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3a > Gynae + GUM > Flashcards

Gynae + GUM Flashcards

1
Q

what are the different types of miscarriage?

A

threatened - bleeding, but foetus still alive (can hear HR), good size for dates and os closed
inevitable/incomplete - bleeding, foetus might still be alive, but os is open
complete - all foetal tissue passed (empty sac on scan), os closed, bleeding diminished
septic - uterine contents infected, causing endometritis, offensive loss, tender uterus
missed miscarriage - not picked up till scan, or bleeding a long time after baby stopped developing/died - os closed, uterus small

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2
Q

what causes miscarriage?

A

often unknown - isolated non-recurring chromosomal abnormalities account for >60% of one off miscarriages

if had 3+ consecutively - consider causes of recurrent miscarriage

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3
Q

what are the clinical features suggesting miscarriage?

A

bleeding is main one.
often around 12 weeks.
may have pain from uterine contractions - be careful not to mix up with ectopic

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4
Q

how would you investigate a woman presenting with what you suspect might be a miscarriage?

A

examine - uterine size/cervical os depends on type of miscarriage.
USS for a viable intrauterine pregnancy - if in doubt, repeat scan in a week
blood HCG - levels should rise by >66% in 48h if pregnancy is viable (i.e. take one, then take another in two days and compare)

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5
Q

describe the different management options for miscarriage

A

expectant management - might use if not heavily bleeding, particularly for incomplete miscarriage (offer rescan in 2 weeks to ensure completed)

medical management - mifepristone to prime, then 24-48h later misoprostal/prostaglandin (oral or vaginal). bleeding can continue for 3 weeks. most successful in earlier miscarriages.

surgical management - if heavy or persistent bleeding, or pt request - surgical evac of retain products of concept (ERPC), under GA.

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6
Q

define recurrent miscarriage

A

loss of 3+ consecutive pregnancies at <24 weeks, by same biological father.
affects 1% of women.

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7
Q

list some possible causes of recurrent miscarriage

A

antiphospholipid abs –> thrombosis in the uteroplacental circulation, treat with aspirin and LMWH
chromosomal defects - e.g. a balanced translocation in parents
anatomical factors e.g .uterine abnormalities, more common with late miscarriage though
infection - BV associated with 2nd trimester loss
others - obesity, smoking, PCOS, maternal age, excess caffeine

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8
Q

what happens during days 1-4 of the menstrual cycle?

A

menstruation!
endometrium shed as its hormonal support is withdrawn
myometrial contraction can –> cramps/pain

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9
Q

what happens during days 5-13 of the menstrual cycle?

A

proliferative phase:

  • GnRH pulses (from hypothalamus) stimulate LH and FSH release –> follicular growth
  • follicles produce oestradiol and inhib –> suppress FSH (neg feedback), so only one follicle/oocyte matures
  • as oestradiol rises, ‘positive feedback’ on hypothalamus and pituitary –> LH levels to rise sharply
  • ovulation occurs 36h after LH surge
  • oestradiol causes endometrium to re-form + become ‘proliferative’ –> thickens as stromal cells proliferate, glands elongate
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10
Q

what triggers ovulation in menstrual cycle / when does it occur?

A

LH surge - ovulation occurs 36h after.

LH surge occurs after oestradiol levels have risen to certain point (I think)

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11
Q

what happens during days 14-28 of the menstrual cycle?

A

luteal/secretory phase

  • follicle from which egg was released becomes corpus luteum - produces oestradiol and progesterone
  • progesterone levels peak a week later (day 21)
  • this triggers ‘secretory’ changes in endometrium where stromal cells enlarge, glands swell, and blood supply increases
  • towards end of luteal phase, corpus luteum starts to fail if egg not fertilized, so progesterone + oestrogen levels decrease
  • endometrium then breaks down as this hormonal support is removed, and cycle restarts
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12
Q

differentiate between the following:

  • primary amenorrhoea
  • secondary amenorrhoea
  • oligomenorrhoea
A 
amenorrhoea = absence of menstruation
primary = menstruation hasn't started by age 16
secondary = prev normal menstruation stops for >6 months
oligomenorrhoea = menstruation occurs every 35 days to 6 months
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13
Q

what five things need to be ‘normal’ for ‘normal’ menstruation to occur?
OR - what five different things can cause pathological problems with menstruation?

A

for normal menstruation you need:

  • hypothalamic function
  • pituitary function
  • ovarian function
  • endometrial function
  • patent cervix and vagina (‘outflow tract’)

so - menstrual disturbance can be caused by issues on any of these 5 levels

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14
Q

what is ‘physiological’ secondary amenorrhoea?

A

amenorrhoea due to pregnancy or menopause - by far the most common causes of amenorrhoea

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15
Q

give some causes of post-coital bleeding

A

cervical trauma, polyp, cervical/endometria/vaginal carcinoma, cervicitis or vaginitis of any cause

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16
Q

explain how you decide how to investigate primary amenorrhoea?

A

in absence of pubertal development - investigate as for delayed puberty
if normal puberty - exclude genital tract anomaly, then investigate as for secondary amenhorrhoea
abnormal pubertal development - exclude chromosomal anomaly (e.g. Turner’s) and causes of hyperandrogenism

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17
Q

what is the main hypothalamic cause of secondary amenorrhoea? how do you diagnose/treat?

A

hypothalamic hypogonadism - due to psychological factors (stress), low weight/anorexia, excessive exercise

GnRH (+ thus LH/FSH) low - although may see normal LH/FSH

treat - supportive + oestrogen replacement (COCP/HRT)

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18
Q

what pituitary causes of secondary amenorrhoea are there? how do you diagnose/treat?

A

hyperprolactinaemia - due to pituitary hyperplasia or benign adenomas, can be due to thyroid issues

treat - bromocriptine, cabergoline or sometimes surgery

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19
Q

what are the key ovarian disorders that lead to secondary amenorrhoea?

A

PCOS - most common
tumours
ovarian insufficiency/failure aka premature menopause
congenital - Turner’s, gonadal dysgenesis

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20
Q

what tests might you order if a woman came to clinic with secondary amenorrhoea?

A
  • beta HCG
  • serum free androgen index (raised in PCOS)
  • FSH/LH
  • prolactin
  • TFT
  • testosterone levels
  • may do MRI if prolactin levels really high
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21
Q

how would you manage a woman with secondary amenorrhoea?

A

treatment depends on cause
can involve HRT/COCP use to replace oestrogen
correct genital tract anomaly if poss
weight gain/stress management/reduction of extreme exercise

for PCOS - main treatment is weight loss, might use COCP or metformin

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22
Q

define menorrhagia

A

menstrual blood loss >80ml per period

clinically - blood loss affecting quality of life

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23
Q

give some possible causes of menorrhagia

A 
uterine fibroid (30%)
uterine polyps (10%)
thyroid disease, clotting disorder
endometrial carcinoma
endometriosis/adenomyosis
PID
iatrogenic - copper coil, anticoagulants

NO KNOWN CAUSE - ‘dysfunctional uterine bleeding’

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24
Q

how do fibroids cause menorrhagia?

A

1) by enlarging uterine cavity, leading to increased surface are of endometrium for bleeding to come from (this is similar to how polyps cause menorrhagia)
2) might produce prostaglandins, which might cause menorrhagia

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25
Q

what tests might you order for a woman complaining of menorrhagia?

A
  • FBC, maybe also TFTs and clotting studies
  • pelvic/transvaginal USS to assess for polyps/fibroids (endometrial thickness)
  • if woman >40yrs, or women <40y with history/scan results that are suspicious, do endometrial biopsy (via hysteroscopy)
  • hysteroscopy is also the best way to rule out fibroids/polyps for sure
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26
Q

how do you treat a woman suffering menorrhagia?

A

1) correct anaemia, treat any systemic causes/focal pathology
2) medical treatment - Mirena coil 1st line, then transexamic acid, NSAIDs (mefenamic acid) or COCP 2nd line, then high dose progestogens or GnRH agonist (for 6 months only)
3) surgical treatment - only if unresponsive to medications - endometrial ablation (reduces fertility), myomectomy or uterine artery embolization (retain fertility) - if fibroids >3cm and no wish for further fertility then consider hysterectomy

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27
Q

what is a myomectomy?

A

open or laparoscopic removal of fibroids from myometrium

used when woman wishes to retain fertility, as endometrial ablation/hysterectomy renders women infertile

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28
Q

define postmenopausal bleeding

A

vaginal bleeding >12 months after LMP

ALWAYS exclude malignancy

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29
Q

list some causes of postmenopausal bleeding

A

ovary - Ca ovary, oestrogen-secreting tumour
uterus - submucous fibroid, atrophic changes, polyp, endometrial carcinoma/hyperplasia (premalignant)
cervix - atrophy, polyp, squamous Ca or adenocarcinoma
vulva - vulvitis, malignancy, dystrophy
vagina - atrophic vaginitis
withdrawal bleed from HRT
haematuria/PR bleed
PREGNANCY - if not truly menopause!

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30
Q

how would you investigate a woman presenting to clinic complaining of postmenopausal bleeding?

A

perform bimanual examination, speculum exam, might do smear (cytology) if cervical pathology - or refer for colposcopy. pipelle biopsy if suspicious of cancer.
transvaginal US - looking for endometrial thickness, other pelvic pathology
if endometrial thickness >4mm or fluid-filled cavity, do hysteroscopy and biopsy

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31
Q

how do you treat postmenopausal bleeding?

A

depends on cause!
most common cause = atrophic changes - oestrogen replacement, usually topical (creams, rings, vaginal tablets)
might use systemic HRT - must combine with progesterone/progestogen in women with a uterus!

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32
Q

list some causes of intermenstrual/postcoital bleeding

A

cervix - ectopy, polyp, malignancy, cervicitis
intra-uterine - polyps, submucous fibroids, endometrial hyperplasia, endometrial malignancy, endometritis
hormonal - breakthrough bleeding
also anovulatory cycles - irregular bleeding common just after menarche/before menopause

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33
Q

how would you investigate a woman with intermenstrual bleeding?

A
  • FBC
  • might do vaginal/speculum exam
  • cervical smear if needed
  • US pelvis if >35y
  • endometrial biopsy/hysteroscopy if indicated
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34
Q

what is primary vs secondary dysmenorrhoea?

A 
primary = pain without organ pathology
secondary = pain secondary to a pathology
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35
Q

what causes secondary dysmenorrhoea?

A

adenomyosis, endometriosis, PID, fibroids

treat cause, avoid IUCD (copper coil)

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36
Q

what causes primary dysmenorrhoea?

A

excess prostaglandins cause painful uterine contractions, producing ischaemic pain.
hx - crampy, radiates to back/groin, worse in first couple of days

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37
Q

what treatment options are there for dysmenorrhoea?

A

NSAIDs e.g. mefenamic acid - inhibit prostaglandins so reduce contractions and thus reduce pain
COCP can help by stopping ovulation

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38
Q

briefly describe the anatomy of the uterus

A

continuous with cervix and going into vagina.
superior part = fundus, communicates with fallopian tubes via the cornu.
supported by uterosacral and cardinal ligaments
anteverted in 80%, retroverted in 20%
wall made of smooth muscle, lined by glandular epithelium (endometrium)

function = nourish, protects and then expels foetus

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39
Q

briefly describe the blood/lymphatic supply of the uterus

A

uterine arteries supply uterus, there’s an arterial anastomosis with ovarian blood supply at the cornu.
inferiorly there’s an anastamosis with vaginal vessels.
lymph = internal and external iliac nodes

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40
Q

briefly describe the structure/function of endometrium

A

supplied by spiral and basal arteries
spiral arteries are responsible for menstruation and nourishment of growing foetus
endometrium responds to oestrogen and progesterone

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41
Q

what are uterine fibroids?

A

benign tumours of myometrium, aka leiomyomata
20% of women (50% if Afro-Caribbean)
more common closer to menopause, less common in women who’ve had a baby.
might be intramural, subserosal or submucosal

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42
Q

what causes fibroids?

A

their growth is oestrogen and progesterone dependent
tend to regress after menopause due to a reduction in circulating oestrgoen (NB - HRT might mean fibroids continue to grow post-menopause!)

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43
Q

what clinical features might you see in a woman with uterine fibroids?

A

50% asymptomatic, incidental finding.
mentstrual probs - menorrhagia, sometimes IMB
pain - dysmenorrhoea
large fibroids might be pressing on bladder
intramural fibroids can lead to subfertility

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44
Q

what are the effects of fibroids in pregnancy?

A

might have prem labour, malpresentations, transverse lie, obstructed labour, PPH

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45
Q

how might you investigate uterine fibroids?

A

might be initially seen as endometrial thickening on transvaginal US
MRI/laparoscopy/hysteroscopy
if postmenopausal - pipelle biopsy

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46
Q

what are the treatment options for fibroids?

A

if small, slow-growing and asymptomatic, consider no treatment.
medical - could try some stuff but usually need surgery - GnRH analogues (goserelin) taken 3-6m before surgery to shrink. ulliprista acetate can be used like this too.

myomectomy - gives best chance of preserving fertility - if not hysteroscopic, counsel re need fo C section deliveries.

uterine artery embolism - interventional radiology.

hysterectomy - only cure!

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47
Q

what is adenomyosis?

A

where there is endometrium/stroma within the myometrium

most common age 40 ish, associations with endometriosis and fibroids

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48
Q

how might adenomysosis present? how would you investigate?

A

asymptomatic
might have dysmenhorroea/menorrhagia
not easy to see on USS but can diagnose via MRI

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49
Q

how do you treat adenomyosis?

A

trial mirena / COCP+NSAIDs to control menorrhagia/dysmenhorroea
often requires hysterectomy in the end
if asymptomatic just leave it ?? I think

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50
Q

what is endometritis?

A

uterine infection - secondary to STI, surgery, foreign tissue (e.g. IUS, retained POC)
if postmenopausal - often due to malignancy

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51
Q

what clinical features might make you think of endometritis? how would you treat?

A

uterine tenderness, systemically unwell/signs of infection, relevant hx (e.g. recent delivery)
treat w/ abx and surgical evac of retained POC if needed

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52
Q

what are intrauterine polyps?

A

small benign tumours growin into uterine cavity, usually endometrial.
common age 40-50 when oestrogen levels high
occasionally malignant

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53
Q

what clinical features might lead to a diagnosis of uterine polyps? how would this be picked up (investigations)?

A

might be asymptomatic/incidental finding
often menorrhagia and IMB.
diagnosed at USS/hysteroscopy

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54
Q

how do you manage a woman with uterine polyps?

A

resection of poly with cutting diathermy should cure abnormal bleeding - ?done at hysteroscopy/as endometrial ablation - not sure on this

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55
Q

what is a haematometra?

A

menstrual blood accumulating in uterus because of outflow obstruction

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56
Q

briefly describe the anatomy and function of the cervix

A

tubular structure, continuous with uterus, 2-3cm long
made of elastic connective tissue. attached to uterosacral and cardinal ligaments.
supplied by upper vaginal branches and uterine artery
lymph drains to obturator and internal/external iliac nodes, up to common iliac and para-aortic nodes

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57
Q

briefly describe the histology of the cervix

A

endocervix is lined by columnar (glandular) epithelium.
ectocervix (continuous with vagina) is squamous epithelium.
two cell types meet at ‘squamo-columnar junction’.
during pregnancy/puberty, partial eversion of cervix exposes new area of columnar epithelium which undergoes metaplasia to squamous epithelium - this is transformation zone, and is the usual site of cervical carcinoma

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58
Q

what is a cervical ectropion?

A

when columnar epithelium of endocervix is visible as red area around the os - due to eversion of cervix, normal finding in younger women, also common in pregnancy

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59
Q

what clinical features might you see in a woman with a cervical ectropion?

A

asymptomatic

or - change in vaginal discharge, or postcoital bleeding

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60
Q

how do you treat a cervical ectropion?

A

once a smear +/- colposcopy has excluded carcinoma - treat with cryotherapy/cautery with diathermy IF symptomatic/patient wishes

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61
Q

what are cervical polyps? how do they present, how would you treat?

A

benign tumours of endocervical epithelium.
asymptomatic or IMB/PMB
treat - avulsion without anaesthetic, or in older women might need a TV USS or hysteroscopy to exclude intrauterine polyps

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62
Q

what is cervicitis?

A

might be follicular or mucopurulent - presents with discharge. result of infection/inflammation.
causes - chlamydia, gonorrhoea, herpes.
chronic cervicitis usually a mixed infection.
can mask neoplasia on a smear so be careful!

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63
Q

briefly describe the cervical cancer screening programme in England

A

all sexually active women age 25-64yrs

3 yearly for woman 25-50yrs, then 5 yearly until 64 (if normal)

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64
Q

how would you manage a woman with borderline changes or mild dyskaryosis on her smear?

A

do a high-risk HPV test, and if positive refer to colposcopy - if negative, repeat smear in 3 yrs

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65
Q

how would you manage a woman with moderate dyskaryosis on smear?

A

referral to colposcopy - colposcopy appt within 2 weeks

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66
Q

how would you manage a woman with severe dyskaryosis on smear?

A

referral to colposcopy - colposcopy appt within 2 weeks

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67
Q

how would you manage a woman with suspected invasion on smear?

A

referral to colposcopy - colposcopy appt within 2 weeks

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68
Q

how would you manage a woman with abnormal glandular cells on smear?

A

referral to colposcopy - colposcopy appt within 2 weeks

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69
Q

how would you manage a woman with 3 consecutive inadequate smear samples?

A

routine colposcopy referral (6 weeks ish)

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70
Q

what is cervical intraepithelial neoplasia?

A

presence of intraepithelial cells within squamous epithelium - a pre-malignant phase of cervical cancer
severity graded I-III depending on extent to which these cells are found in epithelium - histological diagnosis.

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71
Q

what factors are associated with cervical cancer?

A

HPV 16, 18, 31 and 33 = really associated with CIN/cancer (vaccinations against 16 and 18 currently, plus 6 and 11 which cause warts).

no. sexual contacts thus associated with cancer - note that whether these are same/opposite sex doesn’t make a difference!
other factors = oral contraceptive and smoking.

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72
Q

briefly describe the pathology of cervical cancer

A

as columnar epithelium undergoes metaplasia in transformation zone, exposure to certain HPV results in incorporation of viral DNA into cell DNA - viral proteins inactivate key cell tumour suppressor gene products

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73
Q

what will be performed at colposcopy clinic following suspicious smear test results?

A

cervix inspected using speculum and colposcope
5% acetic acid used as dye - different grades of CIN have characteristic appearances - ‘acetowhite’
biopsy usually taken for histological diagnosis

if strong acetowhite patches ‘see and treat’ - sample taken for biopsy, but then definitive treatment performed immediately - transformation zone excised with cutting diathermy under local anaesthetic.
LLETZ = large loop excision of transformation zone
risks are of post op bleeding and future preterm deliveries.

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74
Q

what are treatment options for cervical cancer (i.e. gone past CIN stage)?

A

depends on staging - cone biopsy, possibly hysterectomy.

if later stages then chemo and radio used

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75
Q

how might cervical malignancy present if not detected and treated via screening and colposcopy?

A

might see postcoital or post-menopausal bleeding, watery vaginal discharge (might be offensive)

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76
Q

briefly describe the anatomy of the ovaries

A

sit in ovarian fossa on lateral pelvic wall, overlying ureters
attached to broad ligament by mesovariaum, and to pelvic wall by infundibulo pelvic ligament
blood supply = ovarian artery
outer cortex covered by germinal epithelium
inner medulla contains connective tissue and blood vessels
cortex contains follicles and theca cells

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77
Q

what are the different types of ovarian ‘accidents’?

A

accidents = acute presentations of ovarian cysts
rupture - of contents into peritoneal cavity, causes intense pain
haemorrhage - into cyst or peritoneal cavity, again pain
torsion - of the pedicle, causes infarction of ovary and tube - severe pain, need urgent surgery and detorsion to rescue ovary

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78
Q

when might you be worried about an ovarian cyst?

A

> 5cm
symptomatic woman
complex/multilobular appearance on scan
postmenopausal woman

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79
Q

what is the classical presentation of ovarian torsion?

A

severe sudden onset lower abdo pain and vomiting - pain may improve after 24h as ovary dies off

cyst rupture presents similarly but likely to also have features of haemorrhagic shock

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80
Q

how would you investigate a woman presenting with acute pain that you suspect is related to an ovarian ‘accident’?

A

TV USS - helps distinguish between benign and malignant masses - if stable!
if unstable - urgent laparotomy

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81
Q

what management options are there for premenopausal women with an ovarian cyst?

A

if <5cm and asymptomatic - do nothing, maybe rescan in 6 weeks to check on it.
if >5cm, suspicious appearance on scan or symptomatic - laparoscopic ovarian cystectomy, taking care not to spill cyst contents into cavity - aiming to preserve fertility

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82
Q

what management options are there for postmenopausal women with an ovarian cyst?

A

determine whether malignant - risk of malignancy index (RMI) - uses US scan, menopausal status, CA125 level, multilocularity, solid areas, metastases, ascites, bilaterally of lesions.
determines risk of malignancy and thus management
low risk <5cm cyst = conservative management with repeat TV US and CA125 every 4 months (discharge after a yr of no change)
moderate risk = bilateral oophorectomy
high risk = staging laparotomy and treat according to staging

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83
Q

give some risk and protective factors for ovarian cancer

A

nulliparity
early menarche and/or late menopause
BRCA 1 and 2
HPNCC

protective - lots of pregnancies, breastfeeding, COCP, tubal ligation (female sterilization)

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84
Q

what is the role of screening in ovarian cancer?

A

still not sure if there is one

consider yearly TV US and CA125 (marker) if there’s an identified gene mutation

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85
Q

how might ovarian cancer present?

A 
often vague and mistaken for IBS/diverticular disease
bloating
unexplained weight loss/loss of appetite
fatigue
urinary symptoms / change in bowel habit
abdo or pelvic pain
vaginal bleeding
palpable mass
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86
Q

what is the mechanism of spread of ovarian cancers?

A

local spread throughout pelvis

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87
Q

how are ovarian cancers managed?

A

staging laparotomy with removal of as much cancer as possible, including hysterectomy and bilateral salpingo-oopherectomy if needed
basically everyone offered chemo

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88
Q

what is lichen simplex? how would you manage it?

A

presents with chronic intractable itching, esp at night, in women with sensitive skin/eczema
chronic inflammatory skin condition - vulva and surrounding area inflamed and thickened with hyper- and hypo-pigmentation.
avoid soap/irritants, use of emollients, moderately potent steroid creams, antihistamines

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89
Q

what is lichen planus and how would you manage it?

A

unknown cause. presents with vulval pain more commonly than itch.
flat, purple, popular lesions.
treat = high potency topical steroids

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90
Q

what is lichen sclerosis? how would you treat it?

A

possibly autoimmune cause, condition where elastic tissue starts to turn to collagen later in life.
severe pruritus, worse at night - might see bruises/bleeding/dyspareunia as result of scratching
initially pink papules, gradually vulva becomes white, flat and shiny.
can cause adnhesions leading to fusion of labia/narrowing of introitus.
biopsy to check for Ca and monitor as may be pre-malignant.
treat = Clobetasol propionate (high potency steroid) cream, if severe and unresponsive to steroids then consider tacrolimus

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91
Q

what are Bartholin’s cysts/abscesses?

A

blockage of duct in the Bartholin’s glands causes cyst formation, or abscess if becomes infected.
becomes severely painful (can’t sit down!) - huge, hot, swollen labium
treat = masupialisation (incision and drainage, then stitched to it stays open to prevent a new cyst)

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92
Q

what is vaginal intraepithelial neoplasia?

A

atypical cells in vulval epithelium - premalignant vulval disease.
usual type = warty, basaloid or mixed. associated with HPV, CIN, smoking - multifocal, red/white/pigmented, plaques/papules/patches, erosions, nodules, warty or hyperkeratosis
differentiated type - rarer, older women - unifocal ulcer or plaque

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93
Q

how might VIN present? how is it treated?

A

pruritus/pain leading to vaginal examination where lesions might be seen - surveillance key, biopsy any suspicious lesions.
some regression seen with use of imiquimod cream.
emollients/steroids to manage symptoms whilst monitoring.
surgical excision if necessary.

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94
Q

what is vulval carcinoma and how may it present?

A

refer any unexplained vulval lumps urgently!
cancer of vulva - 90% squamous, may also be melanoma, BCC or carcinoma of Bartholin’s glands.
presentation - lump, ulcer (often presents late with an ulcer leading to pain and bleeding, as otherwise it might not get noticed).

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95
Q

how is vulval carcinoma treated?

A

small tumour = local excision only
larger = wide local excision+ ipsilateral groin node biopsy
radio/chemo have role in shrinking tumour pre-op

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96
Q

give basic info about vaginal cancer

A

v. rare, possibly HPV related, often metastatic from cervical, uterine or vulval cancers.
most common in upper third of vagina, presents usually with bleeding.
treat with radiotherapy, poor prognosis

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97
Q

list some risk factors for endometrial cancer

A

unopposed oestrogen
obesity/T2DM/HTN
nulliparity (pregnancy = high progesterone = protective)
anovulatory cycles e.g. PCOS (no corpus luteum = less progesterone)
early/late menopause
genetics - HNPCC
breast Ca - similar lifestyle factors + tamoxifen use
oestrogen-only HRT

protective - parity, COCP use

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98
Q

how does endometrial cancer usually present?

A

91% = postmenopausal women
most present with PMB

if premenopausal - heavy/irregular bleeding

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99
Q

how is endometrial cancer investigated/diagnosed?

A

exam often normal
TV USS shows endometrial thickness >4mm - biopsy then performed (pipelle in OPD or can do hysteroscopy)
CT/MRI used to stage

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100
Q

how is endometrial cancer treated?

A

depends on stage and functional status of patient.
If early stages - total hysterectomy with bilateral salpingo-oopherectomy, nothing else needed.
later stages may use radiotherapy, or also high dose progesterones
pretty good prognosis overall

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101
Q

what is a prolapse?

A

descent of uterus and/or vaginal walls beyond normal anatomical confines - result from weakness in supporting structures.
not a risk to health, unless severe enough to cause ureteric obstruction.
exacerbated by menopause

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102
Q

describe the 3 levels of the pelvic supports

A

level 1 - cervix/upper vagina supported by cardinal (transverse cervical) and uterosacral ligaments - attached to cervix, then to pelvic side wall and sacrum
level 2 - midportion of vagina, attached by endofascial condensation (aka fascia) laterally to pelvic sidewall
level 3 - lower third of vagina is supported by levator ani muscles and perineal body

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103
Q

list the different types of prolapse

A 
urethrocele
cystocele
enterocele
rectocele
uterine descent/uterine prolapse/apical prolapse (seen different names in different places)

basically named according to structures involved, can have more than one type at once

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104
Q

what is a urethrocele?

A

prolapse of lower anterior vaginal wall, involving urethra

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105
Q

what is a cystocele?

A

prolapse of upper anterior vaginal wall, involving balder - there’s often also prolapse of urethra (‘cystourethrocele’).
residual urine within cystocele might cause frequency and dysuria.

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106
Q

what is an apical prolapse/uterine prolapse/uterine descent?

A

when whole uterus prolapses down towards vagina, taking cervix and upper vagina with it
- if has had a hysterectomy then the vaginal vault is left and might get a ‘vault’ prolapse

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107
Q

what is an enterocele?

A

prolapse of upper posterior wall of vagina - resulting pouch can contain loops of small bowel

108
Q

what is a rectocele?

A

prolapse of lower posterior wall of vagina - bulgers through weak levator ani - involving anterior wall of rectum
often symptomless, but may prevent defecation - patient might have to put finger in vagina to reduce the bugle so that she can defecate

109
Q

describe how prolapses are graded

A

first degree - lowest part of prolapse descends halfway down vaginal axis to the introitus
second degree - prolapse extends to level of introitus, passes through introitus on straining
third degree - prolapse extends through introitus and outside of vagina
fourth degree/procidentia - completely prolapse - uterus lies outside of vagina

110
Q

list some causal factors that might lead to uterine prolapse

A

anything which affects vaginal support mechanisms

  • vaginal delivery / pregnancy
  • congenital factors - abnormal collagen production e.g. Ehlers Danos
  • menopause - deterioration of collagen connective tissue
  • chronic predisposing factors - obesity, chronic cough, constipation, heavy lifting, pelvic mass
  • iatrogenic - pelvic surgery e.g. hysterectomy, continence procedures
111
Q

what clinical features suggest prolapse?

A 
might be asymptomatic
or 'dragging' sensation
or feel a mass
can have back/hip/groin pain (unusual)
might interfere with sex
cystourethrocele --> urinary symps
constipation/digitation to defecate
112
Q

how do you examine for prolapse?

A

do a bimanual examination to exclude masses, then examine with a Sims speculum.
ask woman to strain/stand if no immediately obvious prolapse

113
Q

what are the management options for prolapses?

A

conservative - weight loss, physio, stop smoking and straining
pessaries - useful in those declining/unfit for surgery - need to be changed every 6m, will affect sexual function, topical oestrogen must be used if postmenopausal - ring, Gelhorn or shelf pessaries.
surgery - if severe, pessaries failed, sexual function needs to be preserved - type of op depends on type of prolapse - includes hysterectomy or pelvic wall ‘repairs’

114
Q

briefly explain the neural control of the bladder/urinary continence

A

parasympathetic nerves aid voiding, sympathetic prevent
voiding reflex = afferent fibres respond to distension of bladder wall + pass to spinal cord - efferent parasympathetic fibres pass back to detrusor muscles and cause contraction + open bladder neck
this reflex is controlled at the level of the pons

115
Q

what structures are involved in maintaining urinary continence?

A

external sphincter and pelvic floor muscles - maintain urethral pressure higher than bladder pressure.
micturition occurs when these muscles relax and detrusor muscle contracts.

116
Q

what are the two main mechanisms causing urinary incontinence?

A

1) uncontrolled increase in detrusor pressure leading to bladder pressure > urethral pressure
2) increased intra-abdominal pressure transmitted to bladder but not to urethra (so bladder press > urethra) because urethra has slipped from abdo - stress incontinence

117
Q

list some investigations that might be performed to assess a woman’s urinary incontinence

A

urinalysis/dipstick - check for diabetes, UTI, also haematuria for bladder Ca or stone
urinary diary - 3 days to week long, of vol fluid intake and output
postmicturition US/catheterization - excludes chronic retention of urine
urodynamic studies - combo of tests looking at ability of bladder to store and void urine
cystoscopy to inspect bladder cavity

118
Q

what is stress incontinence?

A

involuntary leakage of urine on effort or exertion, or on sneezing/coughing etc
caused by urethral sphincter weakness - pregnancy, vaginal delivery, age etc
weak pelvic floor supports mean bladder neck has slipped below it, so when intra-abdo pressure raises the pressure in bladder necks remains the same

119
Q

how would you manage a woman with stress incontinence?

A

encourage weight loss, address causes of chronic cough e.g. smoking, reduce caffeine etc
conservative - pelvic floor exercises / physio
medical - duloxetine is only licensed drug, shouldn’t be used first line
surgery - tension-free vaginal tape / trans-obturator tape first line

120
Q

what is urge incontinence/overactive bladder?

A

present with frequency/urgency/urge incontinence - in absence of infection!
detrusor overactity - urodynamic diagnosis, involuntary detrusor contractions during filling phase
cause usually idiopathic

121
Q

how would you manage a woman with urge incontinence / overactive bladder?

A

conservative - reduce excess fluids and caffeine, bladder training (education, timed voiding with increasing delay, positive reinforcement)
drugs - anticholinergics (antimuscarinics) e.g. oxybutynin - suppress detrusor overactivity
botulinum toxin A injections if none of above works, surgery as last resort

122
Q

what is a vesicovaginal fistula?

A

abnormal communication between bladder and vagina, as a complication of an obstructed labour (rare in developed world these days) - presents with constant dribbling incontinence

123
Q

what is endometriosis?

A

presence/growth of tissue similar to endometrium outside the uterus
oestrogren dependent, so regresses after menopause and during pregnancy
can occur throughout pelvis - common in uterosacral ligaments, on or behind ovaries. can form chocolate cysts in ovaries.
causes inflammation, with progressive fibrosis and adhesions

124
Q

describe the main theories behind the causes of endometriosis

A

1) retrograde menstruation - up and out of fallopian tubes
2) metaplasia of mesothelial cells
3) impaired immunity, in that retrograde menstruation cells have not been destroyed

125
Q

how does endometriosis present?

A

pain - cyclical due to endometrial tissue responding to menstrual cycle, or constant due to formation of adhesions from chronic inflammation
might have severe dysmenorrhoea
deep dyspareunia
dysuria
dyschezia (pain on defecation)/cyclical rectal bleeding

subfertility
asymptomatic - incidental finding

126
Q

how is endometriosis investigated and diagnosed?

A

scans not all that helpful but might be used to exclude other pathology
gold standard = laparotomy and biopsy

127
Q

how do you manage endometrosis?

A

medical - COCP (cyclical or continuous), Mirena, oral progestogens, NSAIDs, goserelin can be used for <6m (useful if attempting IVF as well)
surgical - indicated once medical treatment fails - laparoscopy wih ablation or excision of endometriomas

likelihood is these women will suffer chronic pelvic pain

128
Q

what is menopause?

A

permanent cessation of menstruation resulting from loss of ovarian follicular activity
median age = 51y
12m consecutive amenorrhoea

129
Q 
define the following:
perimenopause
postmenopause
early menopause
premature ovarian failure/primary ovarian insufficiency
A

perimenopause = from first signs of menopause –> 12m after LMP
postmenopause = from LMP, but can’t be called this tille >12m amenorrhoea
early menopause = <45y
premature ovarian failure = <40y

130
Q

list some causes of postmenopausal bleeding (PMB)

A 
endometrial or cervical cancer - MUST exclude these!!
atrophic vaginitis
withdrawal leed from cyclical HRT
cervical polyps
ovarian Ca - exclude this too
131
Q

what symptoms/problems to women face when going through the menopause and postmenopause?

A

cardio - increased risk of stroke and CVD
vasomotor symptoms - hot flushes and night sweats
urogenital problems - oestrogen deficinecy leads to vaginal atrophy - dyspareunia, itching, dryness, sexual dysfunction., also may have urinary symptoms.
osteoporosis - increased risk
sexual problems - loss of arousal, loss of desire, problems with orgasm, dysparunia

132
Q

how do you investigate the menopause?

A

FSH - estimates ovarian reserve reamining - if high, few oocytes remain - useful if early menopause
anti-mullerian hormone - more direct measurement of ovarian reserve - low levels = ovarian failure

might also do DEXA scans if concerned about bone density

133
Q

when would you give oestrogen only HRT?

A

ONLY if they’ve had a hysterectomy - NEVER give to a woman with womb!!

134
Q

give a bit of info about HRT for menopause

A

oestrogen + progesterone - use cyclical progeseterone if women are within 12m of LMP (will have withdrawal bleeds)
use continuous progesterone if >12m from LMB
oestrogen can be given orally, as a patch or gel (transdermal), SC or vaginally
progesterone can be delivered via Mirena, orally or transdermally

135
Q

give some contra-indications to HRT

A
  • oestrogen-dependent cancer
  • prev PE
  • undiagnosed vaginal bleeding
  • raised LFTs
  • pregnancy
  • breaastfeeding
136
Q

what are some of the side effects of HRT?

A

fluid retention, bloating, breast tenderness, nausea, headaches, leg cramps.
if progestogens - mood swings, depression, acne, backache

137
Q

what are some alternative options to HRT?

A

SSRIs can help with vasomotor symptoms
calcium, vit D and bisphosphonates for osteoporosis
vaaginal oestrogens if dryness main problem - also silicone based lubricants

138
Q

what is atrophic vaginitis and how can you treat it?

A

postmenopause, lack of oestrgoen means vagina begins to atrophy - typically complains of dryness and dyspareuni.
treat with topical vaginal oestrogens, vaginal moistruisers, silicone based lubricant

139
Q

describe the normal bacterial environment of the vagina

A 
normal vagina is lined by squamous epithelium and colonized by bacterial flora, predominantly Lactobacilli
acidic pH (<4.5)
normal flora helps defends against infection by pathogens
140
Q

what is candidiasis and what factors increase a woman’s risk of getting it?

A

thrush - infection with Candida albicans (yeast like fungus)

pregnancy, diabetes and use of antibiotics are risk factors

141
Q

how does candidiasis present?

A

‘cottage cheese’ discharage
vulval irritation/itching
maybe superficial dyspareunia and/or dysuria
vagina/vulva can appear inflamed and red

142
Q

how is candidiasis diagnosed and treated?

A

diagnosis is by culture of vaginal swab - although can just treat based on clinical suspicion
treat - topical azoles (e.g. single dose clotrimazole pessary) or oral fluconazole (again, single dose)

143
Q

what is BV?

A

bacterial vaginosis - occurs when normal lactobacilli are overgrown by a mixed flora, incl. anaerobes, Gardnerella, Mycoplasma hominis

144
Q

how might BV present?

A

offensive, fishy dischargedischarge is thin, homogenous and adherent to walls of vagina - may be white or yellow

145
Q

how is BV diagnosed?

A

characteristic discharge + raised vaginal pH + ‘clue cells’ on microscopy (vaginal epithelial cells heavily coated in bacteria)

146
Q

how do you manage BV?

A

oral metronidazole BD 400mg for 5 days
or - 2g metronidazole single dose, metronidazole vaginal gel, clindamycin creams
advise against douching, use of shower gels etc

147
Q

what is toxic shock syndrome?

A

rare complication of retained tampon - toxin producing staph aureus
high fever, hypotension, multisystem failure.
antibiotics and intensive care required.

148
Q

what is trichomoniasis?

A

STI - can be carried for months without symptoms

flagellate protozoan infection

149
Q

how does trichomoniasis present?

A

yellow or green discharge which might be offensive, severe itching/soreness/superficial dyspareunia

150
Q

how is trichomoniasis diagnosed and treated?

A

confirmed by wet film microscopy
Rx - metrionidazole 2g single dose or 400mg BD for 5 days
partner notification needed - don’t resume intercourse with partner(s) until treated.

151
Q

give some risk factors for presence of STIs

A 
age <35y
no condom use
symptoms developed after recent change in sexual partner/multiple contacts
recurrent/persistent symptoms
symptoms in partner
partner's risk behaviour
152
Q

what are ‘triple swabs’ used in STI screening/diagnosis?

A

used in primary care:

1) high vaginal swab - for BV, trichomoniasis, thrush
2) endocervical swab - for gonococcal disease
3) chlamydia swab

153
Q

what tests would be done in a routine STI screen for an asymptomatic female?

A

self-taken vaginal swabs for gonorrhoea and chlamydia NAAT
consider pharyngeal/anal swabs dependent on history/type of sex.
ALL patients should be offered HIV and syphilis bloods
consider hep A/B/C bloods if IVDU/other risk factors - hep B esp if assault victim or sex worker

154
Q

what tests would be done in a routine STI screen for an asymptomatic heterosexual male?

A

first-pass urine sample for gonorrhoea/chlamydia

ALL patients should be offered HIV and syphilis bloods
consider hep A/B/C bloods if IVDU/other risk factors

155
Q

what tests would be done in a routine STI screen for an asymptomatic MSM?

A

depending on receptive/insertive oral/anal sex - first pass urine for gonorrhoea/chlamydia and/or pharyngeal/anal swabs for NAAT.
bloods for hep B
ALL patients should be offered HIV and syphilis bloods
bloods for hep A/C in context of local outbreak or other RFs (e.g. IVDU)

156
Q

what is involved in the national chlamydia screening programme?

A

all young adults under 25yrs should be offered a chlamydia test (self-taken swabs or urine sample) annually for free - often involves postal kits etc.
GPs encouraged to offer when young adults visit, even if consultation for unrelated problem.

157
Q

how does chlamydia typically present?

A

asymptomatic!
women - dysuria, vaginal discharge changes, IMB
men - urethral discharge, dysuria

158
Q

how does gonorrhoea typical present?

A

often asymptomatic
women - vaginal discharge, dysuria, abnormal bleeding
men - urethral discharge, dysuria, tender inguinal lymph nodes

159
Q

what causes chlamydia?

A

chlamydia trachomatis types D-K

obligate intracellular bacterium, incubation period <4 weeks for men, unknown in women

160
Q

what causes gonorrhoea?

A

Neisseria gonorrhoeae - gram neg coccus

incubation period 2-5 days in men, unknown in women

161
Q

how do you manage a patient with chlamydia?

A

doxycycline 100mg BD for 7 days

OR - azithromycin 1g single dose

162
Q

how do you manage a patient with gonorrhoea?

A

ceftriaxone IM single dose
cefixime oral single dose
spectinomycin IM single dose

163
Q

how is chlamydia diagnosed?

A

NAAT (nucleic acid amplification testing) performed on swabs/urine

164
Q

how is gonorrhoea diagnosed/

A

culture/NAAT of endocervical swab (women) or first-pass urine (men)

165
Q

what are genital warts?

A 
can vary in presentation
most common STI in UK
caused by HPV usually
spread via skin to skin contact
incubation period usually 3 months (range 2 weeks - 9 months)
166
Q

how do you diagnose and treat genital warts?

A

diagnosis - visual inspection with bright light
management - offer full STI screen, no cure (only treatment for aesthetic/symptomatic relief)
options - imiquimod, podophyllotoxin, cryotherapy, even surgical excision/cautery

167
Q

how does herpes present?

A

multiple small painless vesicles and ulcers - primary infection. virus then lies dormant and reactivations occur

168
Q

how is herpes diagnosed?

A

examination and viral swabs of lesions for PCR - usually HSV2 virus

169
Q

how is herpes treated?

A

acyclovir - reduces severity and duration of episode, particularly for first episode - reactivations usually much milder

170
Q

how does primary syphilis present?

A

solitary lesion, often painless - can go unnoticed. called a ‘chancre’.
heals within 3-10 weeks.

171
Q

how does secondary syphilis present?

A

occurs 4-8 weeks after primary lesion.
generalised lesions of skin and mucous membranes - symmetrical rash.
also get non-specific constitutional symptoms - flu-like.

this is followed by the latent phase (early = <2 yrs, late = >2yrs)

172
Q

what is tertiary syphilis?

A

more lesions + involvement of neuro, cardio or skeletal systems
NASTY - but rare

173
Q

how is syphilis diagnosed?

A

screening test = ELISA test on bloods, then confirmed with assays for Treponema pallidum
can also do direct testing from lesions

174
Q

what pathogen causes syphilis?

A

treponema pallidum

175
Q

how do you treat a patient presenting with syphilis early on i.e. primary/secondary/early latent?

A

benzathine penicillin G IM single dose

procaine penicillin IM o.d. 10 days

176
Q

how do you treat a patient presenting with syphilis late on i.e. late latent or tertiary syphilis?

A

benzathine penicillin IM weekly for three doses

procaine penicillin IM daily for 17 days

177
Q

what is partner notification/contact tracing?

A

informing current and prev partners of new STI diagnosis - really important for reducing spread.
secondary prevention technique.
GUM clinics have specialist contact tracers - help patient to contact partners, or if provided with contact details can contact directly with no mention of partner’s name.
some places have systems where if patient doesn’t refer partners within window, contact tracing is performed by clinic.

178
Q

how common is transmission of HIV via sexual routes? what increases risk of sexual transmission?

A

actually quite uncommon - risk of 0.1=3.0% per sexual exposure - although may well have multiple sexual exposures with same partner!
oral sex is NOT ‘safe’
risk of transmission increased by - HIV viral load in plasma/genital secretions, co-existing STIs, type of sexual activity and frequency, breech in mucosal barrier (trauma), genital HSV infection.
male circumcision and condom use are protective factors

179
Q

describe the natural course of HIV

A

primary infection - acute transient non-specific illness (fever, malaise, lymphadenopathy etc) - seroconversion illness
chronic infection - asymptomatic for ages, until CD4 count becomes so low that AIDS develops. until then may have non-specific constitutional symps (fevers, night sweats, weight loss).
AIDS - presence of 1+ indictors diseases and presence of HIV on lab testing

180
Q

list some common AIDS-defining disease

A

PCP, oesophageal candida, non-Hodgkin’s lymphoma, TB, cerebral toxoplasmos, Cryptococcus meningitis, Kaposi’s sarcoma

181
Q

briefly summarise management of HIV

A

highly active antiretroviral therapy (HAART) helps restore immune function - reduces clinical disease progression and transmission
should be used when symptomatic or CD4 <350

182
Q

what is endometritis?

A

infection of uterine cavity alone - commonly spreads to pelvis if untreated - results from instrumentation of uterus (e.g. IUCD insertion) or complication of pregnancy e.g. retained products

183
Q

what pathogens are typically responsible for endometritis?

A

Chlamydia and gonococcus, E coli, Staph aureus

184
Q

what are the clinical features of endometritis?

A

lower abdo, possible systemic features of infection, offensive discharge.
tender uterus, open os.

185
Q

how would you investigate and manage a woman with endometritis?

A

tests - high vaginal swabs, blood cultures if septic.
broad spectrum abx (e.g. cefalexin or metronidazole), surgical evacuation of retained products of conception if indicated (scans)

186
Q

list some causes of PID

A

STIs - chlamydia most common cause of PID in UK
uterine instrumentation e.g. hysteroscopy, insertion of IUCD, TOP
post-partum
idea is infection ascends up from vagina etc into pelvis - can actually descend from elsewhere too e.g. appendicitis

187
Q

what are the clinical features of PID?

A

lower abdo pain (bi or unilateral), constant or intermittent.
deep dyspareunis, vaginal discharge, IMB or PCB, dysmenorrhoea, fever - but all these vary in whether they’re present or not
can even present late with subfertility.
O/E - cervical excitability (tenderness)

188
Q

what investigations would you perform if a PID diagnosis was suspected?

A

vulvovaginal/endocervical swabs for chlamydia and gonorrhoea and MC&S
if acutely unwell manage as sepsis.
treat empirically with abx - IM ceftriaxone or azithromcyn, plus doxycycline + metronidazole - covers chlamydia/gonorrhoea. treat as outpatient if well - review in 72h to see progress/check culture results.
admit for IV abx if unwell.

189
Q

what are the possible complications of PID?

A 
tubo-ovarian abscess
Fitz-Hugh-Curtis syndrome (liver capsule inflammation)
recurrent/chronic PID
ectopic pregnancy
subfertility - due to tubal blockage
190
Q

what is chronic PID?

A

unresolved/untreated pelvic infection leads to this - inflammation leads to fibrosis, so adhesions develop in pelvis. bad news - pelvic pain, menorrhagia, secondary dysmenorrhoea, discharge and deep dyspareunia.
laparoscopy differentiates this from endometriosis.

191
Q

explain the Rotterdam criteria for PCOS?

A

2 out of 3 must be present:

  • polycystic ovaries on USS
  • oligo-ovulation/anovulation (reflected in oligomenorrhoea)
  • clinical and/or biochemical signs of hyperandrogenism e.g. hirsutism/acne etc
192
Q

how does PCOS present?

A

oligomenorrhoea with/without hirsutism, acne and subfertility

193
Q

what other causes of irregular cycles might you try to exclude before considering a PCOS diagnosis?

A

thyroid dysfunction, hyperprolactinaemia, CAH, androgen secreting tumours, Cushing’s syndrome

194
Q

briefly run through management options for PCOS

A

first line = weight loss and lifestyle. smoking cessation. treat diabetes, hypertension etc.
metformin can improve insulin sensitivity and menstrual disturbance - can be useful with subfertility.
clomifene citrate - to induce ovulation in infertility (often used after trialling weight loss and metformin, not a primary care thing and no more than 6 cycles)
ovarian drilling - if no response to clomifene
COCP used to control bleeding and reduce risk on unopposed oestrogen on endometrium
norethisterone used to induce regular withdrawal bleeds to protect endometrium (ever 3 months ish, if not taking COCP)
hirsutism - Diannette - co-cyprindiol - anti-androgen

195
Q

define ‘subfertility’

A

generally start investigating if no conception after a year (of regular, unprotected vaginal intercourse - double check!), but can take up to two years in ‘normal’ couples!

196
Q

differentiate between primary and secondary failure to conceive

A 
primary = female has never previously conceived
secondary = she has in the past, but failing now
197
Q

what are the 4 basic conditions needed for pregnancy to occur?

A

1) egg must be produced - anovulation (most common cause female infertility)
2) adequate sperm must be released (male factor = c. 25%)
3) sperm must reach the egg - damaged fallopian tubes (most common structural cause) - also sexual problems, cervical problems
4) embryo must implant

30% ish unexplained
don’t forget may be a mix of factors

198
Q

briefly explain physiology of ovulation

A

LOW oestrogen leads to positive feedback on GnRH, causes anterior pituitary to release FSH + LH - leads to growth/maturation of several follicles at once.
these follicles produce oestradiol
INTERMEDIATE oestrogen levels switch it to negative feedback, so LH and FSH drops
follicles ‘compete’ - one with the most LH receptors will end up dominant while the rest will regress.
as follicles mature, release more and more oestradiol
at HIGH threshold - negative feedback reversed and LH surge triggered - leads to rupture of the ‘ripe’ follicle = ovulation
the follicle becomes the corpus luteum, releasing oestrogen and progesterone to maintain secretory endometrium for implantation
if unfertilised - regression of corpus luteum, oestrogen and progesterone drop - menstruation

199
Q

list some common causes of anovulation (leading to subfertility)

A 
PCOS is the main one.
premature ovarian failure
Turner's syndrome
surgery, chemotherapy
excessive weight loss or exercise
hypopituitarism
Kallman's syndrome
hyperprolactinaemia
200
Q

how do you detect whether a woman is ovulating?

A

raised day 21 progesterone levels strongly indicate ovulation has occurred
OTC ‘ovulation kits’ use urinary LH, which can be fairly reliable but not a recommended test

usually majority of women with regular cycles are ovulatory

201
Q

what blood tests might you do to investigate PCOS?

A

raised FSH can be indicator of anovulation
prolactin, TFTs to asses for other causes

serum androgens to investigate hirsutism

202
Q

list some causes of anovulation (apart from PCOS!)

A

hypothalamic hypogonadism - low GnRH leads to amenorrhoea because there’s reduced stimulation of pituitary –> reduced LH/FSH –> reduced oestrogen. this is the cause in athletes/anorexia/stress.

hyperprolactinaemia - excess prolactin –> reduced GnRH - caused by benign tumours or hyperplasia of pituitary cells

Ovarian causes - premature ovarian failure, gonadal dysgenesis

other - thyroid, androgen-secreting tumours

203
Q

how would you treat subfertility due to PCOS?

A 
clomifine - max. 6 month course, it's an antioestrogen, blocks oestrogen receptors in hypothalamus and pituitart to raise FSH/LH - can help initiate follicle maturation.
metformin
laparoscopic ovariandiathermy (ovarian drilling) - can combine with test for tubal patency
gonadotrophins - used to induce ovulation if clomifine has failed - FSH/LH given SC daily to stimulate follicle growth - risk of OHSS
204
Q

how would you investigate subfertility in a primary care setting?

A

hormonal profile - day 2-5 FSH and LH
TSH, prolactin and testosterone
chlamydia test, check rubella status (vaccinate if non-immune)
mid-luteal progesterone (7 days before expected period e.g. day 21 in 28-day cycle) - checks if ovulation occurring
semen analysis - repeat in 3 months if abnormal after making lifestyle changes and adding selenium/zinc/vit C supplements

205
Q

how would you investigate subfertility in gynae clinic, assuming primary care investigations (21 day progesterone, semen analysis etc) have been performed?

A
  • TV USS to check for PCOS, other masses/fibroids etc
  • hysterosaplingogram (HSG) uses XR and contrast to demonstrate uterine anatomy and tubal patency (hysterosalpingo-contrast songograph is similar but contrast + TV USS)
  • laparoscopy and dye test - gold-standard for assessing tubal patency - methylene blue dye injected, tubes visualised with laparoscope - first line if strong suspicion tubal problems or needs laparoscopy for other reasons -second line if HSG abnormal
206
Q

briefly describe the physiology of sperm production

A

spermatogenesis in the testis depends on pituitary LH and FSH, acting via testosterone production in Leydig cells of testis
FSH + testosterone control the Sertoli cells - in charge of transport and release of sperm
takes around 70 days for sperm to develop fully

207
Q

what’s involved in semen analysis?

A

sample produced after 2-7 days without ejaculation - must be analysed within a couple of hours.
if abnormal - advise lifestyle changes and repeat in 12 weeks before any further investigations of male done.

tests for - volume, sperm count, progressive motility

208
Q

give some causes of abnormal/absent sperm release

A
  • idiopathic oligospermia (reduced quantiy of cells)/asthenozoospermia (reduced/absent motility) are common
  • drugs - alcohol, smoking, drugs (sulfasalazine, anabolic steroids) + exposure to industrial chemicals
  • varicocele - present in 25% of infertile men
  • antisperm antibodies, occurs in 5% - more common after vasectomy reversal (poor motility + clumping together of sperm on sperm analysis)
  • other - infections, mumps orchitis, testicular abnormalities, obstruction in sperm delivery
209
Q

how would you investigate a man with abnormal semen analysis results?

A

repeat in 12 weeks then:
if azoospermia (no sperm) - bloods (FSH, LH, testosterone, prolactin and TSH) to find treatable cause
might do karyotyping for genetic cause e.g. Kleinfelter’s (XXY)
blood tests for cystic fibrosis

210
Q

how would you manage subfertility where male subfertility/infertility is to blame?

A

advise lifestyle - reduce alcohol, keep testicles cool etc
treat any identified cause if poss
assisted conception - intrauterine insemination or IVF, surgical sperm retrieval, donor sperm

211
Q

describe how different parts of female anatomy function to aid fertilisation

A

at ovulation - fallopian tube moves so that fimbrial end collects oocyte from ovary
peristaltic contractions and cilia in tube help sweep the oocyte along towards the sperm - blockage/ciliary damage will impair this
also, at ejaculation, cervical mucous aids transport of sperm into uterus

212
Q

give some causes of tubal damage leading to subfertility, plus some specific management options for them

A

infection - PID (formation of adhesions within/around fallopian tubes) - laparoscopic adhesiolysis and salpingostomy can help.
endometriosis - laparoscopy to remove endometriotic deposits can improve fertility
prev. pelvic surgery - adhesions.

213
Q

give some causes of infertility that aren’t due to tubal problems, anovulation or male problems

A

cervical problems - rare, treat with IUI as bypasses cervix. e.g. infection in vagina/cervix preventing mucus production, ectropion (os swollen shut), woman might product abs against sperm
sexual problems - actually having sex frequently??

214
Q

what lifestyle recommendations would you give to a couple trying to conceive?

A 
weight loss (or gain!) if necessary. lots of fruits and veg. stop smoking and doing drugs, reduce alcohol consumption, regular exercise, folic acid supplements, sex every 2-3 days throughout the month.
avoid timed intercourse and ovulation monitors - increase stress more than benefit!
215
Q

describe what options there are to induce ovulation to attempt to treat subfertility (if anovulatory cause suspected)

A

clomifine - given day 2-6 of cycle, for max 6 months, can help induce ovulation.
gonadotrophins - used if clomifene resistant generally - SC injections daily.
IVF after that.

216
Q

describe the role of surgical interventions in the management of subfertility

A

if tubal disease = proximal can try to resolve with tubal catheterisation or hysteroscopic cannulation (high rates of ectopics!)
endometriosis - laparoscopy to remove tissue
intrauterine adhesions - hysteroscopic adhesionolyis

217
Q

list some indications for IVF

A

anovulatory infertility not responding to clomifene/gonadotrophings
endometriosis
male factor subfertility
tubal disease

218
Q

give some factors that affect success rates of IVF

A

age, duration of subfertility, previous pregnancy (improves chances!), smoking, high BMI

219
Q

briefly explain the process involved in IVF

A

ovaries stimulated (beware OHSS)
ova collected - by transvaginal aspiration under TV US guidance
ova fertilized
3-5 days later, 1-2 embryos returned to uterus
luteal support given (progestagens) - 2 weeks later, do a pregnancy test

220
Q

list and briefly explain some assisted conception options that AREN’T IVF

A

donor insemination - useful when male partner azoospermic or if sperm retrieval failed, or in same-sex female partners

intracytoplasmic sperm injection (ICSI) - sperm taken from ejaculate or sperm retrieval and injected directly into egg.

intrauterine inseminations (IUI) - useful in mild male factor subfertility, coital difficulties, unexplained subfertility, same-sex couples - can be combined with ovarian stimulation (but beware multiple pregnancies)

oocyte donation - often done through ‘egg-sharing’ by women who are themselves having IVF (can reduce their costs)

221
Q

how do COCPs work to prevent pregnancy?

A

exert negative feedback effect on gonadotrophin release, inhibiting ovulation.
also thin endometrium and thicken cervical mucus.
most contain ethinyloestradiol - synthetic oestrogen
‘withdrawal’ bleeds occur during week off

222
Q

list some contraindications for COCP

A

migraine with aura (or without if >1 RF for stroke)
current/past VTE
avoid if: age>35yr, smoker (15+ per day), hx of CVD (stroke, TIA, IHD, PVD)
cancer - hx of breast cancer

223
Q

list some non-pill combined contraceptives

A

patch - transdermal, change every week + break every 4th week
NuvaRing - inserted into vagina, leave for 3 weeks, then remove for break week

224
Q

list some short-term side effects of combined hormonal contraceptives

A

often resolve within 2-3 cycles:
oestrogenic - breast tenderness, nausea, cyclical weight gain, bloating, vaginal discharge
progestogenic - mood swings, PMS, vaginal dryness, sustained weight gain, decreased libido, acne
headache
breakthrough bleeding

225
Q

what are the risks associated with COCP use?

A

VTE risk - doubled (although still way below risk in pregnancy!!)
ischaemi cstroke
breast and cervical cancer (normalises within 10yr of stopping)
mood changes

NB - stop oestrogen containing contraception 4 wks pre-op and arrange alternative contraception

226
Q

briefly outline what to advise a woman if she misses her COCP

A

if delayed over 48h, continue pills as usual, use condoms for 7 days (if 48h included days of break then start new pack straight away).
if 2 pills missed in first week, use emergency contraception.
If <48h - take two pills today, no need for condoms.

227
Q

how do progesterone-only contraceptives work?

A

thicken cervical mucus, reduce receptivity of endometrium and in some women inhibit ovulation.
taken as POP
most have a 3h window in which pill must be taken
Cerazette (desogestrel) = 12 hour window.
efficacy affected by hepatic-enzyme inducing drugs (beware AEDs)

228
Q

what are the side effects of the POP?

A

irregular menstrual bleeding ins the big one, breast tenderness, depression, acne, reduced libido, weight change

229
Q

how does the contraceptive injection work?

A

depo progestogen, given ever 12 weeks usually.
beware osteoporosis risk and risk of weight gain.
often irregular bleeding at first which settles to amenorrhoea.
can be helpful for PMS and menorrhagia.

230
Q

how does the implant work?

A

flexible rod inserted subdermally in arm, lasts 3 years. contains etonogestrel (progesterone). irregular bleeding initially, some women experience prolonged bleeding for first 3 months. around a quarter end up amenorrhoeic.

231
Q

how does the mirena coil work?

A

levonorgestrel
sits in womb making periods less painful and lighter for 5 years.
can be used in breastfeeding, obesity, CVD, women taking hepatic-enzyme inducing drugs.
all round, good time - but hurts to go in

232
Q

how do IUCDs work?

A

copper coil - inhibit fertilization, implantation and sperm penetrating mucus.
change every 5-10 yrs.
can be used for emergency contraception - useful in women presenting late (up 120h after UPSI or 5 days after likely ovulation)
screen for infection before insertion or give azithromycin at time of insertion
advise to check threads after each period.

233
Q

how does EllaOne work/when can it be used?

A

ullipristal acetate
must take within 120h of unprotected sex, but sooner the better.
thought to inhibit/delay ovulation

234
Q

how does Levonorgestrel work as an emergency contraceptive?

A

use within 72h of unprotected sex, ideally within 12 hours.

thought to inhibit ovulation.

235
Q

what is the most effective form of emergency contraception?

A

IUCD

236
Q

define spontaneous miscarriage - when does this occur?

A

foetus dies or delivers dead at <24 weeks gestation (delivered dead >24 weeks is still birth)
typically <12 weeks gestation
rate of miscarriage increases with maternal age

237
Q

what are the different methods used for TOP?

A

surgical - suction curettage between 7-13 weeks, >13 weeks use dilatation and evacuation (give cervical preparation before e.g. misoprostol PV)
medical - antiprogesterone mifepristone, plus prostaglandin (misoprostol) given 36-48h after
medical is most effective method if woman is <7 weeks

238
Q

what is an ectopic pregnancy? where is the most common site?

A

when an embryo implants outside the uterine cavity

most common in ampulla of fallopian tube (more risky if in isthmus as rupture way more likely)

239
Q

give some predisposing factors of ectopic pregnancy

A

PID, previous surgery, previous ectopic, endometriosis, IUCD, POP, subfertility and IVF, smoking

240
Q

what are the symptoms/signs of a miscarriage?

A

always exclude ectopic in sexually active woman with abdo pain/bleeding/fainting or even D&V
pain - can be non-specific, classically unilateral
vaginal bleeding
diarrhoea/loose stools and vomiting
shoulder tip pain - diaphragmatic irritation due to bleeding into peritoneum
collapse
dizziness
normal sized uterus
cervical excitation

241
Q

what investigations would you perform in a suspected ectopic pregnancy?

A

FBC, group and save/cross match
HCG / serum progesterone to detect pregnancy
TV USS - to locate pregnancy

242
Q

what are the different types of management options for an ectopic pregnancy?

A

if stable - can manage expectantly or medically

otherwise will need surgery

243
Q

what criteria must be met to consider using medical/expectant management of an ectopic pregnancy?

A
  • asymptomatic
  • HCG <3000
  • ectopic pregnancy <3cm on scan with no FHR
  • no haematoperitoneum on TV USS
  • full understanding of risks and willing to attend regular follow up, with support at home
244
Q

describe expectant management of an ectopic pregnancy

A

take serum HCG every 48h until confirmed falling, then weekly until <15
if falling slowly/plateauing, reconsider management plan

245
Q

describe the medical management of an ectopic pregnancy

A

methotrexate single dose, then HCG measured on days 4 and 7 - if fallen by <15%, second dose required
must use contraception for 3 months after due to teratogenicity of methotrexate

246
Q

describe surgical management of an ectopic pregnancy

A

laparoscopy is preferred option - salpingotomy/salpingectomy.
if contralateral tube healthy - salpingectomy (removal of ectopic via tubal incision)
if other side unhealthy though, salpingotomy to preserve chances of future intrauterine pregnancy

247
Q

define ‘pregnancy of unknown location’ - what are the different outcomes that are possible

A

no sign of intrauterine or ectopic pregnancy or retained POC, in presence of positive pregnancy test or serum HCG >5
outcomes are:
- early intrauterine pregnancy (too early to see on scan)
- complete miscarriage
- failing PUL that will never appear on scan but will resolve itself
- ectopic pregnancy (10%)
- persistent PUL
- RARELY - HCG secreting tumour

248
Q

how do HCG levels change in a normal intrauterine pregnancy?

A

should see rise of >66% every 48h

249
Q

what is gestational trophoblastic disease?

A

where trophoblastic tissue proliferates in a more aggressive way than normal
premalignant = hydatidiform moles
malignant = choricarcinoma

250
Q

what is the difference between a complete and a partial hydatidiform mole?

A

complete - sperm has fertilized an empty egg - entirely paternal origin (apart from maternal mitochondrial DNA)
partial - usually follow dispermic fertilization of ovum, may feature some foetal tissue (actually have bits of foetus in them usually) - 3x more common, slower growing

251
Q

how do hydatidiform moles present?

A

they are derived from chorion so make loads of HCG –> exaggerated pregnancy symptoms and strongly positive pregnancy test.
most present with miscarriage, heavy bleeding.
large uterus

252
Q

what is the characteristic US feature of a hydatidiform mole?

A

snowstorm effect

253
Q

how is a hydatidiform mole managed?

A

mole tissue removed from uterus via gentle suction. give anti-D if rhesus -ve.
avoid pregnancy until HCG normal for 6 months - HCG should normalise within about 6 months, if not dropping consider chemotherapy as may have been invasive mole ± mets

254
Q

how does a choriocarcinoma present? how is it managed?

A

can be years later, with general malaise or uterine bleeding or signs/symps from metastases.
managed in 3 centres in UK - chemo based on methotrexate.

255
Q

how might genital tract abnormalities present?

A 
sexual problems
primary amenorrhoea
obstructed labour
picked up on examination
subfertility
recurrent miscarriage
256
Q

list some female genital tract abnormalities

A 
vaginal sepatae - relatively common but hard to detect
bicornuate uterus - partially divided into two
unicornuate uterus - part divided into two but one hasn't developed
absent/short vagina or uterus
streak ovaries (Turner's syndrome)
257
Q

what is a haematometra? what about a haematocolpos?

A 
haematometra = uterus filled with blood due to outflow obstruction e.g. due to imperforate hymen, carcinoma
haematocolpos = blood-filled dilated vagina, usually due to imperforate hymen
258
Q

what is OHSS?

A

ovarian hyperstimulation syndrome - complication of ovarian induction or superovulation
can be really severe/dangerous

259
Q

what are the characteristics of OHSS? what are the risk factors?

A

ovarian enlargement, fluid shift from intravascular to extravascular space - leads to accumulation of fluid in peritoneal and pleural spaces

260
Q

how does OHSS present?

A

abdo discomfort, nausea, vomiting, abdo distension ± dyspnoea
usually presents 3-7 days after HCG administration (or 12-17 days if pregnancy occurred)

261
Q

how is OHSS prevented/managed?

A

prevention - give lowest effective gonadotrophin growth
mild/moderate (abdo bloating, mild pain, US evidence of ascites, ovaries 8-12cm) management - outpatient, give analgesia, avoid NSAIDs, bed rest, progesterone luteal support, review
severe (clinical ascites, oligouria, ovarian size >12cm) - admit, analgesia, monitor, strict fluid balance etc

262
Q

what is Turner’s syndrome?

A

chromosomal abnormality - 45,X (or 45,X0) - only 1 X syndrome, oocytes don’t develop properly, present with primary amenorrhoea/delayed pubterty, also short stature, webbed neck, shield chest

263
Q

what is Asherman’s syndrome?

A

rare condition - intrauterine adhesions - causes menstrual disturbance, placental abnormalities, subfertility.
RFs - uterine surgery (e.g. myomectomy, C section), infections, some genetic role, evacuation of RPOC
classical history is of pregnancy ending in surgical management of miscarriage/TOP then secondary amenorrhoea
treatment - can involve surgical removal of adhesions, maybe with balloon to stent open to prevent more adhesions forming

264
Q

what is dyspareunia? what are the two main types and what commonly causes each one?

A

pain during sex
superficial vs deep
superficial - e.g. from infection, vaginal atrophy, lack of sexual stimulation
deep - felt internally, often endometriosis or PID, treat cause if possible

265
Q

what is Kleinfelter’s syndrome?

A

chromosomal abnormality that causes small testicles and infertility
47, XXY

266
Q

ultrasound features of ovarian mass/cyst that suggest malignancy

A 
BAM2S:
Bilateral
Ascites
M2 - metastatic, multilocular
Solid mass

3a (11 decks)

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