalies of the female genital tract:

What are the commonest anomalies of Müllerian duct fusion?

A
  • Septate uterus: ducts fuse, but septum remains between them
  • Unicornuate uterus: single, arc-shaped uterus
  • Bicornuate uterus: double uterus ± double cervix, vagina normal or septate
  • Didelphic uterus: double uterus, double cervix, double vagina
  • Müllerian agenesis: hypoplastic/absent uterus, absent cervix, vaginal atresia (with functional ovaries)
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54
Q

Anomalies of the female genital tract:

What is Asherman’s syndrome? What causes it?

A
  • A condition defined by the presence of intrauterine adhesions
  • Most commonly occurs following vaginal curettage
  • Can also occur after infection (e.g. chlamidya)
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55
Q

Anomalies of the female genital tract:

Clinical features of Asherman’s syndrome?

A
  • Usually asymptomatic
  • Abnormal uterine bleeding
  • Secondary amenorrhoea
  • Infertility
  • Recurrent pregnancy loss
  • Periodic abdominal pain
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56
Q

Anomalies of the female genital tract:

Diagnosis of Asherman’s syndrome?

A

Hysteroscopy to visualise adhesions

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57
Q

Anomalies of the female genital tract:

Management of Asherman’s syndrome?

A

Hysteroscopic resection of adhesions

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58
Q

Anomalies of the female genital tract:

Clinical features of imperforate hymen?

A
  • Asymptomatic before puberty
  • Primary amenorrhoea
  • Periodic abdominal pain
  • Perineal examination: bulging, tense, bluish membrane in vulva
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59
Q

Anomalies of the female genital tract:

Diagnosis and management of imperforate hymen?

A
  • Diagnosis is made clinically

- Management is hymenectomy (surgical excision of the hymen)

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60
Q

Anomalies of the female genital tract:

Pathophysiology of vaginal atresia?

A
  • Agenesis or hypoplasia of the Müllerian duct → atresia of the upper ⅓ of the vagina
  • Normal female phenotype → normal development of secondary sexual characteristics
  • Associated with absent or malformed uterus and cervix
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61
Q

Anomalies of the female genital tract:

Clinical features of vaginal atresia?

A
  • Dyspareunia
  • Primary amenorrhoea
  • Infertility
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62
Q

Anomalies of the female genital tract:

Diagnosis of vaginal atresia?

A
  • Lab tests: normal levels of gonadotrophins, oestrogen, progesterone and testosterone
  • Ultrasound: limited view of the uterus and vagina
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63
Q

Anomalies of the female genital tract:

Treatment of vaginal atresia?

A

Vaginoplasty

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64
Q

Disorders of sex development:

What is androgen insensitivity syndrome?

A
  • X-linked recessive condition resulting in defective androgen receptors, and variable end-organ androgen insensitivity
  • Male genotype (46,XY) with a female phenotype
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65
Q

Disorders of sex development:

Clinical features of androgen insensitivity syndrome?

A
  • Female external genetalia and physique (including female breast development)
  • Blind-ending vaginal pouch
  • Scant/no pubic hair
  • Primary amenorrhoea & infertility
  • Absent male internal genetalia
  • Bilateral undescended testes
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66
Q

Disorders of sex development:

Diagnosis of androgen insensitivity syndrome?

A

Hormone testing:

  • Before puberty → raised testosterone
  • After puberty → raised LH and oestrogen

Genetic testing

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67
Q

Disorders of sex development:

Treatment of androgen insensitivity syndrome?

A

Hormonal treatment:

  • Complete androgen insensitivity: oestrogen replacement
  • Partial androgen insensitivity: high-dose androgen therapy in those with male gender identity

Gonadectomy for intra-abdominal/intralabial testes:

  • Usually done after puberty
  • Prevents malignancy
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68
Q

Disorders of sex development:

What is Klinefelter’s syndrome?

A
  • Nondisjunction of sex chromosomes during meiosis resulting in phenotype of 47,XXY
  • One of the commonest causes of male hypogonadism
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69
Q

Disorders of sex development:

Clinical features of Klinefelter’s syndrome?

A
  • Asymptomatic before puberty
  • Tall, slim stature with long extremities
  • Gynaecomastia
  • Reduced facial and body hair
  • Testicular atrophy
  • Reduced fertility
  • Micropenis
  • May be neurodevelopmental delay
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70
Q

Disorders of sex development:

Conditions associated with Klinefelter’s syndrome?

A
  • Mitral valve prolapse

- Increased risk of breast and testicular cancer

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71
Q

Disorders of sex development:

Diagnosis of Klinefelter’s syndrome?

A

Genetic karyotyping

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72
Q

Disorders of sex development:

Management of Klinefelter’s syndrome?

A

Lifelong testosterone supplementation

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73
Q

Disorders of sex development:

What is Kallman syndrome?

A

Genetic condition resulting in hypogonadotrophic hypogonadism with anosmia

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74
Q

Disorders of sex development:

Clinical features of Kallman syndrome?

A
  • Anosmia or hyposmia
  • In males: cryptorchidism and low sperm count
  • In females: primary amenorrhoea
  • Absent or reduced pubertal changes
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75
Q

Disorders of sex development:

Management of Kallman syndrome?

A
  • Hormone replacement therapy to stimulate pubertal development
  • Gonadotropins or pulsatile GnRH therapy may increase fertility
76
Q

Contraceptives:

How to the hormones produce their contraceptive effects?

A

Oestrogen:

  • Suppresses pituitary release of LH & FSH
  • Decreased FSH prevents folliculogenesis
  • Decreased LH prevents ovulation

Progestogens (synthetic progesterone):

  • Suppresses pituitary release of LH & FSH → anovulation (in high enough doses)
  • Inhibits endometrial proliferation → prevents implantation
  • Thickens cervical mucous, impairs fallopian tube peristalsis → prevents sperm ascension
77
Q

Contraceptives:

COCP overview?

A
  • MoA: inhibits ovulation
  • Effectiveness: typical use = 93%, perfect use = >99%
  • Time to effect: within first 5 days of cycle = instant, started later = takes 7 days

Side effects:

  • Increased risk of VTE
  • Increased risk of breast and cervical cancer
78
Q

Contraceptives:

Progestogen-only pill overview?

A
  • MoA: thickens cervical mucous (desogestrel also inhibits ovulation)
  • Effectiveness: typical use = 93%, perfect use = >99%
  • Time to effect: within first 5 days of cycle = instant, started later = takes 2 days

Side effects:
- Irregular vaginal bleeding common

79
Q

Contraceptives:

Condom overview?

A
  • MoA: physical barrier
  • Effectiveness (typical use): male condom = 82%, female condom = 79%
  • Time to effect: instant

Other notes:

  • High risk of poor compliance
  • Reduces transmission of many STIs
80
Q 
Contraceptives:
Depot provera (medroxyprogesterone acetate; MPA) overview?
A
  • MoA: mainly inhibits ovulation, also thickens mucous
  • Effectiveness: typical use = 96%, perfect use = 99.8%
  • Time to effect: within first 5 days of cycle = instant, started later = takes 7 days
  • Duration: lasts 12 weeks

Side effects:

  • Weight gain
  • Abdnormal vaginal bleeding
  • Delayed return to fertility
  • Increased risk of osteoporosis
81
Q 
Contraceptives:
Mirena IUS (levonorgestrel) overview?
A
  • MoA: prevents endometrial proliferation, thickens cervical mucous
  • Effectiveness: typical use = 99.3%, perfect use = 99.5%
  • Time to effect: within first 5 days of cycle = instant, started later = takes 7 days
  • Duration: lasts up to 5 years

Side effects:

  • Initially = frequent vaginal bleeding and/or spotting
  • Increases proportion of pregnancies that are ectopic (although decreases overall risk due to contraception)
  • Risk of causing PID during insertion
  • Risk of uterine perforation during insertion (rare)
82
Q 
Contraceptives:
Implantable contraceptive (Nexplanon) overview?
A
  • MoA: mainly inhibits ovulation, also thickens mucous
  • Effectiveness: 99.9% (most effective form)
  • Time to effect: within first 5 days of cycle = instant, started later = takes 7 days
  • Duration: lasts 3 years

Side effects:

  • Irregular/heavy vaginal bleeding
  • ‘progestogen effects’ - breast pain, headaches, nausea
83
Q

Contraceptives:

Copper IUD overview?

A
  • MoA: decreases sperm motility and survival
  • Effectiveness: around 99%
  • Time to effect: instant, regardless of when inserted
  • Duration: lasts up to 10 years

Side effects:

  • Heavier, longer, more painful periods
  • Risk of causing PID during insertion
  • Increased proportion of pregnancies are ectopic
  • Risk of uterine perforation during insertion (rare)
84
Q

Contraceptives:

Other, non-hormonal contraceptive methods? What are their success rates?

A
  • Lactational amenorrhoea = ∼98% effective
  • Diaphragm = ∼88% effective
  • “Pulling out” = ∼78% effective
  • Calendar based method = ∼76% effective
  • Spermicides = ∼72% effective
  • Cervical cap = may be as low as 60% effective
85
Q

Contraceptives:

What are the available methods of emergency contraception?

A

Hormonal (‘morning after pill):

  • Levonorgestrel (Levonelle)
  • Ulipristal acetate (EllaOne)

Copper IUD

86
Q

Contraceptives:
Levonorgestrel emergency contraceptive overview?
(MoA, window for use, dose, effectiveness, aftercare, other information)

A
  • MoA: stops ovulation and prevents implantation
  • Window of efficacy: take ASAP, effective for 72 hours after UPSI
  • Dose: 1.5mg oral, double if BMI >25 or weight >70kg
  • Effectiveness: 97-99%
  • Aftercare: hormonal contraception can be started immediately after use

Other:

  • Vomiting seen in 1% → if occurs within 3 hours then take another dose
  • Can be used more than once in a single cycle if needed
87
Q

Contraceptives:
Ulipristal acetate emergency contraceptive overview?
(MoA, window for use, dose, effectiveness, aftercare, other information)

A
  • MoA: inhibits ovulation
  • Window of efficacy: within 120 hours after UPSI
  • Dose: 30mg oral
  • Effectiveness: 98-99%
  • Aftercare: reduces effectiveness of hormonal contraception - restart this 5 days after use of EllaOne, uses barrier contraception during this period

Other:

  • Use with caution in severe asthma
  • Can be used more than once in a single cycle if needed
88
Q

Contraceptives:
Copper coil emergency contraceptive overview?
(MoA, window for use, effectiveness, aftercare, other information)

A
  • MoA: may inhibit fertilisation or implantation
  • Window of efficacy: within 5 days of UPSI (or within 5 days of estimated date of ovulation, whichever is latest)
  • Effectiveness: 99%
  • Aftercare: may be left in-situ to provide long-term contraception, should be kept in until at least the next period

Other:
- Prophylactic antibiotics may be given if pt is high risk for STIs → reduces risk of PID

89
Q

Infertility:

Causes (%):

A
  • Male factor = 30%
  • Unexplained = 20%
  • Ovarian failure = 20%
  • Tubal damage = 15%
  • Other causes = 15%
90
Q

Infertility:

How long does it normally take to conceive?

A
  • 84% of couples conceive within 1 year of regular sex

- 92% within 2 years

91
Q

Infertility:

Basic investigations?

A

Semen analysis:

  • Volume >1.5ml
  • Concentration >15million/ml
  • Vitality >48% live
  • Motility >32% progressive

Mid-luteal progesterone (7 days before next menstrual cycle; day 21 of 28 day cycle)

  • Normal >30nmol/l
  • Repeat = 16-30nmol/l
  • Low = <16nmol/l - repeat, refer if consistently low

Other investigations can be done if a specific cause is suspected

92
Q

Infertility:

Advice for couple struggling to conceive?

A
  • Advise regular intercourse every 2-3 days
  • Aim for BMI 20-25
  • Avoid smoking/drinking
  • Folic acid supplements
93
Q

Infertility:

What is ovarian hyperstimulation syndrome?

A

Potentially life-threatening disorder that can occur as a result of ovarian induction (treatment for ovarian-factor infertility)

Occurs in less than 1% of women undergoing ovarian induction

94
Q

Infertility:

Clinical features of ovarian hyperstimulation syndrome?

A

Rapid enlargement of multiple ovarian cysts, with increased vascular permeability, causing:

  • Hypovolaemic shock
  • AKI
  • Venous or arterial thromboembolism
95
Q

Infertility:

Management of ovarian hyperstimulation syndrome?

A
  • Fluid and electrolyte replacement
  • Anti-coagulation
  • Paracentesis of ascites
  • Pregnancy termination to prevent further hormonal damage
96
Q

Vulvovaginitis:
Bacterial vaginosis overview?
(Pathogen, discharge, treatment, special features)

A
  • Pathogen: Gardnerella vaginalis
  • Discharge: gray/milky, fishy odour
  • Treatment: oral metronidazole for 5-7 days

Special features:

  • “Clue cells”
  • Positive whiff test
  • pH >4.5

N.B. the three special features and the discharge form the criteria for diagnosis (3/4 required)

97
Q

Vulvovaginitis:
Trichomoniasis overview?
(Pathogen, discharge, treatment, special features)

A
  • Pathogen: Trichomonas vaginalis
  • Discharge: frothy, yellow-green, malodorous
  • Treatment: oral metronidazole for 5-7 days or 2g one off

Special features:

  • Strawberry cervix
  • pH >4.5
  • Flagellated protozoa on cervical smear
  • May be asymptomatic in men or may cause urethritis
98
Q

Vulvovaginitis:
Candidiasis overview?
(Pathogen, discharge, treatment, special features)

A
  • Pathogen: Candida albicans
  • Discharge: thick, white, ‘cottage cheese-like’
  • Treatment: clotrimazole pessary, oral itra-/fluconazole, may be used together, only topical treatments if pregnant

Special features:

  • pH < 4.5
  • Itching
  • Satellite lesions may be seen

N.B. if recurrent (>4 per year), investigate for diabetes, consider alternative diagnosis e.g. lichen sclerosus, and give prophylactic treatment

99
Q

Vulvovaginitis:
Gonorrhoea overview?
(Pathogen, discharge, diagnosis, treatment, special features)

A
  • Pathogen: Neisseria gonorrhoeae
  • Discharge: purulent, creamy, odourless
  • Diagnosis: vulvovaginal swab & NAAT in women, first-void urine in men
  • Treatment: single dose of IM ceftriaxone (oral cefixime and oral azithromycin alternative), ciprofloxacin if known sensitive

Special features:
- Gram negative diplococci on culture and microscopy

100
Q

Vulvovaginitis:
Chlamydia overview?
(Pathogen, discharge, treatment, special features)

A
  • Pathogen: Chlamydia trachomatis
  • Discharge: purulent, bloody, odourless
  • Diagnosis: vulvovaginal swab & NAAT in women, first-void urine in men
  • Treatment: doxycycline, azithro-/erythromycin if pregnant

Special features:
- Gram negative intracellular organism

101
Q

Vulvovaginitis:

Complications of chlamydia?

A
  • Epididymitis
  • Pelvic inflammatory disease
  • Endometritis
  • Increased incidence of ectopic pregnancies
  • Infertility
  • Reactive arthritis
  • Fitz-Hugh-Curtis syndrome (RUQ pain, liver adhesions)
102
Q

Vulvovaginitis:

Features and complications of disseminated gonococcal infection?

A

Triad of features:

  • Tenosynovitis
  • Migratory polyarthritis
  • Dermatitis

Complications:

  • Septic arthritis
  • Pericarditis
  • Fitz-Hugh-Curtis syndrome
103
Q

Vulvovaginitis:

What is atrophic vaginits?

A
  • Atrophy of the epithelium lining the vulva and vagina

- Occurs due to low oestrogen levels, e.g. after menopause

104
Q

Vulvovaginitis:

Clinical features of atrophic vaginitis?

A
  • Vaginal soreness and dryness
  • Dyspareunia
  • Occasional spotting (due to friable epithelium)
  • Receding pubic hair
105
Q

Vulvovaginitis:

Management of atrophic vaginitis?

A
  • Non-hormonal emollient if mild symptoms

- Topical oestrogen

106
Q 
Human papillomavirus (HPV):
What are the types and how might they present?
A
  • Low-risk HPV types 6 and 11: anogenital warts
  • High-risk types 16 and 18 (+31 and 33): increased risk of cervical cancer, as well as oral, anal, and oesophageal SCC
  • HPV types 1, 2 and 4: cause skin warts
107
Q

Human papillomavirus:

Testing for HPV?

A

Integrated into the cervical cancer screening programme:

  • In the UK HPV is tested first.
  • If High-risk HPV (HrHPV) is present then cytology is performed
108
Q

Human papillomavirus:

Who is vaccinated against HPV?

A
  • All 12- and 13-year-olds (girls AND boys)

- Should also be offered to MSM aged < 45

109
Q

Pelvic inflammatory disease:

Commonest organisms?

A
  • Chlamydia trachomatis

- Neisseria gonorrhoeae

110
Q

Pelvic inflammatory disease:

Risk factors?

A
  • Multiple sexual partners
  • Unprotected sex
  • History of prior STIs
  • Intrauterine devices (risk of infection during insertion)
  • Risk is lower during pregnancy
111
Q

Pelvic inflammatory disease:

Clinical features?

A
  • Lower abdominal pain
  • Nausea & vomiting
  • Fever
  • Dysuria
  • Abnormal vaginal discharge
  • Deep dyspareunia
  • Cervical excitation
112
Q

Pelvic inflammatory disease:

Investigation?

A
  • Pregnancy test to rule out an ectopic
  • High vaginal swab (often negative)
  • Screen for chlamydia and gonorrhoea

Due to difficult diagnosis, a low threshold is required to initiate treatment

113
Q

Pelvic inflammatory disease:

Management?

A
  • Oral ofloxacin + oral metronidazole
    OR
  • IM ceftriaxone + oral doxycycline + oral metronidazole
114
Q

Pelvic inflammatory disease:

Complications?

A
  • Fitz-Hugh-Curtis syndrome: perihepatitis (inflammation of liver capsule), characterised by violin-string adhesions between the liver and the peritoneum
  • Infertility
  • Ectopic pregnancy
  • Chronic pelvic pain
115
Q

Bartholin’s gland cyst:

Presentation?

A

Painless, unilateral swelling of labia, may cause mild dyspareunia

116
Q

Bartholin’s gland cyst:

Management?

A
  • Small, asymptomatic = conservative (warm compress to encourage rupture of cyst)
  • Larger cyst >3cm or painful = surgical drainage
117
Q

Bartholin’s gland cyst:

What is a Bartholin’s gland abscess?

A

An infected Bartholin’s gland cyst

118
Q

Bartholin’s gland cyst:

Features of a Bartholin’s gland abscess?

A
  • Acute unilateral groin pain and swelling
  • Dyspareunia
  • Fever
119
Q

Bartholin’s gland cyst:

Management of a Bartholin’s gland abscess?

A
  • Surgical incision and drainage
120
Q

Urinary incontinence:

What types of urinary incontinence are there?

A
  • Urge incontinence (commonest in males)
  • Stress incontinence (commonest in females)
  • Mixed incontinence
  • Overflow incontinence
121
Q

Urinary incontinence:

Causes of urinary incontinence?

A 
Patients need 𝗗𝗜𝗔𝗣𝗘𝗥𝗦:
𝗗rugs (e.g. diuretics)
𝗜nfection (UTI)
𝗔trophic urethritis/vaginitis
𝗣sychiatric causes (e.g. depression)
𝗘xcessive urine output (e.g. diabetes, hypercalcaemia)
𝗥educed mobility
𝗦tool impaction
122
Q

Urinary incontinence:

Pathophysiology of stress incontinence?

A
  • Urethral hypermobility in women secondary to weak pelvic floor muscles
  • Sphincter dysfunction, caused by obesity, ageing, prostate surgery (men)
  • Increased intra-abdominal pressure (e.g. laughing, coughing) → increased bladder pressure → sphincter insufficiency
123
Q

Urinary incontinence:

Pathophysiology of urge incontinence?

A

Detrusor overactivity → strong, sudden sense of urgency and urine leakage

124
Q

Urinary incontinence:

Investigation?

A
  • Bladder diary for ≥3 days
  • Vaginal examination to exclude pelvic organ prolapse
  • Check ability to contract pelvic floor muscles (“Kegel exercises”)
  • Urine dipstick and culture
  • Urodynamic studies
125
Q

Urinary incontinence:

Management of stress incontinence?

A
  1. Pelvic floor exercises
  2. Surgical procedures (e.g. retropubic mid-urethral tape)
  3. Duloxetine can be offered if patient declines surgery
126
Q

Urinary incontinence:

Management of urge incontinence?

A
  1. Bladder retraining
  2. Antimuscarinics (oxybutinin, tolterodine)
  3. Mirabegron is preferred in the elderly due to lower falls risk
127
Q

Urinary incontinence:

Features of overflow incontinence?

A
  • Impaired detrusor contractility (e.g. neurogenic bladder) → chronic retention and increased bladder pressure → dribbles out when bladder pressure > outflow resistance
  • Results in frequent, involuntary, intermittent/continuous urine leakage in the absence of an urge to urinate
128
Q

Urinary incontinence:

What is the normal physiology of urination?

A

Parasympathetic nervous system → S2-S4 ventral root → inferior hypogastric plexus → contraction of the detrusor muscle

Somatic nervous system → voluntary relaxation of the external urethral sphincter via the pudendal nerve → micturition

129
Q

Pelvic organ prolapse:

Risk factors?

A
  • Multiple vaginal deliveries and/or traumatic births
  • Low oestrogen levels
  • Increased intra-abdominal pressure e.g. obesity
  • Previous pelvic surgery
130
Q

Pelvic organ prolapse:

Clinical features?

A
  • Pressure/discomfort around the perineum (vaginal fullness)
  • Lower back and pelvic pain
  • Rectal fullness, constipation
  • Weakened pelvic floor muscles and anal sphincter tone
131
Q

Pelvic organ prolapse:

Classification?

A
  • Vaginal wall prolapse: anterior wall (associated with cystocele and urethrocele) or posterior wall (associated with rectocele or enterocele)
  • Cystocele = descent of the bladder
  • Urethrocele = descent of the urethra
  • Rectocele = descent of the rectum
  • Enterocele = herniated section of intestine
  • Vaginal vault prolapse = descent of the apex of the vagina
  • Total prolapse = pelvic organs are everted and located outside the vaginal opening
132
Q

Pelvic organ prolapse:

Management?

A
  • Mild prolapse & asymptomatic → no management needed
  • Conservative management → weight loss, pelvic floor exercises
  • Ring pessary
  • Surgery
133
Q

Pelvic organ prolapse:

Surgical interventions?

A
  • Cystocele/cystourethrocele → colposuspension
  • Uterine prolapse → sacrohysteropexy/hysterectomy
  • Rectocele → posterior colporrhaphy
134
Q

Urinary tract infection:
Commonest organisms?
(More detail in GUM cards)

A 
𝗦𝗘𝗘𝗞 𝗣𝗣
𝗦. saprophyticus
𝗘. coli
𝗘nterocci
𝗞lebsiella
𝗣roteus
𝗣seudomonas
135
Q

Urinary tract infection:

Diagnosis?

A
  • Urinalysis

- Urine M, C and S

136
Q

Urinary tract infection:

Management?

A

Non-pregnant women:
- Trimethoprim or nitrofurantoin for 3 days

Pregnant women:

  • Symptomatic = nitrofurantoin (avoid near term), 2nd line = amoxicillin or cefalexin
  • Asymptomatic bacteuria = nitrofurantoin, amoxicillin or cefalexin for 7 days to prevent progression to pyelonephritis
137
Q

Breast cancer:

Risk factors?

A
  • BRCA1 and BRCA2 gene mutations
  • Increased oestrogen (e.g. obesity, nulliparity, early menarche, late menopause)
  • Advanced age (>65)
  • European descent at highest risk (Afro-Caribbean at highest risk of triple negative breast cancer)
  • Smoking
  • Alcohol consumption
138
Q

Breast cancer:

Classification of breast cancer?

A
  • Divided into what tissue they arise from (e.g. lobular/ductal)
  • Subdivided into neoplasms that have spread to other tissue (invasive) or those which haven’t spread (in-situ)
139
Q

Breast cancer:

Commonest kinds of breast cancer?

A
  • Invasive ductal carcinoma (aka no special type; NST)
  • Invasive lobular carcinoma
  • Ductal carcinoma-in-situ (DCIS)
  • Lobular carcinoma-in-situ (LCIS)
140
Q

Breast cancer:

Overview of ductal carcinoma in situ?

A
  • NON-INVASIVE
  • No penetration of the basement membrane
  • Preceded by ductal atypia
  • Frequently appears on a mammogram as focal 𝗺𝗶𝗰𝗿𝗼𝗰𝗮𝗹𝗰𝗶𝗳𝗶𝗰𝗮𝘁𝗶𝗼𝗻𝘀
  • Higher risk of ipsilateral invasive carcinoma
141
Q

Breast cancer:

Overview of invasive ductal carcinoma?

A
  • Most common form of invasive breast cancer (∼ 80%)
  • Aggressive formation of metastases
  • Unilateral, usually unifocal
142
Q

Breast cancer:

Overview of medullary breast cancer?

A
  • Rare type of invasive ductal carcinoma
  • Most common tumour associated with BRCA1
  • Well-circumscribed soft tumour with smooth border (may appear benign)
  • Usually triple-negative
143
Q

Breast cancer:

Overview of invasive lobular carcinoma?

A
  • ∼10% of all breast cancers
  • Less aggressive than invasive ductal carcinoma
  • Bilateral in ∼20%
  • Frequently multifocal
144
Q

Breast cancer:

Clinical presentation?

A

Early stages:

  • Typically single, non-tender, and firm
  • Poorly defined margins
  • Most commonly located in the upper outer quadrant

Locally advanced disease:

  • Change in size/shape → asymmetrical breasts
  • Skin changes (e.g. retractions, dimpling, peau d’orange)
  • Nipple changes (e.g. inversion, blood-tinged discharge)
145
Q

Breast cancer:

Common sites of metastasis?

A
  • Lymph nodes → lymphadenopathy
  • Bone → bone pain, pathological fractures
  • Liver → abdominal pain, jaundice
  • Lung → cough, haemoptysis, dyspnoea
  • Brain → headaches, seizures, focal neurological deficits
146
Q

Breast cancer:

What is Paget’s disease of the breast?

A
  • A rare type of breast cancer that affects lactiferous ducts and the skin of the nipple and areola
  • Believed to occur due to spreading of underlying DCIS/IDC through the lactiferous ducts (90% have underlying invasive carcinoma)
147
Q

Breast cancer:

Clinical features of Paget’s disease of the breast?

A
  • Erythematous, scaly/vesicular rash affecting the nipple and areola
  • Nipple retraction
  • Pruritus/burning sensation
  • Blood-tinged nipple discharge
148
Q

Breast cancer:

Diagnosis of Paget’s disease of the breast?

A
  • Punch biopsy of nipple tissue
  • Paget cells confirm the diagnosis
  • Perform imaging to look for underlying DCIS/IDC
  • Treatment depends on the underlying lesion
149
Q

Breast cancer:

Outline the screening process

A
  • 3-yearly mammogram for women aged 50-70 years
  • Estimated to save 1,400 lives in the UK per year
  • Women may start screening earlier if they have a strong family history
150
Q

Breast cancer:
Interpreting mammogram findings?
(Appearance, margins, calcifications, further management)

A

Appearance of lesion:

  • Benign = well-defined, circumscribed lesion
  • Malignant = focal mass or density

Margins:

  • Benign = surrounding radiolucent ring (“𝗵𝗮𝗹𝗼 𝘀𝗶𝗴𝗻”)
  • Malignant = poorly defined, spiculated margins

Calcifications:

  • Benign = diffuse microcalcifications or coarse calcification
  • Malignant = focal, clustered microcalcifications

Further management:

  • Benign = regular check-ups, possibly surgical excision
  • Malignant = fine-needle aspiration or core needle biopsy
151
Q

Breast cancer:

What is triple-negative breast cancer?

A
  • Breast cancer that is hormone receptor-negative (oestrogen receptor and progesterone receptor) and HER2-negative
  • Typically high-grade, more aggressive tumours
  • Most common in Afro-Caribbean women
  • Treated with chemotherapy (doesn’t respond to hormone therapy)
152
Q

Breast cancer:

Surgical management of breast cancer?

A

Wide-local excision:
- For single, peripheral, smaller lesions (small tumour-to-breast volume ratio)

Mastectomy:
- For lesions that don’t meet the criteria for wide-local excision

Women should be offered breast reconstruction to achieve a cosmetically suitable result regardless of how it is managed

153
Q

Breast cancer:

When is radiotherapy used?

A
  • As an adjunct for all wide-local excision procedures; reduces recurrence by two-thirds
  • As an adjunct for mastectomy in T3-T4 tumours or those with multiple (≥4) positive lymph nodes
154
Q

Breast cancer:

Hormonal therapy?

A
  • Adjuvant hormonal therapy is used if tumours are hormone receptor-positive
  • Tamoxifen is used for 5 years following diagnosis in pre-/peri-menopausal women
  • Aromatase inhibitors (e.g. anastrozole) is preferred in post-menopausal women

N.B. tamoxifen is associated with increased risk of endometrial cancer, VTE, and worsening menopausal symptoms

155
Q

Breast cancer:

Biological therapy?

A
  • Useful in 20-25% of tumours that are HER2 positive
  • Usually trastuzumab (Herceptin)

N.B. Herceptin is contraindicated in patients with a history of heart disorders - can cause dilated cardiomyopathy

156
Q

Breast cancer:

Chemotherapy?

A
  • Usually combination therapy

- Indicated for triple-negative breast cancer or when there is nodal involvement

157
Q

Cervical cancer:

Risk factors?

A
  • High-risk 𝗛𝗣𝗩 𝟭𝟲 & 𝟭𝟴 (found in 70% of patients)
  • Multiple sexual partners
  • Early-onset sexual activity
  • Multiparity
  • Immunosuppression
  • History of STIs
  • Cigarette smoking
  • COCP use
158
Q

Cervical cancer:

Clinical features?

A
  • May be asymptomatic - detected in screening
  • Abnormal vaginal bleeding (𝗽𝗼𝘀𝘁-𝗰𝗼𝗶𝘁𝗮𝗹, intermenstrual)
  • Abnormal vaginal discharge (blood-stained, purulent)
  • Dyspareunia
  • Pelvic pain
159
Q

Cervical cancer:
Outline the screening process
(+ rough interpretation of results)

A
  • 25-49 years = 3-yearly pap smear
  • 50-64 years = 5-yearly pap smear

HrHPV -ve:
- Return to routine recall

HrHPV +ve, cytology normal:

  • Repeat after 12 months
  • If still positive (cytology still normal), do third smear after another 12 months
  • If 𝘴𝘵𝘪𝘭𝘭 positive, refer for colposcopy
  • If HrHPV negative at any stage → back to routine recall

HrHPV +ve, cytology abnormal:
- Refer straight away for colposcopy

Sample inadequate:

  • Repeat after 3 months
  • Two inadequate samples → colposcopy
160
Q

Cervical cancer:

Diagnosis?

A
  • Colposcopy → cervical leukoplakia/acetowhite epithelium indicate atypical cell changes and warrant biopsy
  • Punch biopsy
    OR
  • Cone biopsy (can also treat CIN)
161
Q

Cervical cancer:

What is cervical intraepithelial neoplasia (CIN)?

A
  • Precancerous lesion characterised by epithelial dysplasia beginning at the basal layer of the squamocolumnar junction and growing outward
  • May progress to an invasive carcinoma if left untreated
162
Q

Cervical cancer:

Grading of CIN?

A
  • CIN I: mild dysplasia, involves ∼ ⅓ of the basal epithelium
  • CIN II: moderate dysplasia
  • CIN III: severe dysplasia or carcinoma in situ
163
Q

Cervical cancer:

Staging of cervical cancer?

A

1A: confined to cervix, < 7mm wide
1B: confined to cervix, clinically visible or >7mm wide

2A: extends to upper ⅔ of the vagina
2B: extends to parametrium (fatty tissue surrounding endometrium)

3A: extends to lower ⅓ of the vagina
3B: extends to the pelvic wall

4A: involvement of bladder or rectum
4B: extends beyond the pelvis

164
Q

Cervical cancer:

Management?

A

1A tumours: hysterectomy ± node clearance
1B tumours: radiotherapy & chemotherapy ± hysterectomy

Stage 2 & 3 tumours: radiotherapy & chemotherapy (cisplatin)

Stage 4 tumours: radiation ± chemotherapy, palliation if necessary

165
Q

Cervical cancer:

Commonest cause of death?

A

Bilateral invasion of ureters → obstruction → hydronephrosis → severe uraemia

166
Q

Fibroids:

Risk factors

A
  • Afro-Caribbean women (50% lifetime risk)
  • Nulliparity
  • Women of reproductive age
  • Rare before puberty, shrink during menopause
167
Q

Fibroids:

Clinical features?

A
  • Can be asymptomatic
  • Abnormal menstrual bleeding, menorrhagia, dysmenorrhoea
  • Urinary frequency/retention if large enough
  • Subfertility
168
Q

Fibroids:

Diagnosis?

A

Transvaginal ultrasound

169
Q

Fibroids:

Management?

A

Asymptomatic fibroids:
- Monitor growth, no management required

Management of menorrhagia:

  • Levonorgestrel
  • Mefenamic acid
  • Tranexamic acid
  • COCP

Treatment to remove fibroids:

  • Myomectomy if patient wishes to maintain fertility
  • GnRH agonists can be used beforehand to shrink them
  • Hysterectomy
170
Q

Fibroids:

What is red degeneration of a fibroid?

A

Haemorrhage into fibroid, usually occurring during pregnancy (affects 5% of pregnancies, very rare in non-pregnant women)

171
Q

Fibroids:

How does red degeneration of a fibroid present?

A
  • Acute-onset constant abdominal pain localising to fibroid
  • Rebound tenderness
  • Fibroid enlarging → may become palpable
  • Tachycardia, tachypnoea
  • Fever

Not generally hemodynamically unstable or hypoxic

172
Q

Endometrial cancer:

Risk factors?

A
  • Unopposed oestrogens (HRT, obesity)
  • Nulliparity
  • Early menarche, late menopause
  • PCOS
  • Tamoxifen

Multiparity and COCP use are protective as they decrease the number of uterine cycles

173
Q

Endometrial cancer:

Clinical features?

A
  • 𝗣𝗼𝘀𝘁-𝗺𝗲𝗻𝗼𝗽𝗮𝘂𝘀𝗮𝗹 𝗯𝗹𝗲𝗲𝗱𝗶𝗻𝗴 (up to 90%)
  • Irregular or intermenstrual bleeding if pre-menopausal
  • Examination typically normal
174
Q

Endometrial cancer:

Investigations?

A
  • Any woman >55 years old with post-menopausal bleeding should have a 2ww referral

TVUS:

  • First-line investigation; can also identify benign causes of bleeding such as polyps
  • Endometrial thickness >5mm yields a 96% chance of endometrial cancer

Next stages:

  • Endometrial biopsy: if TVUS is suspicious
  • Hysteroscopy, dilation and curettage: under GA, done if endometrial biopsy is not tolerated or is not appropriate
  • CT chest, abdomen and pelvis to stage disease
175
Q

Endometrial cancer:

Staging?

A
  1. Cancer is contained to the body of the uterus and hasn’t spread to further sites
  2. Cancer has spread through the body of the uterus and extends to the connective tissue of the cervix (the cervical stroma)
  3. Cancer has spread beyond the uterus to other sites but is still confined to the pelvis
  4. Involvement of distant metastasis
176
Q

Endometrial cancer:

Management?

A

Surgical management is mainstay:

  • Offered to all women who can tolerate surgery
  • Total abdominal hysterectomy, bilateral salpingo-oophorectomy and lymphadenectomy

Radiotherapy

  • May be given as an adjunct to surgery
  • In stage 1B or later

Chemotherapy

  • Not commonly used
  • Sometimes used in stage 3 or 4 disease
  • Has a role in palliation
177
Q

Ovarian cancer:

Risk factors?

A
  • BRCA1 and BRCA2 mutations
  • HNPCC (Lynch syndrome)
  • Many ovulations (early menarche, late menopause, nulliparity)
178
Q

Ovarian cancer:

Classification?

A

Epithelial:

  • 90% of cases
  • Serous carcinoma (70% of all cases)
  • Mucinous carcinoma
  • Endometrioid

Germ cell tumours:

  • Yolk sack tumour
  • Teratoma (multiple cell lines e.g. hair, teeth)
  • Struma ovarii (type of teratoma; ectopic thyroid tissue → secretes T4 → hyperthyroidism)
  • Dysgerminoma

Sex-cord tumours:

  • Sertoli-Lyedig cell tumour
  • Granulosa cell

Metastatic:
- Krukenberg tumour (spread from gastric carcinoma)

179
Q

Ovarian cancer:

Clinical features?

A
  • 90% asymptomatic at diagnosis (often asymptomatic adnexal mass)

Otherwise generally vague symptoms:

  • Abdominal pain and bloating
  • Abdominal and pelvic pain
  • Urinary symptoms e.g. urgency
  • Early satiety
180
Q

Ovarian cancer:

Investigations?

A
  • Initially a CA125

- If this is raised then an urgent ultrasound of the abdomen and pelvis

181
Q

Ovarian cancer:

Diagnosis?

A
  • Difficult, usually involves diagnostic laparotomy

N.B: fine needle biopsy absolutely contraindicated as may directly spread tumour cells to the peritoneum

182
Q

Ovarian cancer:

Management?

A

Usually a combination of surgery and chemotherapy

183
Q

Benign breast conditions:

Fibroadenoma clinical features?

A
  • Commonest breast mass in women < 35 years

- Well-defined, non-tender, mobile, rubbery chest mass

184
Q

Benign breast conditions:

Mastitis clinical features?

A
  • Commonest in breastfeeding mothers

- Tender, swollen, erythematous breast (usually unilateral)

185
Q

Benign breast conditions:

Fat necrosis clinical features?

A
  • Peak incidence 50 years
  • Irregularly defined periareolar breast mass
  • Skin retraction, bruising, erythema
  • Typically following minor trauma in women with large breasts
186
Q

Benign breast conditions:

Mammary duct ectasia clinical features?

A
  • Perimenopausal women
  • Unilateral greenish/bloody discharge
  • Nipple inversion
  • Firm, stable, painful mass under the nipple
187
Q

Benign breast conditions:

Investigation?

A
  • Breast lumps should still be investigated at any age

- Ultrasound scan, mammogram and/or core needle biopsy

Medicine Finals (18 decks)

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