Menstruation and Menstrual disorders Flashcards
What checking for a normal menstrual cycle…
- When does ovulation occur?
- When is the progesterone peak?
- How long does the luteal (2nd half; 1st half is follicular) phase last?
- ovulation = day 14
- with peak in LH and FSH & oestrogen drop
- progesterone peak = day 21 in 28d cycle
- when progesterone decreases –> menses @ end of menstrual cycle & signifying the START
- luteal phase (after ovulation) = always 14 days
Menstruation:
follicular (variable) –> ovulation –> luteal
What type of feedback loop do progesterone, testosteronoe and oestrogen have?
- Progesterone & testosterone always -ve feedback
- Oestrogen can also cause +ve feedback
What is the name for the variable first half of the menstrual cycle and the fixed 14d part 2 of the menstural cycle?
variable = 1st part till ovulation = follicular
fixed @14 days after ovulation until menstruation = luteal phase
Just after menstruation, in the follicular phase which are the first 2 hormones to start to rise?
What do these hormones do?
- LH and FSH start to rise
- (after GnRH stimulates gonadotroph cells of the pituitary to release/synthesise them;
- vs posterior pituitary doesnt make the 2 hormones it has it just stores and secretes them from the hypothalamus)
- FSH –> stimulates granulosa cells –> produce OESTROGEN (from the androgens made by LH)
- LH –> Theca cells –> androgens
FSH –> stimulates granulosa cells –> produce OESTROGEN (from the androgens made by LH via theca cells)
What happens to oestrogen throughout the follicular phase?
Which hormone surge causes ovulation
Unopposed oestrogen
- -ve feedback on HPG axis as we are mono-ovular (also role of inhibin)
- Then when lots of oestrogen—>
- switch to +ve feedback
- –> changes amplitude & frequency of hypothalamus pulses (e.g.? higher peaks and more often)
- –> pituitary LH surge
- Pituitary LH surge –> 36hrs later = ovulation!
in the luteal phase of the menstrual cycle how does the growth of the antral follicles occur?
- Growth of antral follicles occurs in response to inter-cycle rise in FSH –> up to ovulation
- then FSH falls… due to -ve feedback
- @ ovulation time the DOMINANT follicle is selected because although FSH is falling the dominant follicle acquired LH receptors on the granulosa cells
- there is an LH surge -> ovulation of the dominant follicle (due to newly acquired LH receptors)
NB: oocyte completes 1st meiotic division but doesnt divide
due to increasing E2 receptors the uterine tubes undergo tube differentiation. Due to progesterone suppressing E2 receptors there is tube un-differentiation in the uterine tubes.
Therefore, which phases of the menstrual cycle does tube differentation vs tube undifferentiation occur?
What changes happen in both?
- Tube Differentiation (↑E2 receptors) occurs in FOLLICULAR phase (f for first)
- -differentiation
- -secretion
- -cilia growth
- -peristaltic contraction of muscle (pushes egg along for ovulation)
- Tube Un-differentiation (P supresses E2r’s) occurs in LUTEAL phase (L for later); basically everything from tube differentiation undoes
- -un-differentiation
- -secretions halt
- -cells decrease in height
in terms of the endometrium throughout the menstural cycle there is a secretory and a proliferative phase. Which one corresponds with which part of the ovarian cycle. e.g. the follicular and luteal phases?
Proliferative = occurs in follicular phase - makes lining all squashy for new egg
- proliferation of stomal layer
- ciliated surface
- glands expand & coil
- neo-angiogenesis of spiral artries
Secretory phase part 1
- differentiation of new layer
- oedema (inflammatory infiltrater) & ↑vascular permeability & coiling of spiral arteries
- maturation of glands → glycoproteins, lipids GF, cytokines, adhesion molecules
Part 2 - pro-constrictor PGs dominate
- Constriction of spiral arteries (24hrs preceding menstruation) –> ischaemia
- –> vessels themselves become ischaemic & fall apart –> start bleeding from very lowest part of artery that is still patent
In terms of the cervix what changes occur in the 1st half of the menstrual cycle vs 2nd half?
Cervix 1st half MC:
- Vascular changes & oedema → mucus more water to allow passage of sperm
- Mid-cycle E2 changes: glycoproteins become aligned & form microscopic channels sperm swim up
Cervix 2nd half MC:
- More viscous mucous (less water content)
- Glycoproteins now form mesh, acting as barrier
- (mechanism of oral contraceptives, ?so from progesterone then?)
The second half of the menstural cycle, the luteal phase is fixed at 14 days.
once the LH surge has occured and released the dominant follicle for ovulation, what happens to the hormone balance in the body if the woman IS PREGNANT?
- Just after ovulation
- Follicle –> to corpus luteum
- (keeps uterine lining cushy via progesterone for the growing egg)
- –> makes progesterone & oestrogen
- –> p –> -ve feedback on LH & FSH
- Follicle –> to corpus luteum
- IF PREGO
- CL saved by bHCG binding to LH receptors
- –> saves for 1st 7 weeks of pregnancy, after that the placenta takes over
NB: bHCG is a type of gnrh hormone along with LH and FSH then
The second half of the menstural cycle, the luteal phase is fixed at 14 days.
once the LH surge has occured and released the dominant follicle for ovulation, what happens to the hormone balance in the body if the woman IS NOT PREGNANT?
Just after ovulation
- Follicle to corpus luteum (keeps uterine lining cushy via progesterone for the growing egg)
- –> makers progesterone & oestrogen
- –> -ve feedback on LH & FSH
NOT PREGO
- CL undergoes programmed cell death after 14d –> corpus albicans
- Oestrogen & progesterone not made, serum levels drop right down
–> BLEED + back to day 1
(FSH –> follicles & oest and LH on theca w/androgens)
What happens in the luteal phase of the menstural cycle (non pregnancy)?
- Corpus luteum formed from empty follicle (made of cholesterol)
- Corpus albicans is formed from programmed cell death of CL (@14d) –> doesn’t produce oestrogen or steroids
What is the process called of how the dominant follicle forms a corpus luteum just after ovulation?
lutenisation
- the follicle cells collapse –> corpus luteum
- fertilise oocyte prevents death of CL from LH and hCG receptors
- otherwise if not fertilised = 14 day lifespan of CL
- the vasculature breaksdown and CL shrinks -> albicans
- the progesterone released from CL –> supports oocyte in journey, controls cells of tubes & alters secretions of cervix and prepares endometrium
- (secretory phase = new layer differentiation, oedema and vasc perm, on the primed layer by oestrogen in follicular/proliferative phase)
- secretion of oestrogen: for endometrium in luteal phase too (Cl gives P and O)
How are oocytes preapred for ovulation?
- after the domionant follicle released in response to LH surge - ovulation –> oocyte completes 1st meiotic division (but doesnt divide)
- –> this arrested 1st meiotic division keeps all DNA and size as long as possible
- 1/2 the chromosomes are put into 1st polar body egg (NOT split into another secondary oocyte)
- oocyte begins and arrests in 2nd meiotic division (until fertilisation)
What is the ovulation cascade?
The travelling of the oocyte down the fallopian tube by peristalsis & action of cilia
- increase blood flow & vascular permeability to follicle causes increased intra follicular pressure
- stigma / apex appearance on ovary wall & local protease action causes HOLE
- oocyte and cumulus cells released (from cortex) & collected by fimbria of uterine tubes
- (to travel down tube by peristalsis etc)
What disorders of menstrutation exist?
- amenorrhoea/oligomenorrhoea
- inter-menstrual bleeding
- post-coital bleeding
- menorrhagia
What is the definition of amenorrhoea?
no periods for >6 months
-
1o:
-
never bled by 16 years - 95% will have
- (doesnt mean theres a problem but much more likely to be)
- or no bleeding + no secondary characteristics by 14 yrs
-
never bled by 16 years - 95% will have
-
2o:
- cessation of periods for 6 months (4 P’S as causes)
- Pregnancy
- Prolactinoma (high pro affects P and O in menstural cycle)
- PCOS
- Premature ovarian insufficiency
- cessation of periods for 6 months (4 P’S as causes)
What is the #1 rule with amenorrhoea?
ALL WOMEN ARE PREGNANT UNTIL PROVEN OTHERWISE
What are the hypothalamic causes of amenorrhoea?
hypothalamus –> GnRH –> anterior pituitary –> FSH & LH
e.g. hypogonadotrophic hypogonadism –> there is no LH or FSH
- Non-functional hypothalamic hypogonadism
- Tumour
- Kallman syndrome - X-linked recessive disorder characterised by failure of migration of GnRH cells.
- Functional hypothalamic hypogonadism
- Anorexia
- (lack of body fat - Leptin initiates menstruation,
- BMI<17
- they stop & can take up to 2yrs for )
- Excessive exercise (lack of fat) –> loss of GnRH pulses
- Iatrogenic e.g. Radiotherapy, surgery
- Pseudocyesis (phantom pregnancy)
- Anorexia
What are the pituitary causes of amenorrhoea?
e.g. hypogonadotrophic hypogonadism –> there is no LH or FSH
hypothalamus –> GnRH –> anterior pituitary –> FSH & LH
- Raised prolactin
- prolactinoma (inc. pro affects P &O),
- anti-psychotics,
- renal failure?? (CKD = increased PRL retention & production)
- Breast feeding
- (the raised prolactin is the contraceptive method behind breast feeding amenorrhoea)
- Pituitary adenoma
- (macroadenoma, microadenoma)
- Pituitary failure
- SOL e.g. acromegaly, Cushing’s syndrome
- Sheehan syndrome - massive PPH causes hypotension & injury to lactotrophs in pituitary –> hypopituitarism e.g. amenorrhoea and no milk produced
- Iatrogenic e.g. radiation, surgery
- Autoimmune destruction of pituitary
-
Post-contraception amenorrhoea -
- prolonged use of contraceptives can cause LT downregulation of pituitary gland & irregular/absent periods or lack of ovulation which persists;
- most commonly seen with Depo-Provera (can take 18months for menses to resume)
A lady has just given birth, it was a traumatic birth with massive PPH causing severe hypotension. In the end both the baby and herself recovered however, she has come to clinic due to an inability to produce breast milk. She has not gotten her periods back.
How would you investigate this syndrome?
Sheehan syndrome - massive PPH causes hypotension & injury to lactotrophs in pituitary –> hypopituitarism). Symptoms –> lack of post-partum milk production, amenorrhoea following delivery with hx massive PPH
Ix = bloods =>
- PRL,
- gonadotrophin stinulation tests (hypopituitarism)
The most common cause of amenorrhoea is due to ovarian causes.
What are the differentials for ovarian causes of amenorrhoea?
- PCOS
- (hyper-oestrogenic, anovulatory)
- (high testosterone, low Sex Hormone Binding Globulin)
- Premature ovarian failure
- (hyper-gonadotrophic) - <40yrs - main reason we check - cause by chemotherapy or bad luck…
- Turners 45 XO
- amenorrhoea,
- failure to develop secondary sexual characteristics and
- almost universal infertility
- short stature,
- webbed neck and aortic coarctation.
- short stature,
- Gonadal dysgenesis
A 16 year old girl presents with amenorrhoea, lack of pubic hair and breast buds. She is short of stature with webbed neck.
What is the likely cause and what other malformation would be likely found?
Turners 45 XO
- aortic coarctation, almost universal infertility, (streak ovaries)
What endometrial problems can cause amenorrhoea?
inter-uterine adhesions
(Asherman syndrome)
(also consider TB)
on hyteroscopy a patient has inter-uterine adhesions…
what is the name of this syndrome?
what else would need considering?
Asherman syndrome
- also consider TB
Outflow disorders of the vagina and cervix can cause amenorrhoea - by obstruction.
What can cause cervical/outflow obstruction?
- Mullerian agenesis
-
MKHR syndrome (Mayer-Rokitansky-Kuster-Hauser syndrome)
- – agenesis of the Mullerian-duct system in varying degrees;
- congenital absence of the uterus and upper two thirds of the vagina and therefore a cause of primary amenorrhoea.
- – agenesis of the Mullerian-duct system in varying degrees;
-
MKHR syndrome (Mayer-Rokitansky-Kuster-Hauser syndrome)
- Transverse vaginal septum - septum between upper & lower embryological origins of vagina
- Imperforate hymen
- Cervical stenosis
- Asherman’s syndrome (inter-uterine adhesions)
What endocrine causes of amenorrhoea are there?
- Androgen insensitivity
- (genetically male, phenotypically female bc -
- -> gonad selection is male but receptors insensitive so female outside, male inside)
- Adrenal
- e.g. congenital adrenal hyperplasia - CAH (too much androgens > mineral/glucocorticoids)
- & deficiency of 21 hydroxylase enzyme (the most common cause of CAH)
- Obesity (excess oestrogen –> -ve feedback
- Cushing’s
- Clinical hypo/hyperthyroidism
A 15y/o female has presented with never having had a period (primary amenorrhoea). She has had breast development. (2o sexual characteristic).
What are your differentials?
- Mullerian agenesis
-
MKHR syndrome (Mayer-Rokitansky-Kuster-Hauser syndrome) – agenesis of the Mullerian-duct system in varying degrees;
- congenital absence of the uterus and upper two thirds of the vagina and therefore a cause of primary amenorrhoea.
-
MKHR syndrome (Mayer-Rokitansky-Kuster-Hauser syndrome) – agenesis of the Mullerian-duct system in varying degrees;
- Androgen Insensitivity
- (genetically male, phenotypically female bc –> gonad selection is male but receptors insensitive so female outside, male inside)
- Vaginal Septum
- Imperforate Hymen
- Constitutional delay
A 13 year old girl has had no pubertal maturation (no breast buds) and absent menses.
karyotype has ruled out 46XY, 46X0 and confirmed she is 46XX.
What are your differentials?
- Prolactinomas
- Kallmann Syndrome
- x linked recessive disorder = failure of migration of GnRH cells; people with this also have no sense of smell
- Other CNS
- Stress, Weight Loss, Anorexia
- PCOS
- Congenital adrenal hyperplasia
- (too much androgen e.g. due to 21OH enzyme deficiency)
- Constitutional Delay
- Other
Female patient X presents after 6 months of not menstrutating (the limit in someone who was previously mensturating).
After checking her hormone levels you find that they are normal what does this imply?
an anatomic cause e.g. Asherman syndrome (intrauterine adhesions blocking outflow of period)
Female patient X presents after 6 months of not menstrutating (the limit in someone who was previously mensturating).
After checking her hormone levels you find that they there is high FSH. What differentials does this lead to?
high FSH indicates gonadal failure (e.g. ovaries not responding)
- 46, X0 (biphasic rise in the girls in early childhood then in late childhood/adolescence)
- Abnormal karyotype
- Idiopathic premature ovarian failure/ post-chemoradiation ovarian failure
- Menopause
Female patient X presents after 6 months of not menstrutating (the limit in someone who was previously mensturating).
After checking her hormone levels you find that they there is low or normal FSH. What differentials does this lead to?
low/normal FSH shows its not gonadal failure (as FHS would be high)
TF w/low or normal FSH, Ddx =
- Weight loss/anorexia/excess exercise
- Non-specific hypothalamic
- Pituitary tumour,
- Chronic anovulation including PCOS
- Hypothyroidism (alters SHBG, PRL & GnRH)
- Cushing syndrome (cortisol can suppress GnRH–>LH/FSH)
- Pregnancy
What are the causes of oligomenorrhoa?
e.g. >35days w/o periods
(normal periods = 21-25d cycle)
- PCOS
- Contraceptive/hormonal treatments
- Perimenopause
- Thyroid disease/ diabetes
- Eating disorders/ excessive exercise
- Medications e.g. anti-psychotics e.g. INC PRL, anti-epileptics
What Ix should be done for oligomenorrhoea?
(NB: lots of causes of oligomenorrhoea overlap with secondary amenhorrhoea)
- Beta-hCG to exclude pregnancy
- TransVag ultrasound - anatomy & physiology of genital tract
- Karyotype - genetic causes
- Bloods -
- FSH, LH, PRL - pituitary & hypothalamus
- FSH/LH low hypothalamic-pituitary cause (e.g. FSH<lh>
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- FSH/LH low hypothalamic-pituitary cause (e.g. FSH<lh>
- FSH, LH, PRL - pituitary & hypothalamus
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* E2, testosterone - ovary & adrenal
* Testosterone >5nmol/L ?androgen-secreting tumour or late-onset CAH
* SHBG, serum free androgen index (PCOS get high oest, high test and low SHBG)
* TFTs (4% of women with amenorrhoea have abnormal thyroid function)
A woman presents with oligomenorrhoea and her blood results are as follows:
- high FSH and LH
- low oestrogen
underlying problem?
Rx?
- If there is high FSH / LH in 2o amenorrhoea & low oestrogen -> gonadal failure suggested
-
Rx premature ovarian failure
- cannot be reversed e.g. no Rx
- hormone replacement therapy –>
- control symptoms of oestrogen deficiency - COCP/HRT may improve symptoms
- & protection against osteoporosis
- control symptoms of oestrogen deficiency - COCP/HRT may improve symptoms
- oocyte donation and IVF can lead to pregnancy in these women (so if fertility is desired = egg donation)
A female patient is experiencing oligomenorrhoea (>35d cycle)
You check their blood hormone levels and they are as follows:
- low GnRH
- normal/low FSH and LH giving LOW LH:FSH ratio
- low oestrogen
What does this indicate? & what is the Rx based off this?
(as Rx is related to cause in oligomenorrhoea)
- hypothalamic problem source –> gonadotrophin deficiency
- Rx: –>
- replace the gonadotrophs if fertility is desired,
- if fertility is NOT desired give COCP
A female patient is experiencing oligomenorrhoea (>35d cycle)
You check their blood hormone levels and they are as follows:
- low GnRH
- Raised PRL
What does this indicate?
(as Rx is related to cause in oligomenorrhoea)
- prolactinoma
- may have galactorrhoea if prolactinoma too
A female patient is experiencing oligomenorrhoea (>35d cycle)
You check their blood hormone levels and they are as follows:
- normal FSH and high LH = raised LH:FSH
- Raised/normal testosterone
What does this indicate?
(as Rx is related to cause in oligomenorrhoea)
PCOS!
(high LH e.g. think of as LOTS of LH that just keeps making cysts of ovaries of stimulated follicles, and then + high testosterone)
Rx depends on if fertility is desired or not
- if yes, fertility desired Rx = weight loss, metformin, ovulation induction
- if no, fertility not desired Rx = weight loss / COCP
What is the definition of menorrhagia a.k.a. heavy menstural bleeding?
Definition =
- too heavy bleeding which interferes with a woman’s quality of life – either on its own or in combination with other symptoms; definition of ‘excessive’ is set by the woman who presents with the problem (NICE)
- -or >80ml per period
- -most common cause is dysfunctional uterine bleeding (DUB) i.e. excessive bleeding of no obvious organic cause
A women presents complaining of heavy menstural bleeding which interferes with her quality of life. What other presenting features of menorrhagia should you ask about?
What is the guidance for management of menorrhagia?
- Presentation:
- bleeding,
- fatigue,
- SOB (if associated anaemia)
- Management:
- <40yrs treat empirically;
- >40yrs investigate first
- (TransVag USD +/- hysteroscopy)
Causes of menorrhagia can be structural or non-structural.
The acronym for structural causes of menorrhagia is PALM.
What does PALM stand for?
- Polyp
- Adenomyosis
- Leiomyoma (Fibroid)
- Malignancy & hyperplasia
Causes of menorrhagia can be structural or non-structural.
The acronym for Non-Structural causes of menorrhagia is COEIN.
What does COEIN stand for?
- Coagulopathy
- Ovulatory dysfunction
- (e.g. dysfunctional uterine bleeding e.g. excessive bleeding of no obvious cause/DUB)
- Endometrial
- Iatrogenic
- (copper coil, warfarin)
- Not yet classified
Define inter-menstrual bleeding
- bleeding etween normal menses
- if >40y/o = endometrial cancer until proven otherwise, >40yrs
- if <20yrs = chlamydia
- Following mid-cycle fall in oestrogen production
- Cervical polyps;
- ectropion (cervix, glandular cells on outside surface)
- carcinoma;
- cervicitis/vaginitis;
- hormonal contraception (spotting); IUCD;
- Chlamydia;
- pregnancy-related (?ectopic too, but pain preceeds bleeding)
What are the differentials of post coital bleeding?
- the main worry to rule out
- <20 y/o
- >40y/o
- for all ages?
- post coital bleeding = cervical cancer until proven otherwise
- <20 = cervical ectropion => chlamydia
- >40 = need to exclude endometrial patholgy
- inc. polyps,
- hyperplasia,
- cancer
- –> US & biopsy
- ALL - need to exculde cervical pathology
- –> cancer,
- polyp,
- ectropion
What are the gynae red flags for cancer?
- Age >35 and symptoms >4 weeks
- History of abnormal smears
- Systemic symptoms - weight loss, night sweats
- A recent change in sexual partner
- History or lower abdominal pain and fever
- Abnormal looking cervix or vaginal walls on examination
- Presence of an unexplained cervical or vulval mass
What are the causes of menorrhagia in the
- ovary,
- endometrium,
- myometrium,
- Endocrine
- clotting
- other
- Overy = PCOS
- (not many but VERY heavy, hyper-oestrogenic but this is unopposed so very proliferated endometrium - anovulatory bleeding)
- endometrium = endometrial polyps, IUCD (copper), dysfunctional uterine bleeding (DUB, molecular issue), endometrial hyperplasia (can be premalignant) [rule out pregnancy, ectopic pregnancy]
- myometrium = fibroids:
- (submucosal not intramural or sub-serosal), adenomyosis (heavy, painful periods - endometrium in myometrium, 30yrs +, multifarious - childbirth gets the endometrium there somehow, very different population to endometriosis patients)
- endocrine = biochemical hypothyroidism, obesity
- clotting = VWD, anticoagulation, ITP (AI, de novo or SLE)
- other = endometrisosis
- (young, thin, white women, nulliparous by definition not in uterus - PAINFUL)
What are the causes of inter mentstrual bleeding in the..?
- endometium
- vag/cerix
-
endometrium =
- endometrial polyps,
- endometrial cancer (>45y/o)
-
vag/cervix =
- cervical cancer,
- polyps,
- ectropion,
- cervicitis/vaginitis,
- hormonal contraception (spotting),
- chlamydia,
- pregnancy-related
What are th causes of PCB from the vagina/cervix?
- cervical cancer,
- cervical ectropion
- (endocervical columnar epithelium comes right out to cervical-vaginal junction
- e.g. Caused by pill,
- polyp,
- STI/PID
- (chlamydia, gonorrhoea –> cervicitis),
- trauma
- (endocervical columnar epithelium comes right out to cervical-vaginal junction
What bedside and blood tests are done for erratic bleeding e.g. IMB, PCB and Menorrhagia, amenorrhoea?
- Pregnancy test *ERRATIC BLEEDING IS THERE ANY CHANCE THEY ARE PREGNANT - ECTOPIC??*
- Cervical smear
- STI swabs (high vagina, endocervical) (C&G)
- Bloods
- Sexual health bloods
- HIV,
- syphilis
- FBC (if bleeding is heavy,) clotting
- (if since menarche or FHx)
- TFTs
- (4% of women with amenorrhoea have abnormal thyroid function)
- Other hormone testing - not routine but considered if other clinical features e.g. suspicion of PCOS
- FSH, LH, PRL - pituitary & hypothalamus
-
E2, testosterone - ovary & adrenal
- Testosterone >5nmol/L ?androgen-secreting tumour or late-onset CAH
- SHBG, serum free androgen index (PCOS)
- Sexual health bloods
What imaging can be done for erratic bleeding (bloods and bedside have already been done)?
(e.g. men/amenorrhoea, PCB, IMB)
- TV ultrasound - anatomy & physiology of genital tract
- Hysteroscopy & endometrial biopsy (Pipelle biopsy) - indications:
- Post-menopausal bleeding (PMB) & endometrial thickness on TVUSS >4mm
- Heavy menstrual bleeding (HMB) >45yrs
- HMB associated with IMB
- Treatment failure
- Prior to ablative techniques
What is the management of erratic vaginal bleeding?
- Exclude serious abnormalities
- Treat the underlying cause e.g. polyp
- Volume control
- Cycle control
- Suppression of periods
Why does dysfunctional uterine bleeding occur?
- Derangements of endometrial tissue necrosis (superficial layer during cycle or lots during menses) due to unopposed oestrogen (anovulatory DUB)
- or irregular progesterone stimulation due to a dysfunction CL (ovulatory DUB) [so sloughing off of endometium happens randomly]
NB: DUB has no obvious organic cause of bleeding TF ?molecular as above
Dystunctional uterine bleeding (DUB) has 4 different treatment methods Rx in A&E, hormonal, medical & surgical.
What would the Rx in A&E for DUB be?
- high dose progesterone –> provera, norethierone
- Switches endometrium off in a matter of days
Dystunctional uterine bleeding (DUB) has 4 different treatment methods Rx in A&E, hormonal, medical & surgical.
What would the hormonal Rx for DUB be?
- *Mirena IUS (1st line)
- (average reduction in blood loss is 90%, 1/3rd women completely amenorrhoeic) - last 5yrs
- *1st line for menorrhagia
-
COCP (2nd line)
- (continuously so doesn’t bleed while raising iron)
- Progestagens e.g. high dose progesterone (3rd line)
- (luteal phase/cyclical) e.g. Norethisterone 15mg daily (cyclical pattern)
Dystunctional uterine bleeding (DUB) has 4 different treatment methods Rx in A&E, hormonal, medical & surgical.
What would the medical Rx for DUB be?
-
NSAIDs
- e.g. mefanamic acid
- (correct their abnormal PGs in endometrium - normally: PGs released from destruction of endometrial cells, the PG and other inflamm mediators cause uterus to contract (periods), TF thought to be major factor in primary dysmenorrhoea)
- Anti-fibrinolytics
- e.g. transexamic acid - blocks conversion of plasminogen to plasmin that degrades blood plasma protein (outpatient kinda management)
- iron (FeSO4)
- (Ovulation induction agent if anovulatory DUB & patient desires ovulation for fertility)
Dysfunctional uterine bleeding (DUB) has 4 different treatment methods Rx in A&E, hormonal, medical & surgical.
What would the surgical Rx for DUB be?
Surgical would be for failed medical (e.g, mefanamif acit, transexamic acid, iron)
- Minimally invasive endometrial ablation
- (diathermy, microwave laser)
- –> PERMANENT & cannot conceive after
- 90% reduction in blood loss, 1/3rd women completely amenorrhoeic
- But 1 in 5 women need another one after 5 yrs
- Resection of fibroid (if cause)
- Hysterectomy (Vag Hysterectomy/ Lap Assisted Vag Hyst/ Trans Abdo Hysterec) - laparoscopic or vaginally
What should be done if a patient has any of these symptoms?
- Ovarian: ascited or pelvic/abdo mass not obviously fibroids
- endometrial: post-menopausal bleeding (unexplained vaginal bleeding ?12m after mensturation has stopped due to menopause)
- cervical: appearance of cervix consistent with cervical cancer
- vaginal: unexplained palpable mass in or at vaginal entrance
- vulval: unexplained vulval lump, ulceration or bleeding
these are red flags..
–> 2 WEEK REFERRAL (gynae.onc)
A patient experiencing IMB has FBC, pregnancy test, cervical screening, chalmydia test… What do you do if patient is <40 OR has no persistent symptoms?
regulate cycle w/COCP or norethisterone (high dose progesterone)
A patient experiencing IMB has FBC, pregnancy test, cervical screening, chalmydia test… What do you do if patient is >40 OR has persistent symptoms?
- USS scan
- check endometrium, look for endometrial polyp
- if USS scan is normal = follows medication advics e.g. COCP or norethisterone 5mg TDS 5-25
- if USS is abnormal = refer to gynaecology
A patient is experiencing PCB. FCB, preg test, cervical screening and chlamydia test are done. What do you do if:
- normal examination and only PMB once
- VS
- recurrent symptoms or abnormal cervical screening
- observe - if normal examination and PMB only occurs once
- refer to colposcopy if there are recurrent symptoms or abnormal cervical screen
O/E (speculum) a cervical polyp is found. What should be done?
- if asymptomatic just leave cervical polyp
- if symptomatic, twist and remove in surgery (and if clinically comptent) –> histology
A patient complains of Bloating, weight gain that seems to occur with period, Mastalgia, Abdominal cramps, Fatigue, Headache, Depression, Irritability. What could be going on?
Premenstrual Syndrome:
- cyclic presence of physical, somatic, psychological and emotional symptoms that worsen as menses approaches (luteal phase of menstrual cycle) and improves with the onset of menstrual flow
Aetiology:
- unknown, but cyclical ovarian activity and the effects of oestradiol and progesterone on certain neurotransmitters, including serotonin, appear to play a role.
A patient complains of Bloating, weight gain that seems to occur with period, Mastalgia, Abdominal cramps, Fatigue, Headache, Depression, Irritability.
What should you recommend in order to diganose?
use symptom diary for diagnosis & assessing effect of treatment
As criteria for PMS diagnosis =>
- Cyclic symptoms/only during luteal phase
- Symptoms increase in severity
- Relieved by onset menses and absent by day 3
- Must be a post-menstrual symptom free period of at least 7 days
- Present for at least 3 consecutive cycles
- –> use symptom diary for prospective diagnosis (retrospective is unreliable)
- Symptoms of a severity to interfere with daily activities
What are the 6 criteria for PMS diagnosis?
- Cyclic symptoms/only during luteal phase (e.g. so can be for 2w before period)
- Symptoms increase in severity
- Relieved by onset menses and absent by day 3
- Must be a post-menstrual symptom free period of at least 7 days
- Present for at least 3 consecutive cycles
- –> use symptom diary for prospective diagnosis (retrospective is unreliable)
- Symptoms of a severity to interfere with daily activities
A patient complains of Bloating, weight gain that seems to occur with period, Mastalgia, Abdominal cramps, Fatigue, Headache, Depression, Irritability.
What lifestyle & psychological recommendations can you make?
Lifestyle -
- diet modification,
- exercise,
- stress/relaxation exercises,
- smoking cessation,
- weight loss
Psychological -
- CBT (especially if co-existing psychopathology!)
A patient complains of Bloating, weight gain that seems to occur with period, Mastalgia, Abdominal cramps, Fatigue, Headache, Depression, Irritability.
What medical recommendations can you make?
1st line -
- vitamin B6 (unlicensed use),
- COCP (most effective regime appears to be taking 2-3 packets continuously, then breaking),
- luteal phase low-dose SSRIs (fluoxetine)
2nd line -
- estradiol patches (100mcg) + progestogen
- (e.g. dydrogesterone 10mg PO day 17-28 or Mirena),
- higher dose SSRI’s continuously or luteal-phase e.g. fluoxetine 20mg/day PO
3rd line -
- suppress ovulation –> GnRH analogues + addback HRT
- (e.g. goserelin 3.6mg sc every 28 days with tibolone 2.5mg PO daily)
- But symptoms return when ovarian activity recommences & bone thinning after 6 months
- Goserelin (e.g. stopping periods via GnRH analogue) is better used to predict the severely affected women who may benefit from hysterectomy with oophorectomy
- (96% satisfaction rates - these women can then have oestrogen replacement)
A patient complains of Bloating, weight gain that seems to occur with period, Mastalgia, Abdominal cramps, Fatigue, Headache, Depression, Irritability.
medical recommendations are 1st, 2nd & 3rd line. Surgery is 4th line… what surgical recommendations can you make?
4th line -
- Total hysterectomy plus bilateral salpingo-oophorectomy + HRT, including testosterone replacement
- (if possible, laproscopic-assisted vaginal hysterectomy or total laparoscopic hysterectomy and BSO because recovery is quicker than with abdominal hysterectomy)
A patient complains of Bloating, weight gain that seems to occur with period, Mastalgia, Abdominal cramps, Fatigue, Headache, Depression, Irritability.
What complementary medical therapy exists?
Best evidence exists for
- calcium and vitamin D,
- magnesium and
- Agnus castus (chaste tree)
No evidence for the benefit of vitamin B6
Evening primrose oil may benefit those with mastalgia but not other PMS symptoms.
