gynaecology Flashcards
When is cervical ca most common?
- peak at 25-29 and in 80s
Describe the pathophysiology of cervical cancer5
Usually develops from cervical intraepithelial neoplasia over the course of 10-20yrs but not all CIN progresses to cancer- most spontaneously regress.
Most are caused by HPV 16 and 18 infection- inhibits p53 tumour surpressor gene
give 4 RFs for cervical ca other than HPV infection
- smoking
- other STIs
- long term (>8yrs) COCP use
- immunodeficiency
Describe the clinical features of cervical cancer
- abnormal vaginal bleeding (post coital, intermenstrual, post menopausal) is most common presenting complaint
- other features inc vaginal discharge (blood stained, foul smelling), dyspareunia, pelvic pain and weight loss
- often asymptomatic and picked up on screening
- if advanced: odema, loin pain, rectal bleeding, radiculopathy and haematuria
- Seculum: bleeding, discharge, ulceration
- bimanual: pelvic mass
How should suspected and confirmed cervical cancer be investigated?
- premenopausal: test for chlamydia, if -ve or +ve and symptoms persist after treatment: colposcopy and biopsy
- post menopause: colposcopy and biopsy
- if diagnosis confirmed: bloods, CT CAP for mets, MRI pelvis and PET for staging, possibly also EUA with further biopsies
Describe the staging of cervical cancer
Stage 0- in situ ca
Stage 1- confined to cervix: a= identified only on microscopy, b= gross lesions
Stage 2- beyond cervix but not pelvic sidewall/ involved vagina but not lower 1/3rd
Stage 3- extends to pelvic sidewall/ involves lower 1/3rd vagina/ hydronephosis not explained by other cause
Stage 4- extends to bladder or rectum or metastases
How can cervical cancer be managed?
Stage Ia-IIa (early): Radical trachelectomy + LN dissection if fertility preservation is a priority and <2cm. If not and <4cm, radical hysterectomy w/ LN dissection, if >4cm then chemo radio is prefered.
Stage IIb-IVa (locally advanced): chemoradiotherapy (radio is external beam and intracavity brachytherapy, chemo is cisplatin based)
- Stage 4b (mets) or reccurent disease: anterior/ posterior/ total pelvic extenteration (removal of all pelvic adnexae plus bladder and/ or rectum) + combo chemo
- chemo can also be used before or after surgery and for palliative intent
- F/U with gynae every 4 months for 2 yrs then 6-12 months for 3 more years
What is a cervical ectropian?
- when there is eversion of the endocervix, exposing the columnar epithelium to the vaginal milieu
- it is benign and commonly seen on examination of adolescents, in pregnancy and in women taking oestrogen containing contraceptives but cervical ca and CIN need to be excluded before treatment or reassurance offered
What is the pathophysiology behind cervical ectropians?
- the stratified squamous epithelium of the ectocervix undergoes metaplasia to become simple columnar epithelium (same as endocervix) this is thought to be induced by high levels of oestrogen
- the columnar epithelium contains mucus glands, which causes some pts to experience vaginal discharge
- the fine blood vessels present in the columnar epithelium cause post coital bleeding
Describe the clinical features of a cervical ectropian
- most commnly asymptomatic
- occasionally present with post coital bleeding, intermenstrual bleeding or excessive discharge (non purulent)
- O/E the everted columnar epithelium has a reddish appearance- usually arranged in a ring around the external os
How should cervical ectropian be investigated? which differentials are these investigations excluding
- pregnancy test- pregnancy
- triple swabs- infections, cervicitis
- cervical smear- CIN or cervical ca, if frank lesion then biopsy should be taken
how should cervical ectropian be managed?
- regarded as a normal variant that doesnt need management unless symptomatic
- first line treatment is to stop any oestrogen containing meds eg COCP
- if symptoms persist the columnar epithelium can be ablated, typically using cryoptherapy or electrocautery- will get significant vgainal discharge until healing is completed
- boric acid pessaries to decrease vaginal pH have been suggested also
How should CIN be managed?
- colposcopy and histological analysis
- if CIN I (confined to upper 1/3 epithelium): low risk, repeat smear in 12 months to check its regressed
- if CIN II or III (deeper or more abnormal):Large loop excision of transformation zone (LLETZ procedure). Cone biopsy, cyroablation and hysterectomy rarely done now
What is thought to cause cervical polyps
- chronic inflammation
- abnormal response to oestrogen (polyps are associated w/ endometrial hyperplasia)
- localised congestion of cervical vasculature
Describe the clinical features of cervical polyps
- usually asymptomatic and identified by routine cervical screening
- most common feature is abnormal vaginal bleeding- can be menorrhagia, intermenstrual, post coital or post menopausal
- can also cause increased vaginal discharge or rarely block the cervical canal and cause infertility
- on speculum exam they are visible as polypoid growths projecting through the external os
Who is invited for cervical screening?
- females age 25-64
- every 1- 3 years depending on results
How should cervical polyps be investigated and managed?
- triple swab and cervical smear to check for differentials
- small risk of malignant transformation (0.5%) so common practice is to remove them whenever they are identified (even if asymptomatic)
- small polyps can be removed in primary care (polypectomy forceps and twist several times)
- larger polyps removed by diathermy loop excision in colposcopy clinic or under general if it has a broad base
- excised polyps should be sent for histology to exclude malignancy. they have a recurrence rate of 6-12%
- risks of polypectomy inc infection, haemorrhage and uterine perforation (very rare)
What is the difference between primary and secondary dysmenorrhoea?
primary- menstrual pain occuring with no underlying pelvic pathology
secondary- menstrual pain associated with pelvic pathology
What causes pain in mensturation?
- corpus luteum regresses
- decline in oestrogen and progesterone production
- causes endometrial cells to secrete prostaglandin
- this causes vasospasm (leading to ischaemic necrosis and shedding of superfical layer of the epithelium) and increased myometrial contractions
- primary dysmenorrhoea is thought to be due to excessive release of prostaglandins by endometrial cells
give 4 RFs for dysmenorrhoea
- early menarche
- long menstrual phase
- heavy periods
- smoking
- nuliparity (it may resolve following pregnancy)
What may cause secondary dysmenorrohea?
- endometrosis
- Adenomyosis
- PID
- adhesions
how should primary dysmenorrhoea be investigated?
- rule out underlying pathology:
- high vaginal swab to screen for infection
- transvaginal USS if pelvic mass is palpated
How should primary dysmenorrhoea be managed?
- stop smoking
- analgesia 1st line= NSAIDs (mefenamic acid/ ibuprofen) then + paracetamol
- 2nd line= hormonal contraception (monophasic COCP usually 1st line then IUS)
- non parm: local application of heat (water bottle or patch) and transcutaneous electrical nerve stimulation (TENS)
What is heavy menstrual bleeding and abnormal uterine bleeding?
HMB is describtion o excessive menstrual loss which interferes with a womans QoL.
40-50% of these cannot be attributed to any uterine, endocrine, haem or infective pathology, these cases are called abnormal uterine bleeding.
What can cause heavy menstrual bleeding? (structural and non structural)
Structural (PALM): - polyp - adneomyosis - leiomyoma (fibroid) - Malignancy and hyperplasia Non structural (COEIN): - Coagulopathy - Ovulatory dysfunction - Endometrial - Iatrogenic (contraceptive hormones/ copper IUD) - Not yet classified
What are the main RFs of heavy menstrual bleeding?
- age (menarche and approaching menopause)
- obesity
- other RFs associated with causes eg C section with adenomyosis
How should heavy menstrual bleeding be assessed?
- ask about symptoms of anaemai
- take menstrual cycle history (frequency (<24 days is frequent, >34 infrequent), duration (>8 days is long,<4.5 is short), volume (>80ml is heavy, 40ml average, <5ml light), flooding or clots, how many pads per day etc, date of last menstrual period, assess impact on QOL- impact on work, soiling, through clothing etc
- smear history, contraception, medical hx and meds
- general exam: pallor
- abdo exam, speculum and bimanual:
- palpable pelvic or uterine masses, is uterus irregular (fibroids) or tender (endometriosis/ Adenomyosis)
- inflammed cervix/ polyp/ endometriosis
- vaginal tumour
- pregnancy test (may be a miscarriage)
What features in the HMB history suggests von willebrands disease?
- HMB since menarche
- PPH
- surgical related bleeding or dental related bleeding
- easy bruising/ epistaxis
- bleeding gums
- fhx bleeding disorder
What are the two most common causes of ovarian dysfunction causing HMB?
- polycystic ovary syndrome
- hypothyroidism
How should HMB be investigated?
- FBC, TFT, coagulation screen and VWb test, other hormone test if suspicion (eg PCOS)
- urine pregnancy test
- pelvic USS (transvag) if abnromal exam or pharm treatment fails
- smear (if not up to date)
- high vag and endocervical swabs
- pipelle endometrial biopsy (Endometrial thickenss >4mm, persistent intermenstrual bleeding >45 yrs, and or failure of pharm treatment)
- hysteroscopy and endometrial biopsy (if higher risk)
- if low risk: fbc only for anaemia and then give first line treatment, if no better then investigate further
Describe the pharmacological management of HMB when there is no suspected pathology
1st: levonorgestral- releasing intrauterine system (acts as contraceptive, licensed for 5 yrs, thins endometrium and can shrink fibroids)
2nd: tranexamic acid, mefanamic acid or COCP (choice dependant on fertility wishes, tran acid only taking during menses to reduce bleeding, no fertility, mefanamic acid is NSAID and also no effect on fertility)
3rd: progesterone only (oral norethinsterone (taken day 5-26 of cycle, depo or implant (norethinsterone DOESNT work as a contraceptive when taken like this)
Describe the surgical management options for HMB
- endometrial ablation: only if they no longer want to conceive (but they still need contraception), in outpts under local
- hysterecomy (causes amenorrhoea and ends fertility, can be subtotal (leaves cervix) or total
Define primary and secondary amenorrhoea and oligomenorrhea
Primary amen- failure to commence menses:
- in girl age 16+ in presence of secondary sexual characteristics
- girls 14+ with no secondary sexual characteristics
Secondary amen: cessation of periods for more than 6 months after menarche (after pregnancy excluded)
Oligomenorrhea: irregular periods with intervals between menstrual cycles of more than 35 days and/ or less than 9 periods per year
Name and describe hypothalamic and pituitary causes of amenorrhoea
Hypothalamic (reduced GnRH):
- functional disoders (eg eating disorders, high levels of exercise)
- severe chronic conditions eg psychiatric disorders, thyroid disease and sarcoidosis
- kallmann syndrome (x linked recessive, failure of migration of GnRH cells)
Pituitary causes: (high GnRH, low LH/FSH)
- prolactinomas
- other pituitary tumours
- sheehans syndrome (post parum pituitary necrosis secondary t massive obstetric haemorrhage)
- destruction of pituitary due to radiation or autoimmune disease
- Post contraception amenorrhoea (prolonged contraceptive use can cause long term downregulation of pituitary gland, most common with depo- provera which can take up to 18 months for menses to resume)
Give ovarian, adrenal and genital tract abnormalities that may cause anemorrhoea
Ovarian:
- PCOS (usually oligo)
- turners
- premature ovarian failure (primary ovarian insufficiency before age 40 with menopausal symptoms)
Adrenal:
- late onset/ mild congenital adrenal hyperplasia- partial deficiency in 21 hydrocylase needed for cortisol and aldosterone- early pubic hair, irregular or absent periods, hirstuism and acne (high 17 hydroxyprogesterone in blood)
Genital tract abnormalities:
- ashermans syndrome (secondary to instrumentation of uterus - tyically following surgical management of miscarriage, damage to endometrium so intrauterine adhesions which fail to respond to ostrogen stimulus
- importforate hyemn/ transverse vaginal septum
- mayer- rokatansky- kuster- hauser syndrome (agenesis of mullerian duct system to varying degree- congenital absence of uterus and upper vagina)
What may cause oligomenorrhoea?
- PCOS
- contraceptives/ hormonal treatments
- perimenopause
- thyroid disease/ diabetes
- eating disorders/ excessive exercise
- medications/ heave ecercise
- meds: antipsychotics, anti epileptics
how should amenorrhoea and oligomenorrhea be investigated?
- pregnancy test
- bloods: TSH, prolactin, FSH/ :H/ oestradiol, progesterone, testosterone, 17 hydroxyprogesterone for congenital adrenal hyperplasia
- karyotyping- if suspecting a genetic abnormality
- USS- to visualise ovaries and pelvic anatomy
- progesterone challenge test to elicit a withdrawl bleed (bleed suggests adequate levels of oestrogen however pt not ovulating (ie PCOS), no bleed means there could be very low levels of oestrogen or an outflow obstruction
Describe the blood tests results ( LH, FHS, oestogen, testosterone) in PCOS and premature ovarian failure
PCOS: normal, FHS, high LH, testosterone normal or high
premature ovarian failure: high FHS and LH, low oestrogen
