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gynaecology > menstural disorders > Flashcards

menstural disorders Flashcards

1
Q

what are fibroids?

A

benign tumours of myometrium
also known as leiomyomas
can become malignant
stimulated by oestrogen

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2
Q

how can fibroids classified?

A

intramural - within myometrium and do not protrude out or in
submucosal - develops immediately below endometrium and thus protrudes into the uterine cavity
subseroal - protrudes into and distorts the serosal surface of uterus

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3
Q

what are the risk factors for developing fibroids?

A 
early menarche
age
overweight 
FHx
ethnicity
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4
Q

what are the differentials

A

endometrial polyp
leiomyosarcoma
ovarian tumour

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5
Q

what are the clinical features of fibroids?

A

majority are asymptomatic
may have menorrhagia
may have pressure symptoms e.g. urinary frequency, retention, abdo distension
subfertility due to obstructive effects

acute pelvic pain from red degeneration

on examination - non tender uterus but solid mass/enlarged uterus may be palpable on bimanual exam

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6
Q

what is red degeneration?

A

sudden disruption in fibroid blood supply e.g. may be torsion of pedunculated fibroid or in pregnancy where fibroid is rapidly growing

fibroid undergoes necrosis and haemorrhage
leads to N,V and low grade fever and acute abdo pain

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7
Q

what investigations should be performed if a fibroid is suspected?

A

pelvic USS

MRI rarely used unless sarcoma suspected

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8
Q

what is a degenerate fibroid?

A

The fibroid outgrows its blood supply and thus can degenerate.
this mainly occurs slowly but can be rapid (red degeneration)
fibroid dies and releases substances causing pain, swelling and low grade fever

types:
- hyaline degeneration - asymptomatic
- red degermation

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9
Q

what is zolidex?

A

GnRH analogue
can be used to treat fibroid by supressing ovulation to shrink fibroid (useful pre -op)
only can use for 6 months due to osteoporosis risk

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10
Q

what defines heavy menstrual bleeding?

A

excessive menstrual blood loss (>80ml) that impacts a woman physically, emotionally and socially

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11
Q

what is the aetiology behind heavy menstrual bleeding?

A

structural causes: (PALM)
- polyps - endometrial/cervical - usually not painful, PCB/ IMB
- adenomyosis
- leiomyomas/ fibroids
- malignancy/ hyperplasia - may be vaginal/cervical hyperplasia provoked by ovarian tumour
non-structural: (COEIN)
- Cogaulopathy
- ovarian dysfunction - hypothyroid, PCOS
- endometriosis
- iatrogenic - intrauterine copper device
- not classified = dysfunctional uterine bleeding (60% of cases)

other = pregnancy = ectopic, miscarriage, placenta praevia
also obesity

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12
Q

what is adenomyosis

A

presence of endometrial tissue in the myometrium of the uterus
(variant of endometriosis)
the endometrial tissue breaks through into myometrium

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13
Q

what are the clinical features of heavy menstrual bleeding?

A

menorrhagia
symptoms associated with anaemia - SoB, tired, pallor
symptoms depending on cause
examination may reveal cause e.g. bimanual examination may be able to feel irregular uterus as a sign of fibroids

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14
Q

what investigations could you do in someone presenting with menorrhagia?

A

FBC, INR, sometimes TFTs, specific blood tests for cause e.g. von Willebrand factor (if history of clotting disease, heavy periods since puberty)

pregnancy test
cervical smear
high vaginal and endocervical swabs
transvaginal USS to assess endometrium and ovaries

hysteroscopy +/- endometrial biopsy

  • can use pipelle/ curettage
  • indicated if persistent heavy bleeding, >45yrs or failure of pharm methods
  • to exclude endometrial malignancy hypoplasia
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15
Q

how is heavy menstrual bleeding managed (1st, 2nd and 3rd line treatments)

A

Levonorgestrel - releasing intrauterine system (LNG-IUS) - first line

  • max 5 years of use , min 12 months, warn patient of irregular bleeding and persist for 6 months for it to settle
    - contraceptive too.

transexamic acid/ mefenamic acid or COCP - second line

- no contraceptive effect for first 2 
- COCP has contraceptive  effect too

progesterone only (oral, depo, implant) - 3rd line

  • oral norethisterone (taken day 5-26) does not work as a contraceptive when taken this way but still effects fertility
    - depo and implant will act as contraceptive too.
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16
Q

how does levonorgestrel - releasing intrauterine system (LNG-IUS) help with heavy menstrual bleeding?

A

progesterone

Thins the endometrium and can shrink any fibroids

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17
Q

how does transexamic acid work to help with heavy menstrual bleeding?

A

Transexamic acid:

- binds plasminogen and prevents fibrinolysis. taken during menses to reduce bleeding.

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18
Q

what are the side effects of transexamic acid?

A 
nausea, 
dizziness
tinnitus 
rash 
abdo cramps
indegrestion, diarrhoea 
headache
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19
Q

when is transexamic acid contraindicated?

A

fibrinolytic disorders
DVT risk
following DIC
history of convulsions

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20
Q

what is mefenamic acid? how does it help in heavy menstrual bleeding?

A

type of NSAID
inhibits COX to reduce prostaglandin release, less spasming of spiral arteries and thus reduced ischaemia and shedding of endometrium
less myometrial contractions

also offers analgesic effect

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21
Q

what is ulipristal acetate

A

progesterone receptor modulator
shrinks fibroids/ endometrial tissue to reduce bleeding
can also be useful pre-op before fibroid removal

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22
Q

what surgical management is available for heavy menstrual bleeding?

A

endometrial ablation

hysterectomy - only definitive treatment (can do subtotal or total (cervix removed too))

uterine artery embolization

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23
Q

what is endometrial ablation?

A

removal of endometrium including basal layer but myometrium is left.
good for women who no longer want to get pregnant
can be performed with laser, cold coagulation, microwaves or resection
under local anaesthetic as an outpatient

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24
Q

what are the side effects of endometrial ablation?

A

pain and period cramping
vaginal discharge
hyponatraemia

less common = infection, perforation, bleeding

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25
Q

when is uterine artery embolization used?

A

only for fibroids (when a cause of heavy menstrual bleeding)
causes reduction in blood supply to fibroid and thus degeneration/ shrinkage for those >3cm

can be performed by radiologist via femoral artery

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26
Q

what is the treatment for fibroids?

A

Can just leave them if not causing much trouble

medical:

  • levonorgestrel IUS
  • Ulipristal acetate
  • Zolidex

surgery:

  • endometrial ablation - for fibroid <3cm
  • uterine artery embolization - for fibroids >3cm
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27
Q

what is the treatment for fibroids?

A

Can just leave them if not causing much trouble

medical:

  • levonorgestrel IUS
  • Ulipristal acetate
  • Zolidex

surgery:

  • hysteroscopy and transcervical resection of fibroid
  • myomectomy (good if children wanted in future) -open or hysteroscopic
  • endometrial ablation - for fibroid <3cm
  • uterine artery embolization - for fibroids >3cm
  • hysterectomy - last resort for big fibroids with impact on quality of life
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28
Q

what are the features of adenomyosis?

A

endometrial tissue grows into myometrial wall

  • dysmenorrhoea
  • menorrhagia
  • bulky tender uterus
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29
Q

what should be considered for fibroids >3cm

A 
unlikely medical management will have much effect 
consider
  - uterine artery embolization
  - myomectomy 
  - hysterectomy
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30
Q

what should be considered for fibroids <3cm?

A

1st line LNG - IUS
2nd line tranexamic acid/ mefenamic acid/ COCP
3rd line progesterone

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31
Q

what are the problems with myomectomy?

A

adhesions, pain

haemorrhage (rarely)

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32
Q

Define amenorrhoea. What are the 2 types ?

A

lack of periods
can be primary - never had a period:
- diagnosed at 14 if no other sexual characteristics
- diagnosed at 16 if sexual characteristics
or can be secondary - periods stopped for >6months

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33
Q

what is the aetiology behind amenorrhoea?

A

physiological - pregnancy, pre-puberal, menopause

hypothalamus:
- suppression - low BMI, excessive exercise can supress GnRH secretion
- psychiatric disorder, sarcoidosis, thyroid can supress it
- kallman syndrome

pituitary

  • tumours e.g. mass effect (acromegaly, cushings) or hyperprolactinaemia
  • sheehans syndrome
  • radiation, autoimmune
  • post contraception - prolonged suppression, takes a while to reset

ovarian:
- turners, PCOS, premature ovarian failure

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34
Q

what is the aetiology behind amenorrhoea?

A

physiological - pregnancy, pre-puberal, menopause

hypothalamus:
- suppression - low BMI, excessive exercise can supress GnRH secretion
- psychiatric disorder, sarcoidosis, thyroid can supress it
- kallman syndrome

pituitary

  • tumours e.g. mass effect (acromegaly, cushings) or hyperprolactinaemia
  • sheehans syndrome
  • radiation, autoimmune
  • post contraception - prolonged suppression, takes a while to reset

ovarian:
- turners, PCOS, premature ovarian failure

adrenal: congenital adrenal hyperplasia
genital tract: ashermans (uterine adhesions), imperforate hymen
thyroid - hypo or hyperthyroidism

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35
Q

what is the mechanism by which pituitary tumours can cause amenorrhoea?

A

prolactinoma - hyperprolactinaemia supresses GnRH

other tumours can have a mass effect to supress GnRH

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36
Q

what is:

  • Kallman syndrome?
  • Sheehans syndrome?
A

Kallman syndrome = X linked recessive disorder, GnRH neurons fail to migrate

sheehans: post partum pituitary necrosis due to massive obstetric haemorrhage

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37
Q

what is congenital adrenal hyperplasia?

A

21 hydroxylase enzyme deficiency results in ability to make cortisol, ACTH is thus very high and causes hyperplasia.
this results in androgen excess (clitoromegaly, acne, hirsutism, early pubic hair)
amenorrhoea (due to high androgens)

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38
Q

what is cryptomenorrhoea?

A

amenorrhoea due to blockage e.g. imperforate hymen

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39
Q

how does imperforate hymen present?

A

cyclic adbo pain but no periods

40
Q

what is the mechanism behind which hypo and hyperthyroidism can cause amenorrhoea?

A

hypothyroid –> results in high TSH and TRH which promotes prolactin release. hyperprolactinaemia inhibits GnRH and LH/FSH

hyperthyroid –> increases SHBG due to increased T3/4. thus less free oestrogens

41
Q

what defines oligomenorrhoea?

A

irregular periods with intervals >35days or <9 periods / yr

42
Q

what are the common causes of oligomenorrhoea?

A 
PCOS
contraceptive hormones 
perimenopause 
thyroid/ diabetes 
eating disorders
medications - antiepileptics/ psychotics
43
Q

For someone presenting with primary amenorrhoea what should we look for in examination?

A

signs of turners, galactorrhoea, growth retardation, mass pituitary tumour effects, thyroid disease, androgen excess

44
Q

what factors are suggestive of premature ovarian failure?

A

low LH/ FSH
<40
high prolactin
low O +P

45
Q

what investigations should be done if there is secondary amenorrhoea?

A

pregnancy test
bloods - TFT, prolactin, LH/FSH/O/P
if suspected ashermans - refer to gynae for USS to visualise pelvic cavity

46
Q

how is CAH tested for?

A

17 hydroxyprogesterone (raised in CAH) because levels build up when it cant be converted to cortisol

47
Q

how is amenorrhoea and oligomenorrhoea managed?

A

osteoporotic prophylaxis - if O is low there is a risk of osteoporosis - treat underlying cause, give ADCAL, consider COCP/HRT

depends on cause to how its managed

  • PCOS - metformin,
    • hirsutism - spirolactone and cryproterone acetate
    • acne - Abx and benzyl peroxide
  • infertility - clomifene / IVF
48
Q

what is PCOS?

A

Polycystic ovarian syndrome - characterised by excess androgens and polycystic ovaries (multi immature ovaries = cysts)

49
Q

what is the pathophysiology behind PCOS?

A

There is excess LH secretion due to increased GnRH pulses
LH causes androgen secretion by ovaries.
although there is excess LH, the excess androgens prevent LH surge and ovulation and thus instead all follicles develop and none dominate - follicles arrest and cysts develop

there is also insulin resistance
high insulin inhibits hepatic production of SHBG means more free androgens
ovaries are insulin sensitive and respond by making more androgens
also abnormal lipid levels.

multifactorial aeitology

50
Q

what are the risk factors for PCOS?

A

diabetes
obesity
family history

51
Q

what are the clinical features of PCOS?

A 
variable
amenorrhoea/ oligomenorrhoea
infertility 
acne, hirsutism , male pattern baldness
chronic pelvic pain
HTN
acanthosis nigricans
depression
obesity - central fat deposition
52
Q

what are the differentials for PCOS?

A

Hypothyroid - obese, hair loss, insulin resistance
cushings - central fat, acne, hirsutism, insulin resistance, depression
hyperprolactinaemia - amenorrhoea, acne, hirsutism

53
Q

what is the Rotterdam criteria?

A

2 or more needed for diagnosis:

  • clinical/ biochemical features of hyperandrogenism
  • oligo/amenorrhoea (<6/9 menses/year)
  • polycystic ovaries on imaging (12 or more follicles in one ovary or ovarian volume >/= 10cm3

new criteria says top one must be present and either or of the other 2

54
Q

what blood tests are needed for PCOS diagnosis?

A

LH - raised
FSH - normal
(LH:FSH raised is most important indicator even if both in normal range - a level of 3:1 is enough)

Testosterone is raised
SHBG is low
progesterone is low

rule out differentials - TFT, prolactin
(note mildly elevated prolactin can be seen in PCOS)

55
Q

how is PCOS investigated?

A

Hx
bloods
transvaginal USS - numerous peripheral ovarian follicles and volume >10cm3

56
Q

how is PCOS managed?

A

amenorrhoea:

  • these women have high O and no P (no ovulation) and thus at risk of endometrial hyperplasia and cancer.
  • can give low dose COCP to help with cycles/ protect
  • or progesterone only (Dydrogesterone)
  • aim for atleast 3 bleeds/ year to protect the endometrium

obesity/ insulin resistance

  • diet/ exercise to loose weight and improve insulin sensitivity
  • orlistat can be used - pancreatic lipase inhibitor
  • metformin - improves insulin sensitivity and ovulatory function

infertility:
- clomifene +/- metformin - first line for those wishing to conceive with BMI >25 (due to risks limited use to 6cycles/ months min)

hirsutism

  • treated cosmetically
  • antiandrogen drugs - spironolactone, cyproterone or finasteride (avoided in pregnancy because teratogenic)
  • eflornithine - topical cream that can help reduce the growth rate of facial hair

also may give statins

57
Q

what risks are associated with treating PCOS infertility with clomifene?

A

ovarian hyperstimulation syndrome
multiple pregnancy
ovarian cancer

58
Q

what are the complications of PCOS?

A 
diabetes
infertility 
endometrial cancer
TIA/stroke 
HTN

miscarriage, gestational diabetes

59
Q

what is offered to women wanting to conceive who have a BMI <25 or clomifene is contraindicated?

A

laparoscopic ovarian drilling - diathermy / laser to reduce amount of androgen producing tissue

can also offer gonadotrophins

60
Q

what is primary and secondary dysmenorrhoea?

A

primary - painful periods without underlying pelvic pathology
secondary - painful periods with underlying pelvic pathology

61
Q

what are the risk factors for dysmenorrhoea?

A 
early menarche
long periods
heavy periods
smoking
nulliparous
62
Q

what are the clinical features of dysmenorrhoea?

A

painful periods - lower abdominal / pelvic pain can radiate to lower back and anterior thighs - usually cramping in nature.
nausea, vomiting, dizziness, malaise
may have diarrhoea too
on examination may be unremarkable or tender uterus

63
Q

what are the differentials for dysmenorrhoea?

A 
endometriosis
adenomyosis 
IBD
PID 
IUD - painful on insertion 
adhesions
64
Q

what are the red flags for dysmenorrhoea?

A

post coital bleed
intermenstrual bleeding
pelvic mass

65
Q

what should be covered in history of someone presenting with dysmenorrhoea?

A

work out if primary or secondary - more likely primary if started at menarche
associated symptoms
- rectal pain, changes to bowel habits, bloating can be associated with endometriosis
- vaginal discharge and STI

66
Q

what are you looking for on examination of someone with dysmenorrhoea?

A

unremarkable if primary dysmenorrhoea

tender uterus, fixed retroverted uterus = endometriosis

67
Q

what are the features of primary dysmenorrhoea?

A

starts with menarche
unremarkable examination
starts just before period starts and lasts around 72 hours.

68
Q

how would you investigate someone with dysmenorrhoea?

A

STI screen - high vaginal and endocervical swab

Transvaginal USS / pelvic USS - to exclude pelvic pathologies (endometriosis, adenomyosis)

laparoscopy - gold standard for endometriosis

69
Q

how can transvaginal USS / pelvic USS diagnose endometriosis?

A

may find ovarian endometriomas
can demonstrate ‘kissing ovaries’ where bilateral endometriomas adhere
can demonstrate any bowel involvement from pelvic motility

70
Q

how can transvaginal USS demonstrate adenomyosis?

A

globular uterine configurations
poorly defined endometrial/ myometrial interface
intramyometrial cysts
heterogenous myometrial echotexture

71
Q

how is adenomyosis diagnosed for definite?

A

histologically after hysterectomy

72
Q

what are the typical findings on laparoscopy for endometriosis?

A

chocolate cysts, adhesions, peritoneal deposits

73
Q

how is dysmenorrhoea managed?

A

conservative - stop smoking, hot water bottles

pharmacology:
- analgesia - mefenamic acid/ ibuprofen, paracetamol
- hormonal control - COCP, POP, mirena, GnRH analogies - all help to supress ovulation and thus growth of endometrium, blood loss and inflammation (good for endometriosis, adenomyosis and also primary). Also aromatase inhibitors.

surgical

74
Q

what are the surgical options for endometriosis?

A

removal of endometrial tissue by excision, fulgaration and laser ablation

or hysterectomy and removal of ovaries = ultimate cure (need HRT till menopause)

75
Q

what are the surgical options for adenomyosis?

A

uterine artery embolization - block supply of blood to cause lesion to shrink
endometrial ablation/ resection
hysterectomy

76
Q

what is the pathophysiology behind endometriosis?

A

condition whereby endometrial tissue is found outside of uterine cavity
usually diagnosed between ages 25 to 40

77
Q

what is endometriosis?

A

for unknown reason endometrial tissue can grow in various places:
- ovaries, fallopian tubes, uterosacral ligament, pelvic peritoneum, umbilicus, pouch of douglas, bowels, bladder, lungs

because of this the tissue is responsive to O+P and thus grows and during menstruation there is inflammation and shedding of the tissue leading to pain and bloating or other symptoms depending on site
bouts of inflammation can result in scarring and further problems e.g. can affect fertility e.g if in fallopian tubes

symptoms improve with pregnancy and menopause

78
Q

what are the risk factors for endometriosis?

A

early menarche
short menstrual cycles
long periods
heavy bleeds

family history
defects in ovaries and fallopian tubes

79
Q

what are the differentials of endometriosis?

A

PID - can present with pain and menorrhagia
IBS/IBD - pain, bloating, change in bowel habit
ectopic pregnancy
fibroids

80
Q

what are the clinical features of endometriosis ?

A

cyclic pain / dysmenorrhoea
subfertility
dyspareunia

depends on where it affects:

  • bowels - change in bowel habbit, rectal pain, dyscherzia (pain on defaecation)
  • lungs - haemothorax if bleeding into pleural cavity
  • bladder - dysuria
81
Q

what is found on examination in endometriosis?

A

fixed retroverted uterus
general tenderness
may have uterosacral ligament nodules

82
Q

what are the risk factors for adenomyosis?

A

high parity
uterine surgery
C section
(all of above allow endometrial tissue to break through into myometrium)

family history
often associated with fibroids

83
Q

what is the pathophysiology behind adenomyosis?

A

Thought to occur when the endometrial stroma is allowed to communicate with the myometrium after uterine damage
e.g. after pregnancy, C section, uterine surgery, surgical management of miscarriage/termination

invasion of endometrium can be focal or diffuse

84
Q

where is adenomyosis commonly found?

A

posterior wall of uterus

85
Q

what are the symptoms of adenomyosis?

A

menorrhage and dysmenorrhoea = main 2
pain is cyclic and reduces with menopause (responsive to O)
dyspareunia
irregular bleeding

86
Q

what is found on examination in adenomyosis?

A

symmetrical tender enlarged boggy uterus

87
Q

how is premature ovarian insufficiency diagnosed?

A

women <40yrs
and menopausal symptoms
and elevated FSH on 2 blood samples taken 4-6 weeks apart

88
Q

how is premature ovarian insufficiency managed?

A

HRT, COCP - continue till natural age of menopause unless contraindicated

89
Q

what are the causes of acute pelvic pain?

A

pregnancy related - miscarriage, ectopic, rupture of corpus luteum cyst, placental abruption and uterine rupture
gynaecological - PID, ovulation, dysmenorrhoea, rupture or torsion of ovarian cyst, degenerative changes to fibroid, pelvic tumour, endometriosis

other - IBS, strangulated hernia, appendicitis, interstitial cyst

90
Q

what investigations would you want to do for acute pelvic pain?

A 
urinalysis and MSU
high vaginal and endocervical swabs
pregnancy test 
FBC
urgent USS - for ectopic, torsion of ovarian cyst
laparoscopy
91
Q

how is chronic pelvic pain defined?

A

intermittent / constant pain in lower abdo/pelvis lasting for atleast 6 months and not occurring exclusively with menstruation or sexual intercourse and not associated with pregnancies

92
Q

what is the cause of chronic pelvic pain?

A 
endometriosis
adhesions 
IBS
interstitial cystitis 
MSK
nerve entrapment 
pelvic organ prolapse
fibromyalgia, depression, sleep disorder

may be multifactorial and also pain may exist beyond pathology (central sensitisation)
psychological and social factors can also be involved in the cause
(big emphasis on the fact that its multifactorial and social aspects play a role in the learning objectives)

e.g. can be due to previous sexual abuse

93
Q

what questions should be asked in a history of someone with chronic pelvic pain?

A

pattern of pain
associated symptoms - bowel, bladder, vagina

red flags:

  • IMB, PMB, post coital bleeding
  • bleeding per rectum
  • new bowel symptoms and >50
  • new pain after menopause
  • pelvic mass
  • excessive weight loss
  • suicidal ideation
94
Q

How can we investigate Chronic pelvic pain

A

FBC, CRP, bloods
screen for STI especially chlamydia
MSU and urinalysis
CA125 esp if >50 and IBS type symptoms

transvaginal USS - look for adnexal masses
diagnostic laparoscopy

95
Q

how is chronic pelvic pain managed?

A

due to multifactorial causes, need an MDT approach - address emotional, psychological and physical factors.
- may need psychiatrist or psychosexual counselling

cyclic pain - Mirena coil or COCP can be trailed

analgesia - NSAIDs, neurological agents

manage any underlying cause
sometimes hysterectomy

96
Q

list some causes of:

a) intermenstrual bleeding
b) post coital bleeding
c) post menopausal bleeding

A

a) infection, malignant, fibroid, endometriosis, pregnancy, hormonal contraception
b) cervical ectropion, infection, vaginitis, malignancy
c) malignancy, vaginal atrophy, HRT use

gynaecology (7 decks)

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