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Phase 3a Revision > GYNAE > Flashcards

GYNAE Flashcards

1
Q

MENSTRUAL CYCLE
When is the last menstrual period?
What are the stages of the menstrual cycle?

A
  • 1st day of last period (cycle runs from 1st day of last to 1st day of next
  • Menstruation (D1-5) > proliferation (D6-14) > ovulation (D14) > secretion (D16-28)
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2
Q

MENSTRUAL CYCLE

What 2 cycles exist within the menstrual cycle?

A
  • Ovarian cycle (development of follicle + ovulation)

- Uterine cycle (functional endometrium thickens + shreds)

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3
Q

MENSTRUAL CYCLE

What happens in the menstrual and proliferative phases?

A
  • Old endometrial lining from previous cycle shed marking day 1 (lasts 5d)
  • High oestrogen > thickening of endometrium, growth of endometrial glands + emergence of spiral arteries from stratum basalis to feed the functional endometrium
  • Consistency of cervical mucus changes to make more hospitable for sperm
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4
Q

MENSTRUAL CYCLE

What happens in the follicular phase?

A
  • Independently primordial follicles mature into primary + secondary follicles with FSH receptors
  • Low oestrogen + progesterone = pulses of GnRH > LH + FSH release
  • FSH leads to follicular development + recruitment
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5
Q

MENSTRUAL CYCLE

What happens as secondary follicles grow during follicular phase?

A
  • Theca cells develop LH receptors + secrete androgens
  • Granulosa cells develop FSH receptors + secrete aromatase
  • Leads to increased oestrogen > -ve feedback on pituitary to reduce LH + FSH leading to some follicles to regress
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6
Q

MENSTRUAL CYCLE

What occurs during ovulation?

A
  • Follicle (dominant) with most FSH receptors continues developing
  • Secretes further oestrogen which at a threshold causes spike in LH (+ slight rise in FSH) causing release of ovum on day 14
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7
Q

MENSTRUAL CYCLE

What occurs during the luteal phase?

A
  • Dominant follicle > corpus luteum + luteinised granulosa cells converts cholesterol into progesterone for 10d to facilitate implantation + reduce FSH/LH + oestrogen
  • Also secretes inhibin to reduce FSH
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8
Q

MENSTRUAL CYCLE

What happens if the egg is fertilised?

A
  • Syncytiotrophoblast of embryo secretes human chorionic gonadotropin (hCG) which maintains corpus luteum
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9
Q

MENSTRUAL CYCLE

What happens if the egg is not fertilised?

A
  • hCG absence > corpus luteum degenerates into corpus albicans
  • Fall in progesterone + oestrogen causes endometrium to breakdown + menstruation occurs
  • FSH + LH levels rise
  • Stromal cells of endometrium release prostaglandins to encourage endometrium breakdown + uterine contraction
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10
Q

MENSTRUAL CYCLE

What happens in the early secretory phase of the menstrual cycle?

A
  • Progesterone mediated + signals ovulation occurred to make endometrium receptive, cause spiral arteries to grow longer + uterine glands to secrete more mucus
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11
Q

MENSTRUAL CYCLE

What happens in the late secretory phase of the menstrual cycle?

A
  • Cervical mucus thickens + less hospitable for sperm

- Decrease in oestrogen + progesterone > spiral arteries collapse + constrict + functional layer prepares to shred

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12
Q

1* AMENORRHOEA

What is primary amenorrhoea?

A

Absence of menstruation by –

  • 14y if no secondary sexual characteristics (more indicative of a chromosomal abnormality)
  • 16y with secondary sexual characteristics (breast buds)
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13
Q

1* AMENORRHOEA

What is the difference between hypogonadotrophic hypogonadism and hypergonadotrophic hypogonadism?

A
  • Deficiency in gonadotrophins (LH + FSH) stimulating ovaries due to abnormal hypothalamus or pituitary means they do not respond by producing sex hormones (oestrogen)
  • Gonads fails to respond to stimulation of gonadotrophins meaning no negative feedback + increasing amounts of FSH/LH
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14
Q

1* AMENORRHOEA

What are some causes of hypogonadotrophic hypogonadism?

A
  • Constitutional delay (temporary delay, no pathology, ?FHx)
  • Hypopituitarism
  • Kallmann’s (failure to start puberty + anosmia)
  • Excessive exercise, dieting or stress causes hypothalamic failure
  • Endo = Cushing’s, prolactinoma, thyroid
  • Damage (cancer, surgery)
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15
Q

1* AMENORRHOEA

What are some causes of hypergonadotrophic hypogonadism?

A
  • Turner’s syndrome XO
  • Congenital absence of ovaries
  • Previous damage to gonads (torsion, cancer, infections like mumps)
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16
Q

1* AMENORRHOEA

What are some other causes of primary amenorrhoea and how may they present?

A
  • Congenital adrenal hyperplasia (tall, deep voice, facial hair)
  • Androgen insensitivity syndrome (46XY but female phenotype)
  • Congenital malformations of genital tract (if ovaries unaffected = secondary sexual characteristics but no menses)
  • Gonadal dysgenesis (no ovaries or uterus form)
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17
Q

1* AMENORRHOEA

What are some first line investigations for primary amenorrhoea?

A
  • Examination = signs of puberty, PV exam, BMI, visual fields
  • FBC + ferritin (anaemia), U+E for CKD, anti-TTG for coeliac, urinary beta-hCG crucial
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18
Q

1* AMENORRHOEA

What hormonal blood tests would you do for primary amenorrhoea?

A
  • FSH + LH (low or high)
  • TFTs, prolactin (if indicated)
  • Free androgens raised in PCOS, AIS + CAH
  • Insulin-like growth factor I used for screening for GH deficiency
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19
Q

1* AMENORRHOEA

What other investigations may be useful for primary amenorrhoea?

A
  • XR of wrist to assess bone age + Dx constitutional delay
  • Pelvic USS for structural causes
  • ?MRI head if pituitary
  • Karyotyping for Turner’s syndrome, AIS
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20
Q

1* AMENORRHOEA
What is the management of…

i) constitutional delay?
ii) ovarian causes (PCOS, damage/absence of ovaries)
iii) genital tract abnormalities?
iv) pituitary tumour?
v) stress?

A

i) May only require reassurance + observation
ii) COCP can induce regular menstruation + prevent Sx of oestrogen deficiency
iii) Surgery
iv) Surgery, chemo, radio or bromocriptine if prolactinoma
v) CBT, healthy weight gain, stress reduction

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21
Q

1* AMENORRHOEA

What is the management of hypogonadotrophic hypogonadism?

A
  • Pulsatile GnRH can induce ovulation, menstruation + potentially fertility
  • COCP if pregnancy not wanted to replace sex hormones, induce regular menstruation + prevent Sx of oestrogen deficiency
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22
Q

2* AMENORRHOEA
What is secondary amenorrhoea?
What is oligomenorrhoea?

A
  • Previously normal menstruation ceases for >3m in a non-pregnancy woman
  • Where menses are >35d apart (up to 6m), can be ovarian normality but exclude PCOS
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23
Q

2* AMENORRHOEA

What are the causes of secondary amenorrhoea?

A
  • Pregnancy (most common), breastfeeding, menopause (physiological)
  • Iatrogenic (contraception)
  • Hypothalamic/pituitary
  • Ovarian causes (PCOS, POI)
  • Thyroid, uterine pathology (Asherman’s)
  • Excessive exercise, stress or eating disorders
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24
Q

2* AMENORRHOEA

What are the hypothalamic or pituitary causes of secondary amenorrhoea?

A
  • Sheehan’s syndrome = pituitary necrosis following PPH
  • Pituitary tumour like prolactinoma leading to hyperprolactinaemia which prevents GnRH
  • Trauma, radiotherapy or surgery
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25
Q

2* AMENORRHOEA

How does excessive stress or eating disorders cause secondary amenorrhoea?

A
  • Hypothalamus reduces GnRH in times of stress > hypogonadotrophic hypogonadism to prevent pregnancy in adverse situations
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26
Q

2* AMENORRHOEA

What hormonal tests would you do in secondary amenorrhoea?

A
  • Urine/blood beta-hCG
  • High FSH (POI)
  • Low FSH/LH (hypgonadotrophic hypogonadism)
  • High LH or LH:FSH ratio suggests PCOS
  • Free androgen raised in PCOS
  • Mid-luteal (day 21) progesterone to check ovulation happened
  • Prolactin + TFTs if indicated
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27
Q

2* AMENORRHOEA

What other investigations may you do in secondary amenorrhoea?

A
  • Pelvic USS to Dx PCOS

- MRI head if ?pituitary tumour

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28
Q

2* AMENORRHOEA
What is the management of…

i) hyperprolactinaemia?
ii) hypothalamic failure?

A

i) Bromocriptine or cabergoline (dopamine agonists)

ii) GnRH replacement

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29
Q

CONGENITAL STRUCTURES
What are congenital structural abnormalities and what are the causes?
What can it lead to?

A
  • Abnormal development of pelvic organs prior to birth, may be result of faulty genes or occur randomly in otherwise healthy people
  • Menstrual, sexual + reproductive problems
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30
Q

CONGENITAL STRUCTURES

What is the basic embryology of the female genital tract?

A
  • Upper third of vagina, cervix, uterus + fallopian tubes develop from paramesonpehric (Mullerian) ducts
  • Errors in their development can lead to congenital structural abnormalities
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31
Q

CONGENITAL STRUCTURES

Give 3 examples of congenital structural abnormalities

A
  • Bicornuate uterus
  • Transverse vaginal septae
  • Vaginal hypoplasia + agenesis
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32
Q

CONGENITAL STRUCTURES
What is bicornuate uterus?
Associations?

A
  • 2 horns to uterus giving heart-shape on pelvic USS

- May be associated with adverse pregnancy outcomes (miscarriage, premature birth, malpresentation)

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33
Q

CONGENITAL STRUCTURES

What is a transverse vaginal septum?

A
  • Septum (wall) forms transversely across the vagina, can be perforate (with a hole) or imperforate (completely sealed)
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34
Q

CONGENITAL STRUCTURES

How does transverse vaginal septae present?

A
  • Perforate = still menstruate but difficulty with intercourse + tampon use
  • Imperforate = cyclical pelvic Sx but no menses as sealed, can lead to endometriosis by retrograde menstruation
  • May have infertility + pregnancy related issues
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35
Q

CONGENITAL STRUCTURES

What is the management of transverse vaginal septae?

A
  • Dx by examination, USS or MRI with surgical correction

- Main complications of surgery are vaginal stenosis or recurrence

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36
Q

CONGENITAL STRUCTURES
What is vaginal hypoplasia and agenesis
What causes it?

A
  • Hypoplasia = abnormally small vagina
  • Agenesis = absent
  • Failure of Mullerian ducts to develop properly + may be associated with absent uterus + cervix
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37
Q

CONGENITAL STRUCTURES
In vaginal hypoplasia and agenesis what structure is not affected?
What is the management?

A
  • Ovaries – leading to normal female sex hormones

- Prolonged period with vaginal dilatation for adequate size or surgery

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38
Q

MENORRHAGIA

What is menorrhagia?

A
  • Heavy menstrual bleeding that occurs at expected intervals of the menstrual cycle + interferes with QOL (no measurable quantity)
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39
Q

MENORRHAGIA

What are some causes of menorrhagia?

A
  • Unknown = dysfunctional uterine bleeding
  • Fibroids (most common cause in gynae)
  • Bleeding disorder (vWD)
  • Hypothyroidism
  • Polyps, endometriosis, adenomyosis, PID, contraceptives (IUD)
  • Endometrial hyperplasia or cancer
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40
Q

MENORRHAGIA

What are some investigations for menorrhagia?

A
  • Bimanual exam (?fibroids if bulky non-tender, ?adenomyosis if bulky tender ‘boggy’)
  • FBC for ALL women, ferritin (anaemic), TFTs, clotting screen
  • STI screen
  • Pelvic (TV>TA) USS
  • Hysteroscopy ± endometrial biopsy if ?endometrial pathology
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41
Q

FIBROIDS

What are fibroids?

A
  • Benign tumours of the smooth muscle of the uterus (uterine leiomyomas)
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42
Q

FIBROIDS

What are the different types of fibroids?

A
  • Intramural (most common) = within the myometrium
  • Subserosal = >50% fibroid mass extends outside uterine contours
  • Submucosal = >50% projection into the endometrial cavity
  • Subserosal + submucosal can be pedunculated (on stalk = risk of torsion)
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43
Q

FIBROIDS
What are the issues with…

i) intramural fibroids?
ii) subserosal fibroids?

A

i) As they grow, they change the shape + distort the uterus

ii) Grow outwards + can become very large, filling the abdominal cavity

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44
Q

FIBROIDS

What can cause fibroids?

A
  • Oestrogen dependent so grow in response to it (rare before puberty or after menopause)
  • Associated with mutation in gene for fumarate hydratase
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45
Q

FIBROIDS

What are some risk factors for fibroids?

A
  • Afro-Caribbean
  • Obesity
  • Early menarche
  • FHx
  • Increasing age (until menopause)
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46
Q

FIBROIDS

What is the clinical presentation of fibroids?

A
  • Menorrhagia (#1)
  • Prolonged menstruation, deep dyspareunia
  • Lower abdo cramping pain (worse during menstruation)
  • Bloating
  • Urinary or bowel Sx due to pelvic pressure or fullness
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47
Q

FIBROIDS

What are some investigations for fibroids?

A
  • Abdo + bimanual exam = palpable pelvic mass or bulky non-tender uterus
  • FBC for ALL women (?Fe anaemia)
  • Pelvic (TV>TA) USS for larger fibroids
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48
Q

FIBROIDS

What are some complications of fibroids?

A
  • Red degeneration
  • Benign calcification if centre of larger fibroids not receiving adequate blood supply
  • Reduced fertility (submucosal interfere with implantation)
  • Obstetric issues (miscarriage, premature labour)
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49
Q

FIBROIDS

What is red degeneration of fibroids?

A
  • Ischaemia, infarction + necrosis of fibroid due to disrupted blood supply
  • Fibroids sensitive to oestrogen so can grow rapidly in presence (like pregnancy) + outgrow their blood supply > ischaemia
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50
Q

FIBROIDS

How does red degeneration of fibroids present and what is the management?

A
  • Low-grade fever, pain + vomiting (classically in pregnant woman)
  • Supportive management like analgesia, fluids
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51
Q

FIBROIDS

How is the management of fibroids split?

A
  • Fibroids <3cm
  • Fibroids >3cm (with referral to gynae for investigation + management)
  • Also split into non-hormonal + hormonal depending on if woman wants to get pregnant
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52
Q

FIBROIDS

What is the first line non-hormonal management of fibroids <3cm?

A
  • Tranexamic acid (antifibrinolytic) taken during bleeding to reduce it
  • Mefenamic acid (NSAID) to reduce bleeding + pain
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53
Q

FIBROIDS

What is the first line hormonal management of fibroids <3cm?

A
  • Mirena coil is 1st line (fibroids <3cm with no uterus distortion)
  • 2nd = COCP triphasing (back-to-back for 3m then break)
  • Cyclical oral progestogens
  • Norethisterone 5mg TDS can be used short-term to rapidly stop menorrhagia from 3d before period until bleeding acceptable
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54
Q

FIBROIDS

What is the management of fibroids <3cm that fail medical treatment or are severe?

A
  • Surgery
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55
Q

FIBROIDS

What is the management of fibroids >3cm?

A
  • Same medical Mx but surgery offered too
  • GnRH agonists (goserelin) can be given to shrink fibroids by inducing menopausal state (reduced oestrogen) in short-term (can demineralise bone) for surgery
  • Selective progesterone receptor modulators (SPRMS) like ulipristal acetate can be used instead to avoid SEs
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56
Q

FIBROIDS

What are the 5 main surgical options of managing fibroids?

A
  • Trans-cervical resection of fibroid via hysteroscopy
  • 2nd gen endometrial ablation
  • Uterine artery embolisation
  • Myomectomy
  • Hysterectomy
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57
Q

FIBROIDS
What is…

i) trans-cervical resection of fibroid?
ii) endometrial ablation?
iii) uterine artery embolisation?
iv) myomectomy?
v) hysterectomy?

A

i) Removal of submucosal fibroid, offered to women planning on having more children
ii) Destroys endometrium via radiofrequency ablation, non-hysteroscopic, day case
iii) Blocked arterial supply to fibroid starves of oxygen + shrinks
iv) Removal of fibroid via laparoscopy/laparotomy
v) Removal of uterus + fibroids ± oophorectomy depending on situation (last resort)

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58
Q

FIBROIDS
What management of fibroids is the only one considered to improve subfertility?
What is a risk of this management?

A
  • Myomectomy

- Avoid during pregnancy or c-section as massive haemorrhage risk

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59
Q

ADENOMYOSIS

What is adenomyosis?

A
  • Endometrial tissue inside the myometrium – oestrogen dependent
  • Can occur alone or alongside endometriosis or fibroids
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60
Q

ADENOMYOSIS

What is the epidemiology of adenomyosis?

A
  • More common in later reproductive years + those who are multiparous (contrast to fibroids)
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61
Q

ADENOMYOSIS

How does adenomyosis present?

A
  • Dysmenorrhoea, menorrhagia + dyspareunia are classic Sx
  • Cyclical pain worse as period starts but can last 2w after it stops (much longer than endometriosis)
  • May cause infertility or pregnancy-related issues
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62
Q

ADENOMYOSIS

What are the investigations for adenomyosis?

A
  • Bimanual exam = bulky + tender uterus, ‘BOGGY’
  • TVS is 1st line investigation
  • Gold standard - histological examination of uterus after hysterectomy (not always suitable though)
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63
Q

ADENOMYOSIS

What are some complications of adenomyosis?

A
  • Infertility
  • Miscarriage
  • Preterm birth
  • SGA
  • PPROM
  • Malpresentation
  • PPH
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64
Q

ADENOMYOSIS

What is the initial management of adenomyosis?

A
  • Same as fibroids or menorrhagia in general
  • TXA or mefenamic acid
  • Mirena coil 1st line if no uterus distortion
  • COCP triphasing
  • Cyclical progesterone
  • Norethisterone 5mg TDS short-term
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65
Q

ADENOMYOSIS

What is the other management of adenomyosis?

A
  • GnRH analogues like goserelin to induce menopause-like state
  • Endometrial ablation, UAE or hysterectomy (if family completed)
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66
Q

ENDOMETRIOSIS

What is endometriosis?

A
  • Presence of ectopic endometrial tissue outside the uterus
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67
Q

ENDOMETRIOSIS

Where might endometriosis occur?

A
  • Pouch of Douglas > PR bleeding
  • Uterosacral ligaments
  • Bladder + distal ureter > haematuria
  • Pelvic cavity incl. ovaries > endometrioma in ovaries
  • Less common - lungs, nose, umbilicus, previous scars (lump gets big + painful)
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68
Q

ENDOMETRIOSIS

What is the pathophysiology of endometriosis?

A
  • Cells of endometrial tissue outside uterus respond to hormones in same way > oestrogen dependent condition
  • During menstruation, endometrial tissue sheds lining + bleeds leading to irritation + inflammation of nearby tissues
  • Chronic + constant inflammation > cyclical pain
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69
Q

ENDOMETRIOSIS

What is the epidemiology of endometriosis?

A
  • Higher prevalence in infertile women

- Exclusive to women of reproductive age

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70
Q

ENDOMETRIOSIS

What are 3 theories about the cause of endometriosis?

A
  • Sampson’s = retrograde menstruation (endometrial lining flows backwards through fallopian tubes + into pelvis/peritoneum where endometrial tissue seeds itself
  • Meyer’s = metaplasia of mesothelial cells
  • Halban’s = via blood or lymphatics
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71
Q

ENDOMETRIOSIS
What are some risk factors for endometriosis?
What are some protective factors?

A
  • Early menarche, late menopause, obstruction to vaginal outflow (imperforate hymen)
  • Multiparity + COCP
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72
Q

ENDOMETRIOSIS

What is the clinical presentation of endometriosis?

A
  • Dysmenorrhoea, deep dyspareunia + cyclical chronic pelvic pain
  • Pain worse 2–3d before periods + better after
  • Cyclical bowel + bladder Sx = pain on defecation (dyschezia), dysuria, urgency
  • Sub-fertility + cyclical bleeding from various sites
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73
Q

ENDOMETRIOSIS

What are the investigation of endometriosis?

A
  • Bimanual = ?adnexal masses or tenderness, nodules in uterosacral ligaments or fixed + retroverted uterus due to adhesions
  • TVS for ovarian endometrioma (chocolate cyst) = brown fluid as old blood + tissue
  • Gold standard = laparoscopy with biopsy
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74
Q

ENDOMETRIOSIS
What might laparoscopy and biopsy show?
What is the benefit of this investigation?

A
  • White scars or brown spots = ‘powder burn’

- Added benefit of being able to remove deposits during procedure

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75
Q

ENDOMETRIOSIS

What are some complications of endometriosis?

A
  • Subfertility

- Adhesions

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76
Q

ENDOMETRIOSIS

How does endometriosis cause subfertility?

A
  • Areas of endometriosis release cytokines + harmful chemicals which can damage reproductive tract
  • Can cause reduced fallopian tube motility, scarring, bleeding, toxicity to oocyte
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77
Q

ENDOMETRIOSIS

How does endometriosis cause adhesions?

A
  • Localised bleeding + inflammation causes damage + development of scar tissue that binds the organs together (adhesions)
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78
Q

ENDOMETRIOSIS

What is the initial management of endometriosis?

A
  • NSAIDs ± paracetamol first line for Sx relief
  • COCP triphasing (can’t take for longer as if not irregular bleeding
  • POP like medroxyprogesterone acetate
  • GnRH analogues to “induce” menopause, reversible, quicker than triphasing but need HRT + only short-term as risk of osteoporosis
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79
Q

ENDOMETRIOSIS

What fertility-sparing treatments are there for endometriosis?

A
  • Laparoscopic removal of adhesions either by ablation (burning) or excision (cutting) away endometriotic tissue
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80
Q

ENDOMETRIOSIS

What is the last resort treatment of endometriosis?

A
  • Hysterectomy ± bilateral salpingo-oopherectomy as no ovaries = no cycle
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81
Q

PCOS

What is polycystic ovarian syndrome (PCOS)?

A
  • Syndrome of excess androgen production by theca cells of ovaries due to hyperinsulinaemia + increased LH levels (due to pituitary production increase, genetics like Turner’s or Klinefelter’s)
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82
Q

PCOS

How does insulin resistance contribute to PCOS?

A
  • Insulin resistance = pancreas produces more insulin
  • Insulin mimics action of insulin-like growth factor 1 which augments androgen production by theca cells in response to LH
  • Higher insulin = higher androgens (testosterone)
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83
Q

PCOS

How does high insulin levels contribute to PCOS?

A
  • Insulin suppresses sex hormone-binding globulin (SHBG) produced by liver which normally binds to androgens + suppresses their function further promoting hyperandrogenism
  • Also contribute to halting development of follicles in ovaries > anovulation + multiple partially developed follicles (polycystic ovaries)
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84
Q

PCOS

What are the 3 main presenting features of PCOS?

A
  • Hyperandrogenism
  • Insulin resistance
  • Oligo or amenorrhoea + sub/infertility
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85
Q

PCOS

How does hyperandrogenism present in PCOS?

A
  • Acne, hirsutism, deep voice, male-pattern hair loss

- Hirsutism is growth of thick, dark hair often in male pattern (facial hair)

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86
Q

PCOS

What are some differentials of hirustism?

A
  • Ovarian or adrenal tumours that secrete androgens
  • Cushing’s syndrome
  • CAH
  • Iatrogenic (steroids, phenytoin)
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87
Q

PCOS

How does insulin resistance present?

A
  • Obesity, acanthosis nigricans (thickened, rough skin often axilla + elbows with velvety texture), psychological Sx
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88
Q

PCOS

What diagnostic criteria is used in PCOS?

A

Rotterdam criteria (≥2) –

  • Oligo- or anovulation (may present as oligo- or amenorrhoea)
  • Hyperandrogenism (biochemical or clinical)
  • Polycystic ovaries (≥12) or ovarian volume >10cm^3 on USS
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89
Q

PCOS

What hormone tests may be used in PCOS?

A
  • Testosterone (raised)
  • SHBG (low)
  • LH (raised) + raised LH:FSH ratio (LH>FSH)
  • Prolactin (normal), TFTs (exclude causes)
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90
Q

PCOS

What other investigation may be useful at indicating PCOS?

A

2h 75g OTT for DM –

  • IFG = 6.1–6.9mmol/L
  • IGT (at 2h) = 7.8–11.1
  • Diabetes (at 2h) = >11.1
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91
Q

PCOS
What is the gold standard for visualising the ovaries?
What might it show?

A
  • TVS
  • “String of pearls” appearance where follicles arranged around periphery of ovary (≥12 cysts or >10cm^3 ovarian volume)
  • Can also visualise endometrial thickness
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92
Q

PCOS

What are some associations and complications of PCOS?

A
  • DM, CVD + hypercholesterolaemia
  • Obstructive sleep apnoea, MH issues, sexual problems
  • Endometrial hyperplasia or cancer
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93
Q

PCOS

Why does PCOS increase risk of endometrial hyperplasia + cancer?

A
  • Oligo/anovulation means endometrial lining continues proliferating with unopposed oestrogen as no corpus luteum releasing progesterone
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94
Q

PCOS

What is the most crucial part of PCOS management?

A
  • Weight loss as can improve overall condition
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95
Q

PCOS

How is the risks of obesity, T2DM, CVD etc. managed in PCOS?

A
  • Lifestyle > diet + exercise, weight loss to reduce insulin resistance, smoking cessation
  • Orlistat (lipase inhibitor that stops fat absorption in intestines) may be given to assist weight loss if BMI >30kg/^m2
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96
Q

PCOS
What are the PCOS risk factors for endometrial cancer?
How is the risk of endometrial cancer managed in PCOS?

A
  • Obesity, DM, insulin resistance, amenorrhoea
  • Mirena coil for continuous endometrial protection
  • Induce withdrawal bleed AT LEAST every 3m with COCP or cyclical progesterones medroxyprogesterone 10mg 14d)
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97
Q

PCOS

How is infertility managed in PCOS?

A
  • Weight loss initial step to restore regular ovulation
  • Clomiphene to induce ovulation
  • Metformin may help (+ helps insulin resistance)
  • Laparoscopic ovarian drilling or IVF last resort
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98
Q

PCOS

How is hirsutism + acne managed?

A
  • Hair removal cream, topical eflornithine to treat facial hirsutism
  • Co-cyprindiol is COCP licensed for hirsutism + acne as anti-androgen effect but only used for 3m as increased VTE risk
  • Spironolactone by specialist (mineralocorticoid antagonist with anti-androgen effects)
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99
Q

BREAST CANCER
What is the pre-malignant form of breast cancer?
How is it detected?
What is the pathology?

A
  • Non-invasive ductal carcinoma in situ (DCIS)
  • Asymptomatic on screening
  • Epithelial lining of breast ducts thickens as cells proliferate, often with central necrosis
  • Microcalcification on mammography, unifocal lesion in one area of breast
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100
Q

BREAST CANCER

What are the 2 most common histological types of invasive breast cancer?

A
  • Invasive ductal carcinoma (70%) = invaded basement membrane, grows as little hard nots in breast
  • Lobular carcinoma (10%) = harder to feel, less likely to be visible on mammography, more diffuse so difficult to excise
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101
Q

BREAST CANCER

What are some other types of breast cancer?

A
  • Inflammatory breast cancer (presents like mastitis, no Abx response)
  • Medullary cancers (younger)
  • Colloid/mucoid cancers (elderly)
  • Breast sarcomas, phyllodes tumour + lymphoma rare
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102
Q

BREAST CANCER

What is Paget’s disease of the nipple?

A
  • Eczematous change of nipple due to underlying malignancy (invasive or in-situ)
  • Suspect if nipple eczema unresolved with 2w of steroid or anti-fungal cream
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103
Q

BREAST CANCER
What causes Paget’s disease of the nipple?
What is the management?

A
  • Infiltration of tumours cells through the ducts onto nipple surface where they infiltrate the epidermis
  • Needs biopsy, excision via mastectomy or central (nipple excising) wide local excision
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104
Q

BREAST CANCER

What is the epidemiology of breast cancer?

A
  • 1 in 8 women will develop breast cancer in their lifetime

- Most common cancer in women + second most common cause of death

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105
Q

BREAST CANCER

What are some modifiable risk factors of breast cancer?

A
  • Weight
  • Exercise
  • Smoking
  • Alcohol
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106
Q

BREAST CANCER

What are some non-modifiable risk factors of breast cancer?

A
  • Female (99%)
  • Breast density
  • Age of menarche + menopause
  • BRCA1/2 status + FHx
  • Increasing age
  • Nulliparous
  • Not breastfeeding
  • HRT use >5y
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107
Q

BREAST CANCER

What are some protective factors of breast cancer?

A
  • Breastfeeding
  • Multiparity
  • Late menarche + early menopause
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108
Q

BREAST CANCER

What are the 2 main genes involved in breast cancer and how do they act?

A
  • BRCA1 = mutation of C17, 60-80% lifetime risk, stronger incidence
  • BRCA2 = mutation of C13, 45% lifetime risk
  • Tumour suppression genes that act as inhibitors of cellular growth
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109
Q

BREAST CANCER

What are some other genetic mutations associated with breast cancer?

A
  • TP53 (Li Fraumeni)

- Peutz-Jeghers

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110
Q

BREAST CANCER

What is the classic clinical presentation of breast cancer?

A
  • Normal appearing breast with palpable painless lump
  • Pain + tenderness uncommon
  • Visually = nipple inversion, bloody nipple discharge
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111
Q

BREAST CANCER

What are some clinical signs of breast cancer?

A
  • Hard, irregular, painless, fixed lesions tethered to skin or chest wall
  • Indrawn nipple, peau d’orange (skin tethering), oedema or erythema
  • Palpable axillary nodes (axillary > supraclavicular > infraclavicular > neck)
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112
Q

BREAST CANCER
What warrants an urgent 2ww cancer referral?
What happens under the 2ww referal?

A
  • ≥30 with unexplained breast lump ± pain
  • ≥50 with discharge, retraction or other change of concern
  • Triple assessment
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113
Q

BREAST CANCER
What is the triple assessment?
What happens at end?

A
  • Clinical assessment (Hx + Examination)
  • Imaging (<35 USS as dense tissue, >35 USS + mammography)
  • Biopsy (histology + cytology) with core needle biopsy (or fine needle aspiration)
  • Each scored /5 (1=ok, 5=malignant), aim for score concordance (repeat test if one really high)
  • Pt discussed + reviewed in breast MDT
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114
Q

BREAST CANCER

What imaging choices are there for investigating breast cancer and what would influence your choice?

A
  • Mammography, high resolution USS (good at Dx + targeting biopsy)
  • MRI (good assessment of implants, dense breasts or high-risk screening)
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115
Q

BREAST CANCER

If someone has breast cancer, what would you like to check now?

A
  • Oestrogen receptor (ER)
  • Human epidermal growth factor 2 (HER2)
  • Progesterone
  • Ki67 status
  • Nottingham Prognostic index = grade, size + nodal status to predict survival
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116
Q

BREAST CANCER

What staging is used in breast cancer?

A
  • CT CAP for TNM staging
  • T1 = confined to breast, mobile
  • T2 = confined to breast + LN in ipsilateral axilla
  • T3 = fixed to muscle, locally advanced disease
  • T4 = fixed to chest wall, metastatic
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117
Q

BREAST CANCER

What tumour marker can be used to monitor response to breast cancer treatment and disease recurrence?

A
  • CA 15-3
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118
Q

BREAST CANCER
What is the NHS breast screening programme?
What is the process?

A
  • Women 50–70 invited triennially for dual-view mammography
  • Breast pressed between 2 plates to flatten + improve resolution
  • Cranio-caudal (CC) + medio-lateral oblique (MLO) views
  • Graded 1 (normal) to 5 (likely malignant)
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119
Q

BREAST CANCER

What are the pros and cons of breast cancer screening?

A
  • Earlier detection, reduces morbidity + mortality, detects asymptomatic cancers before present, not overly invasive
  • ?Overdiagnosis (frail women Dx with small low-grade cancers), anxiety if recalled, low dose XR > small amount of malignancies
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120
Q

BREAST CANCER

What are some reasons that a woman may be recalled for further views, USS or biopsy?

A
  • Mass (well or poorly defined, rough edges, spiculated = carcinoma)
  • Microcalcification (associated with DCIS)
  • Parenchymal deformity
  • Asymmetrical density
  • Clinical or technical recall
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121
Q

BREAST CANCER

What is the high risk screening for breast cancer?

A

BRCA1/2 screening –

  • 30–40 annual MRI
  • 40–50 annual MRI + mammograms
  • 50–60 annual mammogram (+ MRI if dense breasts)
  • 60–70 triennial mammograms (+ MRI if dense breasts)
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122
Q

BREAST CANCER

What is the management of BRCA1/2 women?

A
  • Genetic pedigree to identify at risk
  • Additional screening, lifestyle advice
  • ?Prophylactic tamoxifen or aromatase inhibitors
  • ?Risk reducing salpingo-oopherectomy or mastectomy
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123
Q

BREAST CANCER

What are some complications of breast cancer?

A
  • Locally advanced (rare), try shrink with radio, chemo, or hormone therapy to try operate, salvage surgery + stage for mets
  • Metastatic breast cancer (2Ls 2Bs) = Lungs, Liver, Bones, Brain
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124
Q

BREAST CANCER
How may metastatic breast cancer present?
What is the management?

A
  • Bony pain or #

- Bisphosphonates + denosumab, radio/chemo + Sx control

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125
Q

BREAST CANCER
What is breast conservation treatment?
What are the indications?
What factors affect the outcome?

A
  • Lumpectomy or wide local excision where remaining breast tissue gets localised radiotherapy
  • Small tumour relative to breast (<25%), DCIS, no previous radiotherapy, not underneath nipple, pt choice
  • Tumour size relative to breast, position of tumour in breast (lateral more favourable), radiotherapy fibrosis
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126
Q

BREAST CANCER
What is mastectomy?
What are the indications?

A
  • Uni or bilateral removal of breast
  • Large tumour relative to breast size, >1 cancer in same breast, tumour under nipple, immediate or delayed reconstruction, pt choice
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127
Q

BREAST CANCER
What is full axillary clearance?
What are the indications + benefits?
What are the risks?

A
  • Removal of all glands
  • Glands clinically involved, good control, no need for further surgery or axillary radiotherapy
  • 10% lymphoedema, high complication rate (seromas, arm stiffness, drains, axillary numbness), extends surgical time
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128
Q

BREAST CANCER
What is limited axillary surgery?
What are the benefits?

A
  • Clinically normal glands but removal of targeted ‘hot’ node by sentinel LN biopsy or blindly removes 4–6 nodes
  • Day surgery, no significant complications, no drains, no effect on mortality but may need full clearance if +ve
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129
Q

BREAST CANCER

What adjuvant endocrine therapy may be given to women?

A
  • All ER+ve women need endocrine therapy as increases survival
  • Bisphosphonates to reduce rate of bone mets in ER+ve
  • Trastuzumab (Herceptin) used in HER2+ve + chemo
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130
Q

BREAST CANCER
What endocrine therapy is given if…

i) pre-menopausal?
ii) post-menopausal?

A

i) Tamoxifen –inhibits oestrogen receptor on breast cancer cells
ii) Anastrozole (aromatase inhibitors) – inhibits aromatase which converts androgens > oestrogen

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131
Q

BREAST CANCER
What are the important side effects of…

i) tamoxifen?
ii) anastrozole?

A

i) Menopausal Sx, rarely VTE + endometrial cancer as acts on oestrogen receptors there
ii) Hot flushes, reduced bone density, joint pains but no rare SEs like tamoxifen

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132
Q

BREAST CANCER

What other adjuvant treatment may be offered?

A
  • Radiotherapy = always after WLE, sometimes after mastectomy if high risk (cons = skin viability risk, fibrosis, fat necrosis, loss of elasticity)
  • Chemotherapy = high/risk or aggressive disease (HER2+ve, ER-ve, node+ve)
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133
Q

BREAST CANCER
Reconstruction surgery can either be primary (immediately) or delayed.
What are the pros and cons of primary reconstruction?

A
  • Increased skin preservation options, reduced psychological trauma
  • May delay chemo/radiotherapy if complications, radiotherapy may ruin results (fibrosis)
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134
Q

BREAST CANCER
Reconstruction surgery can either be primary (immediately) or delayed.
What are the pros and cons of delayed reconstruction?

A
  • Minimal risks of delay in adjuvant therapies, healthy tissue used to recreate breast
  • Limited skin preservation options, psychological impact (no breast)
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135
Q

BREAST CANCER

What are some options for breast mound recreation?

A
  • Implant based (implant alone or implant augmented latissimus dorsi)
  • Autologous (own tissues) such as TRAM flap, lat dorsi
  • Lat dorsi uses muscle ± skin ± fat but C/I if chronic back pain or physical hobby
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136
Q

BREAST CANCER

What are some risks with breast mound recreation?

A
  • Capsule formation
  • Shape changes with age, gravity
  • Rupture
  • Infection
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137
Q

BENIGN BREAST DISEASE

What are 3 main causes of benign breast lumps?

A
  • Nodularity
  • Fibroadenoma
  • Breast cyst
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138
Q

BENIGN BREAST DISEASE
What is nodularity?
What is the management?

A
  • Normal variation, some ladies have lumpy breasts, often cyclical (more prominent pre-menstrual)
  • Re-examine after period as nodularity should lessen or disappear
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139
Q 
BENIGN BREAST DISEASE
What is a fibroadenoma?
What are some features?
Rule with fibroadenomas?
How does it present? Management?
A
  • Benign tumours of stromal/epithelial breast duct tissue
  • Most common benign lump in <35, most <3cm diameter
  • 1/3 shrink, 1/3 same, 1/3 enlarge
  • Very mobile on exam, reassurance + only remove if large
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140
Q

BENIGN BREAST DISEASE
What are breast cysts?
What are features of a benign cyst?
How is it managed?

A
  • Abnormal response of part of the breast to hormonal stimulation, commonly seen in 40–60y
  • Fluid not blood stained, no residual lump, same cyst does not continually refill
  • Dx confirmed on aspiration
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141
Q

BENIGN BREAST DISEASE

What are some causes of nipple discharge?

A
  • Duct ectasia
  • Duct papilloma
  • Galactorrhoea
  • Infection
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142
Q

BENIGN BREAST DISEASE

What are some features of surgically significant nipple discharge?

A
  • Persistent
  • Unilateral + unifocal
  • Spontaneous
  • Bloody or clear
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143
Q

BENIGN BREAST DISEASE

What are some differentials of bloody nipple discharge?

A
  • Duct papilloma
  • Duct ectasia
  • Occasionally invasive/in-situ Ca
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144
Q

BENIGN BREAST DISEASE
What is duct ectasia?
How does it present?
What is the management?

A
  • Ducts become dilated + fill with debris, prone to secondary infections
  • Yellow, green, thick + occasionally bloody nipple discharge
  • Expectant management
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145
Q

BENIGN BREAST DISEASE
What is duct papilloma?
How does it present?

A
  • Benign warty growth behind nipple

- Bloody or clear discharge

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146
Q

BENIGN BREAST DISEASE
What is galactorrhoea?
How does breast infection nipple discharge present?

A
  • Milky (physiological or iatrogenic)

- Purulent

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147
Q

BENIGN BREAST DISEASE

What are the 2 types of breast infection (mastitis)?

A
  • Lactational (usually peripheral in breast)

- Non-lactational (associated with duct ectasia + so central)

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148
Q

BENIGN BREAST DISEASE

What is the management of lactational mastitis?

A
  • Continue breastfeeding
  • Rx if systemically unwell with flucloxacillin or erythromycin if allergic
  • May develop abscess (lump + erythema) so need drainage
149
Q

BENIGN BREAST DISEASE

What is the management of non-lactational mastitis?

A
  • Same as lactational mastitis (flucloxacillin or erythromycin) but + metronidazole
150
Q

BENIGN BREAST DISEASE
What is the most common cause of mastitis?
What is there a caution with?

A
  • S. Aureus then anaerobes (esp. non-lactational)

- Repeated incision in non-lactational abscess as can develop mammary fistula which is difficult to treat

151
Q

BENIGN BREAST DISEASE
What is mastalgia?
What are the two types?

A
  • Breast pain
  • Cyclical = worse prior to and better after period
  • Non-cyclical (responds well to NSAIDs)
152
Q

BENIGN BREAST DISEASE

What is the management of cyclical mastalgia?

A
  • Supportive bra, reassurance, PO/topical analgesia
  • Danazol (weak androgen) but SEs = breast shrinkage, acne, weight gain
  • Tamoxifen (risk of endometrial cancer)
  • Goserelin
153
Q

BENIGN BREAST DISEASE
What is gynaecomastia?
What is a differential?

A
  • > 2cm lump of breast tissue behind male nipple

- Pseudo-gynaecomastia (deposition of fat in overweight men)

154
Q

BENIGN BREAST DISEASE

What are the two broad causes of gynaecomastia?

A
  • Physiological = oestrogen + testosterone imbalance (puberty)
  • Pathological
155
Q

BENIGN BREAST DISEASE

What are some pathological causes of gynaecomastia?

A
  • Drugs (spironolactone, oestrogen, anabolic steroids)
  • Marijuana
  • Liver failure
  • Testicular failure or tumour (Can produce beta-hCG)
156
Q

BENIGN BREAST DISEASE

What is the management of gynaecomastia?

A
  • Older men >50 exclude breast cancer by biopsy
  • Remove or reverse cause/drug
  • Reassure teenagers
157
Q

BENIGN BREAST DISEASE

When investigating breast disease, what are features of a benign disease?

A
  • Breast exam = soft + mobile mass

- Mammography = rounded mass, smooth edged, well-defined margins, low score

158
Q

CERVICAL CANCER
What is cervical cancer?
What is the histological type of cervical cancer?

A
  • Most common cancer in women <35

- Squamous cell carcinoma 80%, then adenocarcinoma (small cell rare)

159
Q

CERVICAL CANCER

What has a strong association with development of cervical cancer?

A
  • Human papillomavirus (HPV) types 16 + 18 primarily a STI

- Also associated with anal, vulval, vaginal, penis, mouth + throat cancers

160
Q

CERVICAL CANCER

What genes may be implicated in cervical cancer?

A
  • P53 + pRb are tumour suppressor genes
  • HPV produces two oncoproteins (E6 + E7)
  • E6 inhibits P53, E7 inhibits pRB
161
Q

CERVICAL CANCER

What are some risk factors for cervical cancer?

A
  • Increased risk of catching HPV = early (unsafe) sex, lots of sexual partners
  • Smoking (limits availability to clear HPV)
  • HIV
  • COCP
  • High parity
  • Previous CIN/abnormal smear or FHx
162
Q

CERVICAL CANCER

How does cervical cancer present?

A
  • Asymptomatic + smear detected
  • Abnormal PV bleeding (POSTCOITAL, intermenstrual or postmenopausal)
  • PV discharge, pelvic pain, dyspareunia
163
Q

CERVICAL CANCER

How would advanced cervical cancer present?

A
  • Menorrhagia
  • Ureteric obstruction
  • Weight loss
  • Bowel disturbance
  • Vesico-vaginal fistula
164
Q

CERVICAL CANCER

What are some initial investigations for cervical cancer?

A
  • Speculum + swabs to exclude infection
  • Abnormal cervix (ulcerated, inflamed, bleeding, visible tumour) = urgent referral for colposcopy
  • Bimanual = rough + hard cervix
165
Q

CERVICAL CANCER

How would you confirm a diagnosis of cervical cancer?

A

Colposcopy –

  • Acetic acid causes abnormal cells to appear white “acetowhite”
  • Schiller’s iodine test = healthy cells stain brown, abnormal do not stain
  • Punch biopsy or large loop excision of transformation zone (LLETZ) for histology
166
Q

CERVICAL CANCER

How is cervical cancer staged?

A

FIGO staging –

  • 1 = confined to cervix
  • 2 = invades uterus or upper 2/3 vagina
  • 3 = invades pelvic wall (e.g. ureter) or lower 1/3 vagina
  • 4 = invades beyond pelvis
167
Q

CERVICAL CANCER

What is the cervical cancer screening?

A
  • Sexually active women 25–64 (triennially 25–50, 5y 50–64) smear test
  • Exceptions = HIV pts screened annually, women with previous CIN may require additional tests
168
Q

CERVICAL CANCER

What is the process of cervical smears?

A
  • Smear test where cells collected from cervix + placed in preservation fluid for microscopy
  • Aims to identify precancerous changes (dyskaryosis) in epithelial cells of cervix for early treatment
  • Samples initially tested for high-risk HPV before examined
169
Q

CERVICAL CANCER
What is dyskaryosis?
What results would warrant investigating?

A
  • Abnormal nucleus in cell
  • Borderline/mild = test sample for HPV (-ve = routine recall, +ve = normal 6w colposcopy referral)
  • Moderate = consistent with CIN II (urgent 2w colposcopy)
  • Severe = consistent with CIN III (urgent 2w colposcopy)
170
Q

CERVICAL CANCER

How do you manage smear results?

A
  • Repeat inadequate smears within 3m or after 2 consecutive refer for colposcopy
  • HPV +ve but normal cytology = 12m, if +ve, 12m, if +ve at 24m > colposcopy (if HPV -ve then normal recall)
171
Q

CERVICAL CANCER

What is used to grade the level of dysplasia, or premalignant change, in the cells of the cervix after colposcopy?

A
  • Cervical intra-epithelial neoplasia (CIN)
  • CIN I = mild, affects 1/3 thickness of epithelial layer, likely to return to normal without Tx
  • CIN II = mod, affects 2/3 thickness of epithelial layer, likely to progress to cancer without Tx
  • CIN III or cervical carcinoma in situ = severe, v likely to progress to cancer without Tx
172
Q

CERVICAL CANCER

After treatment for CIN, when do patients have screening?

A
  • Screening at 6m for test of cure
173
Q

CERVICAL CANCER

What is the prophylaxis for cervical cancer?

A
  • Children 12–13 HPV vaccine (6+11 genital warts, 16+18 cervical cancer)
  • Cervical screening
174
Q

CERVICAL CANCER
What is the management of…

i) CIN or early stage 1A cervical cancer?
ii) Stage 1B-2A
iii) Stage 2B-4A
iv) Stage 4B

A

i) LLETZ or cone biopsy with -ve margins (maintain fertility)
ii) Radical hysterectomy + removal of pelvic LN with chemo (cisplatin) + radiotherapy
iii) Chemo + radiotherapy
iv) Combination of surgery, chemo/radio + palliative care

175
Q

CERVICAL CANCER

What is the difference between LLETZ and cone biopsy?

A
  • LLETZ = LA during colposcopy, loop of wire with electrical current to cauterise tissue
  • Cone = GA where cone-shaped piece of cervix removed with scalpel
176
Q

CERVICAL CANCER

What are the side effects of LLETZ and cone biopsy?

A
  • Bleeding + abnormal discharge weeks after, intercourse + tampon avoided as infection risk, may increase preterm labour
  • Pain, bleeding, infection, increased risk of premature labour + miscarriage
177
Q

CERVICAL ECTROPION
What is cervical ectropion?
What is it associated with?

A
  • Columnar epithelium of endocervix extends out to ectocervix
  • Endocervix cells more fragile so prone to trauma + to bleed (post-coital)
  • High oestrogen > young women, COCP, pregnancy
178
Q

CERVICAL ECTROPION

How does cervical ectropion present?

A
  • Increased vaginal discharge

- Abnormal PV bleeding (IMB + PCB)

179
Q

CERVICAL ECTROPION

How does cervical ectropion present on speculum?

A
  • Well-demarcated border between redder, velvety columnar epithelium extended from os + pale pink squamous epithelium of ectocervix
  • ‘Red ring’ around cervical os (transformation zone)
180
Q

CERVICAL ECTROPION

What is the management of cervical ectropion?

A
  • Problematic bleeding = cauterisation (silver nitrate or cold coagulation during colposcopy)
181
Q

OVARIAN CANCER
What is ovarian cancer?
When do patients present?

A
  • Cancer of ovaries, usually presents late as non-specific Sx > worse prognosis
  • ≥70% present after spread beyond pelvis (most commonly para-aortic LN + liver)
182
Q

OVARIAN CANCER

What are the 4 causes of ovarian cancer?

A
  • Epithelial cell tumours (85–90%)
  • Germ cell tumours (common in women <35)
  • Sex cord-stromal tumours (rare)
  • Metastatic tumours
183
Q

OVARIAN CANCER

What are some types of epithelial cell tumours?

A
  • Serous carcinoma (#1)

- Endometrioid, clear cell, mucinous + undifferentiated tumours too

184
Q

OVARIAN CANCER

What are germ cell tumours?

A
  • Often benign teratomas containing various tissue types like skin, teeth, hair
  • Rokitansky’s protuberance
185
Q

OVARIAN CANCER

What are sex-cord stromal tumours?

A
  • Arise from stroma (connective tissue) or sex cords (embryonic structures associated with the follicles)
  • Sertoli-Leydig + granulosa cell tumours
186
Q

OVARIAN CANCER

What are metastatic tumours?

A
  • Secondary tumours

- Krukenberg = metastasis in ovary, usually from GI (stomach) > CLASSIC “SIGNET-RING” CELLS ON HISTOLOGY

187
Q

OVARIAN CANCER

What are some risk factors of ovarian cancer?

A 
Unopposed oestrogen + increased # of ovulations –
- Early menarche
- Late menopause
- Increased age
- Endometriosis
- Obesity + smoking
Genetics (BRCA1/2, HNPCC/lynch syndrome)
188
Q

OVARIAN CANCER

Hence, what are some protective factors of ovarian cancer?

A
  • COCP
  • Early menopause
  • Breast feeding
  • Childbearing
189
Q

OVARIAN CANCER

How does ovarian cancer present?

A
  • Abdo pain, discomfort + bloating (IBS like)
  • Early satiety or loss of appetite
  • Urinary Sx as pressure on bladder (freq, urgency)
  • Change in bowel habit (obstruction later)
  • Abdo or pelvic mass, ascites
  • Germ cell = rapidly enlarging abdo mass (often causes rupture or torsion)
190
Q

OVARIAN CANCER

What warrants a 2ww gynae oncology referral?

A
  • Ascites
  • Abdo or pelvic mass (unless clearly fibroids)
  • ≥250 risk of malignancy index score
191
Q

OVARIAN CANCER

How is the risk of malignancy index calculated?

A
  • Menopausal status = 1 (pre) or 3 (post)
  • Pelvic USS findings = 1 (1 feature) or 3 (>1 feature)
  • CA-125 levels IU/mL as marker for epithelial cell ovarian cancer
192
Q

OVARIAN CANCER

What are concerning pelvic USS findings?

A
  • Ascites
  • Metastases
  • Bilateral lesions
  • Solid areas
  • Multi-locular cysts
193
Q

OVARIAN CANCER

What can cause falsely elevated CA-125 levels?

A
  • Endometriosis
  • Fibroids + adenomyosis
  • Pelvic infection
  • Pregnancy
  • Benign cysts
194
Q

OVARIAN CANCER

What other investigations should be performed in ovarian cancer?

A
  • CT CAP for Dx + staging
  • Biopsy for histology
  • Paracentesis if ascites to test ascitic fluid for cancer cells
195
Q

OVARIAN CANCER

What staging is used in ovarian cancer?

A

FIGO staging –

  • 1 = confined to ovary
  • 2 = past ovary but contained to pelvis
  • 3 = past pelvis but inside abdomen (can be microscopically in lining of abdomen)
  • 4 = spread to other organs
196
Q

OVARIAN CANCER

What is the management of ovarian cancer?

A
  • Abdominal hysterectomy + bilateral salpingo-oopherectomy

- May need bowel resections + chemo

197
Q

OVARIAN CYST

What is a cyst?

A
  • Fluid-filled sac
198
Q

OVARIAN CYST

What are the 4 types of ovarian cysts?

A
  • Functional (physiological)
  • Benign epithelial neoplasms
  • Benign germ cell neoplasms
  • Benign sex-cord stromal neoplasms
199
Q

OVARIAN CYST
What are functional cysts?
Who are they seen in?
How do they present

A
  • Cysts relating to fluctuating hormones in the menstrual cycle
  • Pre-menopause, COCP is protective (inhibits ovulation)
  • Simple cysts = 2-3cm (can be up to 10cm), clear serous liquid, smooth internal lining, thin walls
200
Q

OVARIAN CYST

What are the three types of functional cysts?

A
  • Follicular (most common)
  • Corpus luteum
  • Theca lutein
201
Q

OVARIAN CYST
What are follicular cysts?
How is it managed?

A
  • Non-rupture of dominant follicle or failure of atresia > growth
  • Commonly regress after several cycles
202
Q

OVARIAN CYST
What are corpus luteum cysts?
When are they seen?

A
  • Corpus luteum fails to breakdown, may fill with fluid or blood
  • May burst causing intraperitoneal bleeding
  • Early pregnancy
203
Q

OVARIAN CYST
What are theca lutein cysts?
Association?

A
  • Stimulates growth of follicular theca cells so usually bilateral as resting follicles on both sides
  • Overstimulation of hCG (multiple + molar pregnancy as hCG v high)
204
Q

OVARIAN CYST

What are some features of neoplastic cysts?

A
  • Often complex
  • > 10cm
  • Irregular borders
  • Internal septations appearing multi-locular
  • Heterogenous fluid
205
Q

OVARIAN CYST

What are the 2 benign epithelial neoplasms?

A
  • Serous cystadenoma (most common epithelial tumour)

- Mucinous cystadenoma

206
Q

OVARIAN CYST

How does serous cystadenoma present?

A
  • May be bilateral, filled with watery fluid, 30–50y
207
Q

OVARIAN CYST

How does mucinous cystadenoma present?

A
  • Often very large + contain mucus-like fluid
  • Pseudomyxoma peritonei where abdo cavity fills with gelatinous mucin secretions if rupture
  • 30–40y
208
Q

OVARIAN CYST

What are benign germ cell neoplasms?

A
  • Dermoid cysts or teratomas
  • Common in women <35
  • May contain various tissue types (skin, teeth, hair + bone)
  • Can be bilateral, associated with ovarian torsion as heavy
209
Q

OVARIAN CYST

What is an example of sex cord-stromal neoplasms?

A
  • Fibromas (small, solid benign fibrous tissue tumour)

- Associated with Meig’s syndrome

210
Q

OVARIAN CYST

What are some risk factors of ovarian cysts?

A
  • Obesity, tamoxifen, early menarche, infertility
  • Dermoid cysts = most common in young women, can run in families
  • Epithelial cysts = most common in post-menopausal (?malignant)
211
Q

OVARIAN CYST

What is the clinical presentation of ovarian cyst?

A
  • Unilateral dull pelvic ache + may have dyspareunia
  • Pressure effects (frequent urination or bowel movements)
  • Abdo swelling or mass (ascites suggests malignancy, ruptured mucinous cystadenoma or Meig’s syndrome)
212
Q

OVARIAN CYST
What is Meig’s syndrome?
Who is it commonly seen in?
What is the management?

A
  • Triad of fibroma, pleural effusion + ascites
  • Older women
  • Removal of fibroma = complete solution
213
Q

OVARIAN CYST

What clinical presentation would suggest ovarian cyst rupture?

A
  • Acute, sharp abdo/pelvic pain
  • PV bleed, N+V (esp. torsion)
  • Shoulder tip pain if referred diaphragmatic pain
  • If peritonitis + shock occurs (fever, syncope, low BP, high HR)
214
Q

OVARIAN CYST

What investigations should be done for ovarian cysts?

A
  • Beta-hCG to exclude uterine or ectopic
  • FBC for infection or haemorrhage
  • CA-125 if >40
  • Germ cell tumour markers if <40 with complex ovarian mass
  • Imaging (TVS or MRI abdo if larger mass)
  • Diagnostic laparoscopy (gold standard in ruptured cyst)
  • May need USS guided aspiration + cytology to confirm benign
215
Q

OVARIAN CYST

What are the germ cell tumour markers?

A
  • Lactate dehydrogenase
  • Alpha-fetoprotein
  • Human chorionic gonadotropin
216
Q

OVARIAN CYST

What are some complications of ovarian cysts?

A
  • Torsion leading to ovarian ischaemia = pain may be intermittent if untwists or stop if necrotic
  • Haemorrhage into cyst = sudden increase in size + pain (follicular + corpus luteal cysts)
  • Rupture of contents into peritoneum = peritonitis (associated with sex)
217
Q

OVARIAN CYST

What is the management of a ruptured ovarian cyst?

A
  • ABCDE approach + admission
  • Stable = analgesia, fluids
  • Unstable or bleeding = surgery (?laparotomy)
218
Q

OVARIAN CYST

What is the management of simple cysts in pre-menopausal women?

A
  • Small <5cm = likely to resolve within 3 cycles, no follow up
  • Mod 5–7cm = routine gynae referral + yearly USS
  • Large >7cm = ?MRI + surgical evaluation
219
Q

OVARIAN CYST

What is the management of post-menopausal women presenting with an ovarian cyst?

A
  • Risk of malignancy index calculation
  • Simple cysts <5cm + normal CA-125 = monitor with 4–6m USS
  • Complex cyst or raised CA-125 = 2ww gynae oncology referral
220
Q

OVARIAN CYST
What is the surgical management of ovarian cysts?
What are the indications?
What are the cautions?

A
  • Laparoscopic ovarian cystectomy ±oophorectomy
  • Persistent or enlarging cysts, Sx, ovarian torsion or Sx of rupture
  • Caution of chemical peritonitis with dermoid cysts if contents spill
221
Q

OVARIAN TORSION

What is ovarian torsion?

A
  • Ovary twists in relation to surrounding connective tissue, fallopian tube + blood supply (adnexa) leading to ischaemia ± necrosis if persists
222
Q

OVARIAN TORSION

What are some risk factors of ovarian torsion?

A
  • Pregnancy
  • Ovarian tumours/cysts
  • Previous surgery
  • Reproductive age
223
Q

OVARIAN TORSION

What is the clinical presentation of ovarian torsion?

A
  • Sudden onset, severe unilateral iliac fossa pain
  • Colicky if twists/untwists
  • May occur during exercise
  • N+V
  • Fever + pain stopping may indicate necrotic ovary
224
Q

OVARIAN TORSION

What are the investigations for ovarian torsion?

A
  • Localised tenderness ± palpable mass in pelvis
  • Beta-hCG to exclude ectopic
  • USS with colour doppler
225
Q

OVARIAN TORSION

What might USS show in ovarian torsion?

A
  • Free fluid in pelvis + oedema of ovary
  • “Whirlpool sign” = wrapping of vessels around central axis
  • Doppler studies may show lack of blood flow
226
Q

OVARIAN TORSION

What are some complications of ovarian torsion?

A
  • Delay in treatment may lead to loss of function > infertility or menopause if other ovary non-functional
  • Necrotic ovary may become infected > abscess > sepsis (or rupture causing peritonitis + adhesions)
227
Q

OVARIAN TORSION

What is the management of ovarian torsion?

A
  • Laparoscopy for definitive diagnosis + treatment
  • Untwist ovary + fix into place (detorsion)
  • Oophorectomy based on visual appearance (necrotic)
  • Analgesia + fluid resus
228
Q

ENDOMETRIAL CANCER
What is endometrial cancer?
What is the prognosis?

A
  • Cancer of endometrium (lining of uterus) = oestrogen dependent
  • 90% women are >50, good prognosis, 5-year survival in stage 1 = 80%
229
Q

ENDOMETRIAL CANCER
What is the most common histological type of endometrial cancer?
What are some others?

A
  • Adenocarcinoma (80%)

- Adenosquamous, squamous, papillary serous, clear cell + uterine sarcoma

230
Q

ENDOMETRIAL CANCER

What are some risk factors for endometrial cancer?

A

Unopposed oestrogen –

  • Obesity (adipose tissue contains aromatase)
  • Nulliparous
  • Early menarche
  • Late menopause
  • Oestrogen-only HRT
  • Tamoxifen
  • PCOS
  • Increased age
  • T2DM
  • HNPCC (Lynch syndrome)
231
Q

ENDOMETRIAL CANCER

What are some protective factors for endometrial cancer?

A
  • COCP
  • Mirena coil
  • Multiparity
  • Cigarette smoking (Seem to have anti-oestrogenic effect)
232
Q

ENDOMETRIAL CANCER

What is the clinical presentation of endometrial cancer?

A
  • PMB is endometrial cancer until proven otherwise
  • May have abnormal bleeding (PCB, IMB, menorrhagia)
  • Abnormal PV discharge + pain less commonly
233
Q

ENDOMETRIAL CANCER

What is the first line investigation for endometrial cancer?

A
  • TVS = endometrial thickness should be <4mm

- Recommended for >55 w/ unexplained PV discharge + visible haematuria

234
Q

ENDOMETRIAL CANCER

What other investigations is recommended in endometrial cancer?

A
  • Pipelle biopsy via speculum (highly sensitive so useful for exclusion in low risk)
  • Hysteroscopy with endometrial biopsy
  • 2WW urgent gynae oncology referral if PMB in ≥55y
235
Q

ENDOMETRIAL CANCER

What is the staging for endometrial cancer?

A

FIGO staging –

  • 1 = confined to endometrium + uterus
  • 2 = tumour invaded cervix
  • 3 = cancer spread to ovary, vagina, fallopian tubes or LN
  • 4 = cancer invades bladder, rectum or beyond pelvis
236
Q

ENDOMETRIAL CANCER

What is the management of stage 1 + 2 endometrial cancer?

A
  • Total abdominal hysterectomy with bilateral salpingo-oopherectomy + pelvic LN
237
Q

ENDOMETRIAL CANCER

What other treatments are there for endometrial cancer?

A
  • Surgery = radical hysterectomy ± pelvic LN
  • Radiotherapy = adjuvant (brachytherapy/external beam)
  • Chemo, progesterone therapy to slow progression of cancer
238
Q

ENDOMETRIAL POLYP
What is an endometrial polyp?
What is the main differential?

A
  • Benign growths of endometrium, some may be (pre)cancerous

- Fibroids

239
Q

ENDOMETRIAL POLYP

What are some risk factors of endometrial polyps?

A
  • Being peri or post-menopausal
  • HTN
  • Obesity
  • Tamoxifen
240
Q

ENDOMETRIAL POLYP

What is the clinical presentation of endometrial polyps?

A
  • Irregular menstrual bleeding (IMB, PMB), menorrhagia

- Infertility in younger as competing with foetus for space

241
Q

ENDOMETRIAL POLYP

What are the investigations for endometrial polyps?

A
  • TVS/TAS

- Hysteroscopy ± endometrial biopsy

242
Q

ENDOMETRIAL POLYP

What is the management of endometrial polyps?

A
  • Conservative but monitor or biopsy if concerns
  • GnRH analogues as oestrogen sensitive
  • If post-menopause or pre but symptomatic = hysteroscopic resection or morcellation of polyps
  • Hysterectomy if severe
243
Q

VULVAL CANCER
What is vulval cancer?
What is the most common histological type?

A
  • Rare compared to other cancers

- Squamous cell carcinomas (90%), malignant melanoma less common

244
Q

VULVAL CANCER

What are some risk factors for vulval cancer?

A
  • Vulval intraepithelial neoplasia (VIN) due to HPV in younger women
  • Lichen sclerosus in older women
245
Q

VULVAL CANCER

What is the clinical presentation of vulval cancer?

A
  • Vulval itching, soreness + persistent lump on labia majora
  • Ulceration, bleeding, pain (sometimes on urination)
  • May be lymphadenopathy in groin
246
Q

VULVAL CANCER

What are the investigations for vulval cancer?

A
  • Suspected = 2ww urgent gynae oncology referral

- Biopsy lesion with sentinel node biopsy to see if LN spread

247
Q

VULVAL CANCER

How is vulval cancer staged?

A

FIGO staging –

  • 1 = <2cm
  • 2 = >2cm
  • 3 = adjuvant organs or unilateral nodes
  • 4 = distant mets or bilateral nodes
248
Q

VULVAL CANCER

What is vulval intraepithelial neoplasia (VIN)?

A
  • Premalignant condition affecting squamous epithelium that can precede vulval cancer
249
Q

VULVAL CANCER

What are 2 types of VIN?

A
  • High grade squamous intraepithelial lesion = type of VIN associated with HPV typically in younger women 35–50
  • Differentiated VIN associated with lichen sclerosus
250
Q

VULVAL CANCER

What is the management of VIN?

A
  • Biopsy to Dx
  • Watch + wait with close follow up
  • Wide local excision to surgically remove lesion
  • Imiquimod cream or laser ablation
251
Q

VULVAL CANCER

What is the management of vulval cancer?

A
  • Radical or conservative surgery (WLE ± groin LN dissection)
  • Radio ± chemotherapy
252
Q 
VAGINAL CANCER
What is the most common histological type of vaginal cancer?
What causes it?
What is the prognosis like?
How does it present?
What is the management?
A
  • 90% squamous
  • HPV or metastatic spread from cervix or vulva
  • Poor prognosis, average survival at 5 years 50%
  • Bleeding or discharge, evident mass or ulcer
  • Intravaginal radiotherapy or sometimes radical surgery
253
Q

MENOPAUSE
What is menopause?
What is the average age of onset? When is it premature?

A
  • Permanent cessation of menstruation where ovarian activity ceases to function, can occur after TAH-BSO
  • Average 51, premature <40
254
Q

MENOPAUSE

What is perimenopause?

A
  • Time around menopause where woman may have vasomotor Sx + irregular periods
  • Includes time leading up to LMP + 12m after
255
Q

MENOPAUSE

What is the physiology of menopause?

A
  • Starts with decline in development of ovarian follicles
  • Less oestrogen + progesterone production
  • Absence of -ve feedback loop so FSH + LH rises
  • Falling follicular development = anovulation so irregular menstrual cycles
  • Low oestrogen = endometrium does not develop so amenorrhoea + perimenopausal Sx
256
Q

MENOPAUSE

What are the peri-menopausal symptoms?

A
  • Vasomotor = hot flushes, night sweats, impact on QOL
  • General = mood swings, decreased libido, vaginal dryness, headache, dry skin, loss of energy, joint aches, muscles pains, irregular periods
257
Q

MENOPAUSE

What are some medium-term presentations of menopause?

A
  • Urogenital atrophy leading to dyspareunia, recurrent UTIs + PMB
258
Q

MENOPAUSE
Why does urogenital atrophy occur?
What can it lead to?

A
  • Urogenital tract has oestrogen receptors + continual stimulation keep it strong + supple
  • Urinary incontinence + pelvic organ prolapse
259
Q

MENOPAUSE

What are the investigations for menopause?

A
  • Retrospective diagnosis after 12m of amenorrhoea in women >45y
  • NICE recommends FSH (high) blood test in women <40 with suspected premature menopause or women 40–45 with menopausal Sx or change in menstrual cycle
260
Q

MENOPAUSE

What are the long-term complications of menopause?

A
  • Osteoporosis as oestrogen inhibits osteoclasts + can become hyperactive
  • CVD, stroke (esp. in early menopause) + dementia
261
Q

MENOPAUSE
When is contraception recommended in relation menopause?
Why?

A
  • 2y after LMP in <50, 1y after LMP in >50

- Pregnancy >40 has increased risks + complications

262
Q

MENOPAUSE
What contraception is suitable in older women?
How do hormonal contraceptives affect the menopause?

A
  • UKMEC1 = barrier, IUS/IUD, POP, long-acting progesterone (<45), sterilisation
  • UKMEC2 = COCP after 40 used until 50, try ones with levonorgestrel or norethisterone as lower VTE risk
  • They don’t but may mask Sx
263
Q

MENOPAUSE

What is the initial management of menopause?

A

Lifestyle –

  • Vasomotor symptoms last 2-5y without intervention so ?no treatment
  • Regular exercise can improve hot flushes, mood + cognitive Sx
  • Good sleep hygiene can improve sleep disturbance
264
Q

MENOPAUSE

What is the management of menopause in more severe cases?

A
  • HRT first-line for vaso-motor Sx as most effective
  • Clonidine (alpha adrenergic receptor agonist) second line with low-dose antidepressants like venlafaxine (not C/I in breast cancer Tx) or fluoxetine
  • CBT
  • Vaginal oestrogen cream/tablets + moisturisers for dryness
265
Q

MENOPAUSE

What is the mechanism of action of clonidine?

A
  • Alpha-adrenergic receptor agonist
266
Q

HRT
What is Hormone Replacement Therapy (HRT)?
How does this compare to the COCP?

A
  • Treatment to alleviate Sx associated with menopause by giving physiological dose of oestrogen as replacement for what body is used to
  • COCP gives a supraphysiological dose of oestrogen
267
Q

HRT

What are some indications for HRT?

A
  • Replacing hormones in POI even without Sx
  • Reducing vasomotor + other Sx in menopause
  • Reduce osteoporosis risk in women <60
268
Q

HRT

What are some benefits of HRT?

A
  • Improved Sx control
  • Improved QOL
  • Reduced risk of osteoporosis
269
Q

HRT

What are some risks with HRT?

A
  • Increased risk of breast cancer by adding progesterone
  • Increased risk of endometrial cancer by oestrogen alone
  • Increased risk of VTE
  • Increased risk of stroke + IHD
270
Q

HRT
How can the HRT risks be managed for…

i) breast cancer?
ii) endometrial cancer?
iii) VTE?
iv) IHD?

A

i) Local (Mirena) instead of systemic progesterones, risk declines after 5y stopping
ii) Add progesterone (esp Mirena) to prevent endometrial hyperplasia
iii) Transdermal patch
iv) Do not take for >10y after menopause

271
Q

HRT

What are some contraindications to HRT?

A
  • Undiagnosed PV bleeding
  • Current or past breast cancer
  • Any oestrogen sensitive cancer (endometrial)
272
Q

HRT
What HRT would you give to…

i) woman without uterus?
ii) woman with uterus?
iii) woman with period within past 12m?
iv) woman with period >12m ago?

A

i) Continuous oestrogen-only HRT
ii) Add progesterone (combined HRT)
iii) Cyclical combined HRT
iv) Continuous combined HRT

273
Q

HRT

What preparations of HRT are there?

A
  • Pessary + cream (local Sx like bleeding, pain, UTI), transdermal patch, tablets
  • Tibolone is a synthetic steroid hormone that acts as continuous combined (only used >12m from LMP)
274
Q

HRT
When would patches be used for HRT?
What is the most common side effect?

A
  • Pt choice
  • GI upset (Crohn’s)
  • VTE risk
  • Co-morbidities like HTN
  • Skin irritation #1
275
Q

HRT

How can oestrogen be given?

A
  • Tablets or transdermal (patches or gels)
276
Q

HRT

When would you use cyclical progesterone compared to continuous?

A
  • Perimenopausal women to allow monthly breakthrough bleed during oestrogen-only part of cycle (10–14d/month)
  • Continuous after amenorrhoeic for 2y <50 or 1y >50 as before this can cause irregular breakthrough bleeding
  • After 12m of treatment can switch to continuous
277
Q

HRT

How can progesterone be given?

A
  • Tablets, transdermal (patches) or IUS (Mirena)
278
Q

HRT
What would you give for…

i) cyclical combined HRT?
ii) continuous HRT?

A

i) Sequential tablets or patches

ii) Mirena licensed for 4 years for endometrial protection – also treats menorrhagia

279
Q

HRT
What are the side effects associated with…

i) oestrogen?
ii) progesterone?

A

i) Nausea, bloating, headaches, breast swelling or tenderness, leg cramps
ii) Mood swings, fluid retention, weight gain, acne + greasy skin

280
Q

ATROPHIC VAGINITIS

What is atrophic vaginitis?

A
  • Dryness + atrophy of vaginal mucosa related to lack of oestrogen
281
Q

ATROPHIC VAGINITIS

What is the pathophysiology of atrophic vaginitis?

A
  • Epithelial lining of vagina + urinary tract responds to oestrogen by becoming thicker, more elastic + producing secretions so reduced oestrogen has opposite effect
  • Tissue more prone to inflammation + changes in vaginal pH + microbial flora that contribute to localised infections
282
Q

ATROPHIC VAGINITIS

What are some risk factors for atrophic vaginitis?

A
  • Menopause
  • Oophorectomy
  • Anti-oestrogen (tamoxifen, anastrozole)
283
Q

ATROPHIC VAGINITIS

What is the clinical presentation of atrophic vaginitis?

A
  • Postmenopausal with PV dryness, dyspareunia + occasional spotting
  • Consider with recurrent UTIs, stress incontinence or pelvic organ prolapse
284
Q

ATROPHIC VAGINITIS

What might the PV examination show in atrophic vaginitis?

A
  • Sparse pubic hair
  • Pale mucosa
  • Dryness
  • Thin skin
  • Reduced vaginal folds
  • May be painful
285
Q

ATROPHIC VAGINITIS

What is the management of atrophic vaginitis?

A
  • Vaginal lubricants + moisturisers like Sylk + Replens

- Topical oestrogen like estriol cream, HRT if severe

286
Q

POI

What is premature ovarian insufficiency (POI)?

A
  • Premature menopause before the age of 40
287
Q

POI

What are some causes of POI?

A
  • Majority idiopathic
  • Iatrogenic (chemo/radio, oophorectomy)
  • Autoimmune (coeliac, T1DM)
  • Genetic (FHx, Turner’s)
  • Infections (mumps, TB, CMV)
288
Q

POI

What is the clinical presentation of POI?

A
  • Secondary amenorrhoea (or irregular) + typical peri-menopause Sx before age 40
289
Q

POI

What are some investigations for POI?

A
  • Clinically = menopausal Sx in woman <40y with 4m of amenorrhoea
  • FSH level = >25IU/L on 2 samples >4w apart
  • Hypergonadotrophism + hypoestrogenism
290
Q

POI

What are the complications of POI?

A
  • Higher risk of conditions due to lack of oestrogen > CVD, stroke, osteoporosis, dementia + cognitive impairment + Parkinsonism
291
Q

POI

What is the management of POI?

A
  • HRT imperative until at least average age of menopause to reduce risks
  • HRT or COCP can be used
292
Q

POI

What is the difference between traditional HRT and COCP in POI?

A
  • Traditional HRT associated with lower BP than COCP

- COCP may be more socially acceptable if younger + acts as contraceptive

293
Q

POI

Are there the same risks of HRT in POI as in menopause?

A
  • No increase in breast cancer risk as women normally produce these hormones at that age
  • Slight increased risk of VTE but reduced by transdermal patch
294
Q

URINARY INCONTINENCE

What is urinary incontinence?

A
  • Involuntary leakage of urine at socially unacceptable times
  • Affects 20% of adult women
295
Q

URINARY INCONTINENCE

What is the physiology of micturition?

A
  • Detrusor = smooth muscle, transitional epithelium normally only contracts during micturition = sacral parasympathetic innervation from S2-4
  • M2+3 muscarinic receptors with ACh
  • Sympathetic nerve fibres from T11-L2 maintain relaxation of bladder for storage
296
Q

URINARY INCONTINENCE

What are the 6 main types of incontinence?

A
  • Overactive bladder/urge incontinence
  • Stress incontinence
  • Mixed incontinence (of the 2 above)
  • Overflow incontinence
  • Fistula
  • Neurological
297
Q

URINARY INCONTINENCE

What causes urge incontinence/OAB?

A
  • Overactivity + involuntary contractions of the detrusor muscle
298
Q

URINARY INCONTINENCE
What causes stress incontinence?
What happens?
What can cause it?

A
  • Weakness of pelvic floor + sphincter muscles
  • Detrusor pressure > closing pressure of urethra
  • Low oestrogen in menopause > weakened pelvic support, parity, pelvic surgery
299
Q

URINARY INCONTINENCE

What is overflow incontinence?

A
  • Chronic urinary retention due to outflow obstruction leads to overflow of urine + incontinence without the urge to pass, M>F
300
Q

URINARY INCONTINENCE

What are some causes of overflow incontinence?

A
  • Anticholinergics
  • Fibroids
  • Pelvic tumours
  • BPH (men)
  • Neuro (damage, MS, diabetic neuropathy, spinal cord injuries)
301
Q

URINARY INCONTINENCE
How does

i) fistula
ii) neurology

cause incontinence?

A

i) Between urinary tract + vagina or bowel

ii) Nerve damage, MS or functional

302
Q

URINARY INCONTINENCE

What are some risk factors for urinary incontinence?

A
  • Increasing age
  • Multiparity
  • High BMI
  • FHx
  • Previous pelvic surgery (hysterectomy)
303
Q

URINARY INCONTINENCE

What is the clinical presentation of urge incontinence/OAB?

A
  • Urgency, frequency, nocturia
  • ‘Key in door’ + ‘handwash’ trigger bladder contractions
  • Intercourse
  • May affect activities + QOL as worried about toilet access
304
Q

URINARY INCONTINENCE

What is the clinical presentation of stress incontinence?

A
  • Involuntary leakage when increased pressure (cough, laugh, lifting, exercise)
305
Q

URINARY INCONTINENCE

What are some investigations in urinary incontinence?

A
  • Hx most important
  • Bladder diary (frequency volume chart) first line
  • Urine dipstick + MSU
  • Residual urine measurement
  • Electronic Personal Assessment Questionnaire
  • Urodynamics
  • Cystogram with contrast
306
Q

URINARY INCONTINENCE

What does a bladder diary look at?

A
  • Frequency + quantity of both urination and leakage

- Fluid intake + diurnal variation

307
Q

URINARY INCONTINENCE

What are you looking for in urine dipstick + MSU?

A
  • Nitrites + leukocytes = infection
  • Microscopic haematuria = glomerulonephritis
  • Proteinuria = renal disease
  • Glycosuria = DM, nephropathy
308
Q

URINARY INCONTINENCE

How do you measure residual urine?

A
  • In/out catheter or USS
309
Q

URINARY INCONTINENCE

What is the Electronic Personal Assessment Questionnaire (ePAQ)?

A

Determines impact on QOL + assesses –

  • Urinary (pain, voiding, stress, OAB, QOL)
  • Vaginal (pain, capacity, prolapse, QOL)
  • Bowel (IBS, constipation, continence, QOL)
  • Sexual (dyspareunia, overall sex life)
310
Q

URINARY INCONTINENCE
What is the purpose of

i) urodynamics?
ii) cystogram with contrast?

A

i) Measures pressure in abdomen + bladder to deduce detrusor pressure
ii) Visualise the bladder

311
Q

URINARY INCONTINENCE

What is some lifestyle advice for urinary incontinence?

A
  • Weight loss
  • Stop smoking
  • Reduce caffeine + alcohol
  • Avoid straining + constipation
312
Q

URINARY INCONTINENCE

What are some conservative treatments for urinary incontinence?

A
  • Leakage barriers (pads), skin care + odour control
  • Bladder bypass with urethral, suprapubic or intermittent self-catheters
  • PV oestrogen to reduce urinary Sx
313
Q

URINARY INCONTINENCE

What is the stepwise management of urge incontinence/OAB?

A
  • 1st line = bladder retraining (6w gradually increasing time between voiding)
  • 1st line drugs = anti-muscarinics (oxybutynin, tolterodine, darifenacin)
  • Mirabegron (beta-3-adrenergic agonist) if anti-muscarinics not tolerated
314
Q

URINARY INCONTINENCE
What is the mechanism of action of anti-muscarinics?
What are some side effects?

A
  • Parasympathetic so Pissing = decreases need to urinate + spasms
  • “Can’t see, spit, pee or shit” > caution in elderly as falls esp oxybutynin immediate release in frail
315
Q

URINARY INCONTINENCE
What is the mechanism of action of beta-3-adrenergic agonists?
What is a caution of these?

A
  • Sympathetic so Storage = relaxes detrusor + increases bladder capacity
  • C/I in uncontrolled HTN as stimulates SNS to increase BP, can lead to hypertensive crisis so monitor BP
316
Q

URINARY INCONTINENCE

What are last resort options for urge incontinence?

A
  • Augmentation cystoplasty with bowel tissue
  • Bypass (urostomy)
  • Botox can paralyse detrusor + block ACh release
317
Q

URINARY INCONTINENCE

What is the first line management of stress incontinence?

A
  • Pelvic floor exercises with physio for 3m

- Pelvic floor muscle contraction > clamping of urethra > increased urethral pressure so reduced leakage

318
Q

URINARY INCONTINENCE

What medical management can be used in urinary incontinence?

A
  • Duloxetine (SNRI)
319
Q

URINARY INCONTINENCE

What are the surgical interventions for stress incontinence?

A
  • Colposuspension
  • Tension free vaginal tape (TVT)
  • Autologous sling procedures (TVT but strip of fascia from abdo wall)
320
Q

URINARY INCONTINENCE

What are the aims of surgical interventions of stress incontinence?

A
  • Restore pressure transmission to urethra
  • Support or elevate urethra (anterior wall + pubic symphysis stitches in colposuspension, mesh sling looping urethra in TVT)
  • Increase urethral resistance
321
Q

PELVIC ORGAN PROLAPSE

What is pelvic organ prolapse?

A
  • Descent of ≥1 pelvic organs resulting in protrusion on the vaginal walls
  • Due to weakness + stretching of ligaments + muscles surround uterus, rectum + bladder (levator ani + endopelvic fascia support pelvic organs)
322
Q

PELVIC ORGAN PROLAPSE

What are the 5 types of prolapse?

A
  • Cystocele
  • Rectocele
  • Enterocele
  • Uterine prolapse
  • Vault prolapse
323
Q

PELVIC ORGAN PROLAPSE

What is a cystocele?

A
  • Defect in ant. vaginal wall = bladder prolapses backwards into vagina (can get urethrocele or cystourethrocele)
324
Q

PELVIC ORGAN PROLAPSE
What is a rectocele?
How may this present?

A
  • Defect in post. vaginal wall = rectum prolapses forwards into vagina
  • Faecal loading in that part of rectum may lead to lump in vagina + have to use finger to press lump to aid defecation
325
Q

PELVIC ORGAN PROLAPSE
What is…

i) enterocele?
ii) uterine prolapse?
iii) vault prolapse?

A

i) Defect in upper posterior wall of vagina > intestine protrusion
ii) Uterus descends into vagina
iii) If had total hysterectomy, top of vagina (vault) descends into the vagina

326
Q

PELVIC ORGAN PROLAPSE

What are some risk factors of pelvic organ prolapse?

A
  • Age
  • BMI
  • Multiparity (vaginal)
  • Spina bifida
  • Pelvic surgery
  • Menopause
327
Q

PELVIC ORGAN PROLAPSE

What is the clinical presentation of pelvic organ prolapse?

A
  • “Something coming down” = dragging/heavy sensation in pelvis
  • Pain, lump, discomfort
  • Urinary Sx (cystocele) = incontinence, urgency, frequency, poor stream + retention
  • Bowel Sx (rectocele) = constipation, incontinence + urgency
  • Sexual dysfunction = pain, altered sensation + reduced enjoyment
328
Q

PELVIC ORGAN PROLAPSE

What are the investigations for pelvic organ prolapse?

A
  • Sim’s speculum (U-shaped) to show if something is there

- May have urodynamics, USS or MRI

329
Q

PELVIC ORGAN PROLAPSE

What is the management for pelvic organ prolapse?

A
  • Conservative = pelvic floor exercises, weight loss + diet changes
  • Vaginal pessary = ring (preferred as can have sex), shelf or Gellhorn
  • Surgery (symptomatic or severe like outside vagina, ulcerated, failed Mx)
330
Q

PELVIC ORGAN PROLAPSE
What surgical intervention is provided for…

i) cystocele/cystourethrocele?
ii) uterine prolapse?
iii) rectocele?

A

i) Anterior colporrhaphy or colposuspension
ii) Hysterectomy or sacrohysteropexy
iii) Posterior colporrhaphy

331
Q

PREMENSTRUAL SYNDROME

What is premenstrual syndrome (PMS)?

A
  • Psychological, emotional + physical Sx that occur prior to menstruation
332
Q

PREMENSTRUAL SYNDROME

What is thought to cause PMS?

A
  • Fluctuation in oestrogen + progesterone during the cycle
333
Q

PREMENSTRUAL SYNDROME

How may PMS present?

A
  • Mood = anxiety, swings, stress, fatigue, low confidence
  • Physical = bloating, headaches, breast pain
  • Resolves on menstruation
  • Absent before menarche, during pregnancy or after menopause
334
Q

PREMENSTRUAL SYNDROME

How is PMS diagnosed?

A
  • Sx diary spanning 2 menstrual cycles

- Definitive Dx with GnRH to temporarily induce menopause = Sx resolve

335
Q

PREMENSTRUAL SYNDROME

What is the conservative management of PMS?

A
  • Healthy diet, exercise, alcohol + smoking cessation, stress reduction, good sleep patterns
336
Q

PREMENSTRUAL SYNDROME

What management can be trialled in primary care for PMS?

A
  • SSRIs
  • COCP
  • CBT
337
Q

PREMENSTRUAL SYNDROME

What specialist management can be given for PMS?

A
  • Continuous transdermal oestrogen with progestogens
  • GnRH analogues if severe (add HRT to mitigate osteoporosis risk)
  • Hysterectomy + bilateral oophorectomy to induce menopause if severe
  • Danazol + tamoxifen for cyclical breast pain
  • Spironolactone for breast swelling + bloating
338
Q

DYSMENORRHOEA
What is dysmenorrhoea?
What are the two types?

A
  • Painful menstruation ± N+V

- Primary + secondary

339
Q

DYSMENORRHOEA
What is…

i) primary dysmenorrhoea?
ii) secondary dysmenorrhoea?

A

i) No underlying pathology, may be due to excessive endometrial prostaglandins – presents as suprapubic cramps just before or within few hours of period starting
ii) Secondary to endometriosis, adenomyosis, fibroids, PID, IUDs, cancer

340
Q

DYSMENORRHOEA

What is the management of primary dysmenorrhoea?

A
  • NSAIDs like mefenamic acid during menstruation

- COCP second line

341
Q

FGM

What is female genital mutilation (FGM)?

A
  • All procedures involving partial or total removal of female external genitalia or injury to female organs for non-medical reasons, often pre-pubertal
342
Q

FGM

Is FGM illegal?

A
  • Yes as stated in FGM Act 2003 – legal requirement for HCPs to report cases of FGM to the police
  • Illegal to assist in carrying out FGM (booking flights)
343
Q

FGM

What is the epidemiology in FGM?

A
  • Very common in Africa (Somalia, Egypt, Ethiopia, Sudan)

- UK hotspots = Sheff, London, Manc, Oxford

344
Q

FGM

What is the WHO classification for the types of FGM?

A
  • 1 = partial or total clitoridectomy
  • 2 = excision
  • 3 = infibulation
  • 4 = all other non-medical harmful procedures incl. pricking, piercing, incising
345
Q

FGM
What is…

i) excision?
ii) infibulation?

A

i) Partial or total removal of clitoris + labia minora ± excision of labia majora
ii) Narrowing/closing of vaginal orifice with creation of a covering seal (stitch labia together)

346
Q

FGM

Is female labia reduction illegal?

A
  • <18 = FGM

- >18 = legal but only performed privately

347
Q

FGM

What are some potential reasons for FGM?

A

Based on customs –

  • It will bring status + respect to family (social norm)
  • Rite of passage + being part of woman
  • Preserves girls’ virginity so acceptable for marriage
  • Cleanses + purifies girl with perceived religious requirement
348
Q

FGM

What are some acute complications of FGM?

A
  • Pain
  • Bleeding
  • Infection (BBV)
  • Sepsis
  • Swelling
  • Urinary retention
349
Q

FGM

What are some chronic complications of FGM?

A
  • Dyspareunia
  • Dysmenorrhoea
  • Infertility + pregnancy issues
  • Keloid scar
  • Haematocolpos (period backs up in uterus as cannot be released)
  • PTSD
350
Q

FGM

What is the initial management of suspected or confirmed FGM?

A
  • Report ANY FGM in <18 to police + Record in notes (consider in >18 after risk assessment e.g. others at risk like unborn children)
  • Educate pts + relatives that FGM is illegal + health consequences
  • Services = social, safeguarding, paeds, counselling, FGM specialists
351
Q

FGM

What is the overall management of FGM?

A
  • De-infibulation by specialist in FGM in some type 3 to try restore function
  • Re-infibulation may be requested after childbirth but this is illegal
352
Q

AIS

What is androgen insensitivity syndrome (AIS)?

A
  • X-linked recessive condition (androgen receptor gene mutation) with end-organ resistance to testosterone causing male genotype 46XY but female phenotype
353
Q

AIS

What is the pathophysiology of AIS?

A
  • Absent response to testosterone + conversion of additional androgens to oestrogen result in female secondary sexual characteristics
  • Typical male sexual characteristics (Wollfian structures) do not develop
354
Q

AIS

What is the clinical presentation of AIS?

A
  • Infancy = inguinal hernias with undescended testes
  • Puberty = primary amenorrhoea + infertile
  • Tend to be taller than average, lack of pubic + facial hair as well as male muscle development
  • Female external genitalia (but not internal) + breasts
355
Q

AIS

Why is their female external genitalia but not internal in AIS?

A
  • Undescended testes in abdo or inguinal canal produce AMH which prevents uterus, upper vagina, tubes + ovaries developing (Mullerian duct structures)
356
Q

AIS

What is the clinical presentation of partial AIS?

A
  • More ambiguous
  • Micropenis
  • Clitoromegaly
  • Bifid scrotum
  • Hypospadias
  • Reduced male features
357
Q

AIS

What are the investigations for AIS?

A 
Hormone tests show raised –
- LH
- FSH (or normal)
- Testosterone (or normal for male)
- Oestrogen (for male)
Pelvic USS = absent female internal organs
Karyotyping = 46XY
358
Q

AIS

What is the management of AIS?

A
  • Specialist MDT (paeds, gynae, urology, endo, psychology)
  • Bilateral orchidectomy to avoid testicular cancer
  • Oestrogen therapy
  • Vaginal dilators or surgery to create adequate length
  • In general, raised as female but counselling for support
359
Q

ASHERMAN’S SYNDROME

What is Asherman’s syndrome?

A
  • Adhesion formation within uterus following damage
360
Q

ASHERMAN’S SYNDROME

What is the pathophysiology of Asherman’s?

A
  • Damage to basal layer of endometrium, damaged tissue may heal abnormally, creating scar tissue (adhesions)
  • Adhesions can bind uterine walls together or endocervix, sealing it shut causing obstruction > infertility, 2* amenorrhoea
361
Q

ASHERMAN’S SYNDROME

What causes Asherman’s syndrome?

A
  • Pregnancy-related dilatation + curettage procedures
  • After uterine surgery
  • Pelvic infection like endometritis
362
Q

ASHERMAN’S SYNDROME

What is the clinical presentation of Asherman’s syndrome?

A
  • Secondary amenorrhoea
  • Infertility
  • Significantly lighter periods
  • Dysmenorrhoea
363
Q

ASHERMAN’S SYNDROME

What is the management of Asherman’s syndrome?

A
  • Hysterosalpingography = contrast injected into uterus + XR
  • Sonohysterography = uterus filled with fluid + pelvic USS
  • Hysteroscopy gold standard + can dissect adhesions (recurrence after common)
364
Q

BARTHOLIN CYST
What are the bartholin glands?
What causes a bartholin cyst?
What causes a bartholin abscess? Presentation?

A
  • 2 glands behind labia minora which secrete lubricating mucus for coitus
  • Blockage of duct
  • Infection (Staph or E.coli) = acutely painful (can’t sit), swollen + tender red swelling of labia
365
Q

BARTHOLIN CYST

How is a bartholin abscess managed?

A
  • Abx
  • Incision + drainage (word catheter)
  • Marsupialisation (incision sutured open to reduce risk of reformation)
366
Q

NABOTHIAN CYST

What is a nabothian cyst?

A
  • Columnar epithelium of endocervix produces cervical mucus

- When squamous epithelium of ectocervix slightly cover these it traps mucus + forms cyst

367
Q

NABOTHIAN CYST
What can cause a nabothian cyst?
How does it present?

A
  • After childbirth, minor cervical trauma or cervicitis

- Asymptomatic + incidental, white or opaque swellings on ectocervix near os

368
Q

NABOTHIAN CYST

What is the management of a nabothian cyst?

A
  • Majority resolve spontaneously

- Cryocautery if symptomatic (rare)

Phase 3a Revision (11 decks)

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