Gynae Flashcards
Summary of premenstrual syndrome?
Emotional + physical Sx women experience in luteal phase of normal menstrual cycles
Only in ovulatory cycles, not prior to puberty, in pregnancy, or after menopause.
Emotional: anxiety, stress, fatigue, mood swings.
Physical: bloating, breast pain.
Tx:
Mild: lifestyle, sleep, exercise, smoking, alcohol reg 2-3hrly small balanced meals, complex carbs
Mod: new gen COCP eg Yasmin
Severe: SSRI, continuously or just in luteal phase.
What is primary amenorrhoea?
defined as the failure to establish menstruation by 15 years of age in girls with normal secondary sexual characteristics (such as breast development), or by 13 years of age in girls with no secondary sexual characteristics
Causes of primary amenorrhoea?
gonadal dysgenesis (e.g. Turner’s syndrome) - the most common causes
testicular feminisation
congenital malformations of the genital tract
functional hypothalamic amenorrhoea (e.g. secondary to anorexia)
congenital adrenal hyperplasia
imperforate hymen
Mullerian agenesis (congen absence of part of uterus/ vagina),
5α reductase def (lack enzyme to form DHT, undergo virilisation in puberty),
constitutional delay
Kallman’
What is secondary amenorrhoea?
cessation of menstruation for 3-6 months in women with previously normal and regular menses, or 6-12 months in women with previous oligomenorrhoea
Causes of secondary amenorrhoea?
hypothalamic amenorrhoea (e.g. secondary stress, excessive exercise)
polycystic ovarian syndrome (PCOS)
hyperprolactinaemia
premature ovarian failure
thyrotoxicosis* / hypothyroidism
Sheehan’s syndrome
Asherman’s syndrome (intrauterine adhesions)
Cervical stenosis, prev biopsy, curettage, infection. Absence of external OS + bulky uterus on exam
Pit tumours: compressive, ↑PRL
Depo = takes while to recover
Investigations for amenorrhoea?
exclude pregnancy with urinary or serum bHCG
full blood count, urea & electrolytes, coeliac screen, thyroid function tests
gonadotrophins
- low levels indicate a hypothalamic cause where as raised levels suggest an ovarian problem (e.g. Premature ovarian failure)
- raised if gonadal dysgenesis (e.g. Turner’s syndrome)
prolactin
androgen levels
- raised levels may be seen in PCOS
USS: outflow obstruction, Mullerian agenesis, androgen insensitivity
oestradiol
Management of primary amenorrhoea?
investigate and treat any underlying cause
with primary ovarian insufficiency due to gonadal dysgenesis (e.g. Turner’s syndrome) are likely to benefit from hormone replacement therapy (e.g. to prevent osteoporosis etC)
IVF
Management of secondary amenorrhoea?
exclude pregnancy, lactation, and menopause (in women 40 years of age or older)
HPG disorder: exogenous gonadotropins
treat the underlying cause
IVF
What is cervical ectropion?
Eversion of endocervix, exposing columnar epithelium. Induced by high levels of oestrogen.
Normal physiological condition, adolescents, pregnancy + oestrogen contraceptives.
Features of cervical ectropion?
Vaginal discharge, non-purulent.
Post-coital bleeding, fine BVs in epithelium easily broken intercourse
Asymptomatic
Intermenstrual bleeding
Investigations for cervical ectropion?
Speculum: reddish appearance, ring around external OS.
Pregnancy
Triple swabs: any infection.
Cervical swab: rule out IEN.
Treatment of cervical ectropion?
Doesn’t require Tx unless symptomatic
1st: stop any oest containing meds, effective in majority.
Can be ablated, sig vaginal discharge until healing completed.
What is lichen sclerosus?
Inflammatory condition that usually affects the genitalia and is more common in elderly females.
Lichen sclerosus leads to atrophy of the epidermis with white plaques forming
AI disease
Can be precancerous
Features of lichen sclerosus?
white patches that may scar
itch is prominent
may result in pain during intercourse or urination
Diagnosis of lichen sclerosus?
usually made on clinical grounds but a biopsy may be performed if atypical features are present (woman fails to respond to treatment or there is clinical suspicion of VIN or cancer or pigmented areas)
Management of lichen sclerosus?
topical steroids and emollients
Follow-up: (6m)
increased risk of vulval cancer
What is pelvic organ prolapse?
Descent of pelvic organs into vagina due to weakness + lengthening of ligaments + muscles surrounding uterus, rectum, bladder.
It probably affects around 40% of postmenopausal women
Types of pelvic organ prolapse?
Uterine
Vault: hysterectomy, vault top of vagina.
Rectocele: post vaginal wall, rectum prolapse into vagina.
Cystocele: ant wall, bladder prolapse into vagina. Urethrocele cytourethrocele.
Enterocele: herniation of pouch of Douglas incl small intestine into vagina
RF’s for pelvic organ prolapse?
multiple vaginal deliveries
instrumental, prolonged or traumatic delivery
↑age
postmenopausal
obesity
chronic resp disease (coughing)
chronic constipation (straining)
spina bifida.
Features of pelvic organ prolapse?
Feeling of something coming down in vagina
Dragging or heavy sensation in pelvis
Urinary: incontinence, urgency, freq, weak stream, retention.
Bowel: constipation, incontinence, urgency
Sexual dysfunction: pain, altered sensation ↓enjoyment
Rectocele: constipation, faecal loading, women may use their fingers to press lump back allowing them to open bowels.
Investigation/examination for pelvic organ prolapse?
Empty bladder + bowel before exam
Sim’s speculum: U-shaped, single bladed, support ant/post vaginal wall whilst other vaginal walls examined. Woman can be asked to cough or bear down to assess full descent of prolapse
Grades: 0-4 (0 ischial level, 4 past Introitus)
Management of pelvic organ prolapse?
Pelvic floor exercises, WL, ↓caffeine
Vaginal oest cream
Ring pessary: give extra support to pelvic organs, clean + changed every 4 mnths. Shelf + Gellhorn (flat disc, stem sits below uterus, can’t have sex), donut/cube shaped. Hodge (rectangular, 1 side hooked around post cervix, other extends into vagina).
Surgery: mesh repairs, plastic mesh to support organs but not recommended.
Cystocele/ cystourethrocele: ant colporrhaphy, colposuspension
Uterine prolapse: hysterectomy, sacrohysteropexy
Rectocele: post colporrhaphy
What is pelvic inflammatory disease?
term used to describe infection and inflammation of the female pelvic organs including the uterus, fallopian tubes, ovaries and the surrounding peritoneum.
It is usually the result of ascending infection from the endocervix.
RF’s - UPSI, IUD
Causative organisms of PID?
Chlamydia trachomatis
+ the most common cause
Neisseria gonorrhoeae
Mycoplasma genitalium
Mycoplasma hominis
Features of PID?
lower abdominal pain
fever
deep dyspareunia
dysuria and menstrual irregularities may occur
vaginal or cervical discharge
cervical excitation
Chronic: low grade fever, WL, abdo pain
Investigation for PID?
a pregnancy test should be done to exclude an ectopic pregnancy
high vaginal swab - these are often negative
screen for Chlamydia and Gonorrhoea
Abundant WBC on saline microscopy of vaginal secretions, polymorphonuclear cells.
↑ESR, CRP
Transvaginal USS: tubal wall thickness, incomplete septae within tube, fluid in cul-de-sac, cog-wheel appearance on CS of tubal view tubo-ovarian abscess
Pelvic CT: thickened uterosacral ligaments, inflam changes of tubes + ovaries, abnormal fluid collection, reactive inflam.
Pelvic MRI: thickened, fluid-filled tubes, tubo-ovarian abscess, pyosalpinx.
Management of PID?
due to the difficulty in making an accurate diagnosis, and the potential complications of untreated PID, consensus guidelines recommend having a low threshold for treatment
oral ofloxacin + oral metronidazole OR intramuscular ceftriaxone + oral doxycycline + oral metronidazole
mild - ntrauterine contraceptive devices may be left in
Removal of the IUD should be considered and may be associated with better short term clinical outcomes’
Complications of PID?
perihepatitis (Fitz-Hugh Curtis Syndrome)
> occurs in around 10% of cases
> it is characterised by right upper quadrant pain and may be confused with cholecystitis
infertility - the risk may be as high as 10-20% after a single episode
chronic pelvic pain
ectopic pregnancy
Recurrent PID
Hydrosalpinx: fluid filled fallopian tube
Pyosalpinx: infected fallopian tube filled with purulent matter
Ovarian cancer
What is dyspareunia?
Deep or superficial
Deep indicates pathology: scarring, adhesions, endometriosis, masses restricting uterine motility
Acute onset indicates organic cause.
1°: since onset of sexual activity
2°: acquired over pts life
Bartholin’s: non-infectious occlusion of distal Bartholin’s duct, retention of secretions. Mass at inf aspect of labia majora, 5 or 7 o clock position, vulval pressure or fullness, pain during sitting/ walking. Dyspareunia.
Causes of superficial dyspareunia?
Abnormalities at introitus
Inadequate lube
Vaginismus
Overwork/depression
Relationship problems
Drug/alcohol problem
Hormonal changes
Vaginitis/vulvovaginitis - burning sensation with coitus, vulvar/ vaginal oedema, discharge, pruritis, dysuria, PV bleed, abdo pain, vaginal dryness.
Herpes simplex - intense vulvar pain, dysuria, burning, pruritis, fever + general malaise.
Vaginal atrophy - vaginal dryness, feeling of tearing during intercourse, post-coital bleeding, vaginal spotting, vaginal mucosa pale, lacks rugae.
Iatrogenic: meds, radiotherapy, COCP, antidepressant, some antihypertensives
Intersititial cystitis, UTI
Bartholin’s cyst.
What is vaginismus?
voluntary / involuntary contraction of pelvic floor muscles. Failure of penetration, affects gynae exam, tampon insertion, IUDs.
Management of dyspareunia?
Rule out organic cause
Relaxation techniques, self-exploration of genitals, insertion of vaginal trainers
Couple programs, CBT, sexual counselling
Lidocaine
HRT
Botox injections
Bartholin’s cyst: sitz bath, warm compress, marsupialisation, catheter drainage, surgical excision silver nitrate cauterisation alcohol sclerotherapy
What is female genital mutilation?
refers to all procedures involving partial or total removal of the external female genitalia or other injury to the female genital organs for non-medical reasons.
Illegal FGM Act 2003
Cultural practice in girls before puberty. Africa: Somalia, Sudan, Eritrea, Yemen, Kurdistan, Indonesia, south + west Asia.
Classification of FGM?
Type 1 - Partial or total removal of the clitoris and/or the prepuce (clitoridectomy).
Type 2 - Partial or total removal of the clitoris and the labia minora, with or without excision of the labia majora (excision).
Type 3 - Narrowing of the vaginal orifice with creation of a covering seal by cutting and appositioning the labia minora and/or the labia majora, with or without excision of the clitoris (infibulation).
Type 4 - All other harmful procedures to the female genitalia for non-medical purposes, for example: pricking, piercing, incising, scraping and cauterization.
Features of FGM?
Pain, bleeding, urinary retention, urethral damage
Incontinence
UTI, pelvic/ vaginal infections
Dysmenorrhoea
Sexual dysfunction
Dyspareynia
Infertility, pregnancy complications
Psychosocial issues + depression
↓engagement with healthcare + screening
RF’s for FGM?
From countries that practise FGM, having relatives affected
Pregnant women with FGM + female child.
Siblings/daughters of women affected by FGM
Women who decline exam or cervical screening
Present with complications of FGM
Management of FGM?
Mandatory to report all cases of FGM
Counselling
De-infibulation: T3, correct narrowing of vaginal orifice, improve Sx + try to restore normal function.
Re-infibulation: re-closure of vaginal orifice, requested after childbirth which is illegal.
What is polycystic ovarian syndrome?
complex condition of ovarian dysfunction thought to affect between 5-20% of women of reproductive age.
Ovaries contain large no of harmless follicles. Often unable to release egg, no ovulation.
XS androgen production
The aetiology of PCOS is not fully understood.
Both hyperinsulinaemia and high levels of luteinizing hormone are seen in PCOS and there appears to be some overlap with the metabolic syndrome.
Hyperinsulinemia: theca cells express insulin receptors, XS insulin, division of theca cells, ↑LH receptors, hypothalamus ↑GnRH > ↑LH
Theca cells produce XS androstenedione, too much for granulosa cells to convert. Some goes into blood, converted to estrone by aromatase in adipose tissue, neg feedback. Block ant pit from releasing FSH/ LH, no LH surge, no dominant follicle, remains in ovary as cyst, or degen with other follicles, no ovulation.
XS adipose tissue, aromatase, converts androgens to oestrogen.
Features of PCOS?
subfertility and infertility
menstrual disturbances: oligomenorrhea and amenorrhoea
hirsutism, acne (due to hyperandrogenism)
obesity
acanthosis nigricans (due to insulin resistance)
oily skin or sweating
depression + anxiety
sexual problems
Rotterdam criteria - oligoovulation or an ovulation, hyperandrogegism, polycystic ovaries on US (or ovarian volume of more than 10cm3)
Investigations for PCOS?
pelvic ultrasound: multiple cysts on the ovaries (12+ developing follicles in 1 overt or ovarian volume >10cm)
FSH, LH, prolactin, TSH, and testosterone are useful investigations: raised LH:FSH ratio is a ‘classical’ feature but is no longer thought to be useful in diagnosis. Prolactin may be normal or mildly elevated. Testosterone may be normal or mildly elevated - however, if markedly raised consider other causes
check for impaired glucose tolerance - OGTT
Management of PCOS?
weight reduction if appropriate, stop smoking, orlistat > can restore fertility
if a women requires contraception then a combined oral contraceptive (COC) pill may help regulate her cycle and induce a monthly bleed
Hirsutism and acne:
> a COC pill may be used help manage hirsutism. Possible options include a third generation (dianette) COC which has fewer androgenic effects or co-cyprindiol which has an anti-androgen action. Both of these types of COC may carry an increased risk of venous thromboembolism
> if doesn’t respond to COC then topical eflornithine may be tried
> spironolactone, flutamide and finasteride may be used under specialist supervision
> laser hair removal
> topical Tx for acne - retinoid, clindamycin, azelaic acid, tetracyline.
Infertility:
weight reduction if appropriate
supervised by a specialist.
letrozole, clomifene. 2nd line metformin
There is an ongoing debate as to whether metformin, clomifene or a combination should be used to stimulate ovulation
gonadotrophins - follitropin alfa, follitropin beta, menotrophin.
IVF
Laparoscopic ovarian drilling: puncturing cystic ovary, induces ovulation can damage ovary. Doesn’t resolve overall hormonal imbalance.
RFs for PCOS?
AD
obesity
lack of PE
gestational DM.
Complications of PCOS?
Infertility: ↑testosterone + anovulation
CVD, non-alcoholic fatty liver, hypercholesterolemia, HTN, OSA, endometrial hyperplasia + Ca
Endometrial Ca, unopposed oest causes endometrial hyperplasia.
What is ovarian torsion?
the partial or complete torsion of the ovary on it’s supporting ligaments that may in turn compromise the blood supply. If the fallopian tube is also involved then it is referred to as adnexal torsion.
RFs for ovarian torsion?
ovarian mass: present in around 90% of cases of torsion
being of a reproductive age
pregnancy
ovarian hyperstimulation syndrome
PCOS
PMHx
Features of ovarian torsion?
Usually the sudden onset of deep-seated colicky abdominal pain.
Associated with vomiting and distress
fever may be seen in a minority (possibly secondary to adnexal necrosis)
Vaginal examination may reveal adnexial tenderness
Abdo - guarding, RT
Investigation for ovarian torsion?
Ultrasound may show free fluid or a whirlpool sign. enlarged ovary. Tender on pressure with USS.
FBC: leucocytosis
CRP may be ↑
Laparoscopy is usually both diagnostic and therapeutic.
Management of ovarian torsion?
Surgical emergency
Laparoscopy with uncoiling
Oophorexy
Salpingo-oopherectomy: if severe vascular compromise, peritonitis or tissue necrosis.
What is Nabothian cyst?
a lump filled with mucus on the surface of the cervix or cervical canal
Squamous epithelium of ectocervix slightly covers mucus secreting columnar endocervical epithelium. Mucus becomes trapped + forms cyst. Can happen after childbirth, minor trauma to cervix or cervicitis
RFs for nabothian cyst?
RF: pregnant, child bearing age.
Features of nabothian cyst?
Asymptomatic
Feeling of fullness if large
Smooth rounded bumps on cervix, usually near OS
Fluid filled cyst.
2mm-30mm
Whitish yellow appearance, if raised + discoloured = concern
Harmless, unrelated to cervical cancer.
Rupture: bleeding, discharge, odour.
Investigation for nabothian cyst?
Incidentally on speculum
Dr may break a cyst to confirm diagnosis
Uncertain: colposcopy to examine in detail.
Rarely excised or biopsied.
Management of nabothian cyst?
Reassurance, no Tx needed if diagnosis clear
If discharging may be cauterised.
What are ovarian cysts?
Benign ovarian cysts are extremely common. They may be divided into physiological cysts, benign germ cell tumours, benign epithelial tumours and benign sex cord stromal tumours.
Complex (i.e. multi-loculated) ovarian cysts should be biopsied to exclude malignancy.
Uncommon in premenarchal + postmenopausal.
Fibroadenoma: small, solid benign fibrous tissue tumours. Meigs syndrome (benign ovarian tumour, ascites, pleural effusion)
Thecoma
Polycystic ovaries
Endometrioma, chocolate cysts.
Brenner’s tumour: rare, benign, borderline or prolif + malig variant. Mostly benign, unilat.
Types of physiological cysts?
Follicular cysts
> commonest type of ovarian cyst
> due to non-rupture of the dominant follicle or failure of atresia in a non-dominant follicle
commonly regress after several menstrual cycles
Corpus luteum cyst
> during the menstrual cycle if pregnancy doesn’t occur the corpus luteum usually breaks down and disappears. If this doesn’t occur the corpus luteum may fill with blood or fluid and form a corpus luteal cyst
more likely to present with intraperitoneal bleeding than follicular cysts
Theca-lutein: Stim of theca internal cells of ovarian follicles due to XS gonadotrophins eg βhCG. Associated with molar preg + multiple gest
What are benign germ cell tumours?
Dermoid cyst
> also called mature cystic teratomas. Usually lined with epithelial tissue and hence may contain skin appendages, hair and teeth
> most common benign ovarian tumour in woman under the age of 30 years
> median age of diagnosis is 30 years old
> bilateral in 10-20%
> usually asymptomatic. Torsion is more likely than with other ovarian tumours
What are benign epithelial tumours of ovaries?
Arise from the ovarian surface epithelium
Serous cystadenoma
> the most common benign epithelial tumour which bears a resemblance to the most common type of ovarian cancer (serous carcinoma)
> bilateral in around 20%
Mucinous cystadenoma
> second most common benign epithelial tumour
> they are typically large and may become massive
> if ruptures may cause pseudomyxoma peritonei
RFs for ovarian cysts?
obesity
tamoxifen
early menarche
infertility
fertility Tx
FH
PCOS
hypothyroid
hyperandrogenism
smoking (mucinous cysts)
Features of ovarian cysts?
Asymptomatic
Dull ache or pain in lower abdo (back)
Torsion or rupture: sudden severe sharp abdo pain, fever.
Torsion: intermittent eps of severe pain
Rupture: peritonitis shock, rebound tenderness, guarding, shoulder pain.
Dyspareunia
Swollen abdo, palpable mass
Dull to percussion
Doesn’t appear if bladder emptied
Pressure effects: bladder (freq), venous returns (varicose veins, leg oedema)
Ascites, bloating early satiety
Hormone secreting: virilisation, menstrual irreg, PMB
Affect fertility
Torsion more common in dermoid cysts.
Investigation for ovarian cysts?
Pelvic USS: transvaginal, enlarged ovary, or portion of ovarian tissue may be cystic, solid or mixed. Hypoechoic or anechoic.
CL: simple ovarian cyst, variable wall thickness, ↑vascularity, ring of fire sign. Small central lucency.
TL: multiple bilat, thin walls, clear content, occasionally solid.
Complex cyst (multi lobulated) should be biopsied to excl malig.
CA125: doesn’t need to be done in premenopausal who have had USS of simple ovarian cyst as it is unreliable due to large number of false pos.
Risk of malig index: menopausal status, USS findings, CA125
Rule out germ cell tumours: LDH, AFP, hCG.
All women <40 with complex ovarian mass.
Management of ovarian cysts?
Functional cysts usually resolve on their own.
<50mm diameter: simple doesn’t require follow up.
50-70mm: simple, yearly follow up.
If persistent, unchanged <10cm, normal CA125, likelihood of invasive cancer low. Observation
NSAIDs if painful
Surgery: suspicion of malig, solid ovarian cyst, ↑size, complex ovarian cyst in post-menopausal, pregnant women (symptomatic, non-suspicious cyst, or if >8cm), cystectomy (children + women wishing to be pregnant). Immediate surgical intervention indicated for haemorrhagic cyst.
Solid ovarian cyst: laparotomy + gynaecological oncology review.
What is infertility?
Infertility affects around 1 in 7 couples. Around 84% of couples who have regular sex will conceive within 1 year, and 92% within 2 years
Causes male factor 30% unexplained 20% ovulation failure 20% tubal damage 15% other causes 15%
Investigations for infertility?
Investigations initiated when couple trying for 12mnths w/o success, 6mnths if F>35
semen analysis
Serum FSH + LH: day 2-5. ↑FSH (poor ovarian reserve, little eggs, pit tried to compensate by producing more FSH), ↑LH (PCOS), ↑FSH:LH (PCOS)
Serum progesterone day 21. 7 days before end of cycle/expected period. Rise indicates ovulation. <16 repeat, if consistently low refer, 16-30 repeat, >30 indicates ovulation.
TFTs, PRL, AMH (any time of cycle, most reliable measure of ovarian reserves but not readily available, high is good, released by granulosa cells)
Transvaginal USS: structural abnormalities, PCOS
Hysterosalpingogram: patency of tubes, tubal obstruction, spillage of dye with XR. Dilation of cervix via cannula for contrast can lead to ↑ conception rates.
Laparoscopy + dye test: same idea, done with laparoscopy. Adhesions + endometriosis. Dye injected to see if there is any spillage.
Counselling points for infertility?
folic acid
aim for BMI 20-25
advise regular sexual intercourse every 2 to 3 days
smoking/drinking advice
Male RFs for infertility?
varicocele
CF
cryptorchidism
prior chemo or radiotherapy
congen bilat absence of vas deferens
Klinefelter’s
epididymitis
prostatitis
mumps
orchitis
STD
testicular torsion or trauma
smoking
alcohol consumption
obesity
> 55 (can affect sperm motility)
Female RF for infertility?
> 35
STI
very high/ low body fat
Cannabis, alcohol, caffeine
stress
smoking.
Features of infertility?
BMI: low (anovulation), high (PCOS)
STI: chlamydia, PID
Semen analysis: quality + quantity. Mumps in males. <15 million sperm/mL, <40% motile spermatozoa, <4% normal morphology, >42% sperm necrosis.
Seminal fluid parameters: low volume, ↓pH, presence of fructose, ↑leukocyte count
Rubella immunity in mother
Management of infertility?
General advice: 400mcg folic acid daily, healthy BMI, no smoking or XS alcohol, ↓stress, intercourse 2-3 X a wk, avoid timing intercourse
Anovulation: WL, gonadotrophins (stim ovulation, menotrophin, follitropin alda, lutropin alfa). Clomiphene: SERM, stop neg feedback of oest on hypothalamus. ↑FH + LH secretion, growth of follicle + ovulation. Letrozole: stim ovulation. Ovarian drilling: PCOS.
Tubal + uterine: laparoscopy to remove adhesions, endometriosis or polyps.
IVF: 2 eggs (young women) 5 (women >40)
Sperm: surgical sperm retrieval, surgical correction of obstruction, IU insemination, intracytoplasmic sperm injection, donor insemination
Men: hormonal (chorionic gonadotrophin, follitropin alfa, pulsatile GnRH, clomifene, tamoxifen), ↑PRL due to pit adenoma (bromocriptine, cabergoline), antisperm Ig (IVF), varicocele (percut embolization, microsurgical dissection + ligation).
What is ovarian hyperstimulation syndrome?
complication seen in some forms of infertility treatment. It is postulated that the presence of multiple luteinized cysts within the ovaries results in high levels of not only oestrogens and progesterone but also vasoactive substances such as vascular endothelial growth factor (VEGF). This results in increased membrane permeability and loss of fluid from the intravascular compartment
Whilst it is rarely seen with clomifene therapy is more likely to be seen following gonadotropin or hCG treatment. Provoked by trigger injection hCG 36 hrs before oocyte collection that matures follicles in IVF. RAAS, ↑renin
Up to one third of women who are having IVF may experience a mild form of OHSS
Classification of OHSS?
Mild - Abdominal pain, Abdominal bloating
Moderate - As for mild, Nausea and vomiting, Ultrasound evidence of ascites
Severe - As for moderate, Clinical evidence of ascites, Oliguria, Haematocrit > 45%, Hypoproteinaemia
Critical - As for severe, Thromboembolism, Acute respiratory distress syndrome, Anuria, Tense ascites
RFs for OHSS?
young age
↓BMI
↑AMH, antral follicle count + oestrogen levels during ovarian stim.
PCOS
Features of OHSS?
7 days after injection
Late OHSS: >10days
Peritonitis from rupturing follicles releasing blood
Rapid weight gain
Abdo pain, bloating, ascites, VTE/PE, ARDS
Investigations for OHSS?
During simulation with gonadotropins (FSH), monitoring: ↑oestrogen ↑ risk, USS (follicles, ↑ + larger ↑ risk).
USS: ovaries bigger, large fluid filled follicles
Bloods: U+E, leukocytosis, LFTs
Monitor hematocrit: assess volume of fluid in intravascular space, conc of RBCs in blood, if high, less fluid in intravascular space, indicate dehydration
Management of OHSS?
Prevention: GnRH antagonist instead of agonist, ↓dose of gonadotropins, + hCG injection, alternative to hCG > GnRh agonist or LH
Supportive
Oral fluids
Monitor UO
LMWH: prevent VTE
Paracentesis
IV colloids: human albumin solution.
Don’t give diuretics
Analgesia: paracetamol +/or opioids, NSAIDs avoided.
What is menopause?
The average women in the UK goes through the menopause when she is 51 years old. The climacteric is the period prior to the menopause where women may experience symptoms, as ovarian function starts to fail
Premenopausal: vasomotor Sx + irregular periods. >45. 4 yrs before FMP.
Perimenopause: transition, from onset of Sx until 1 yr after menopause. 45-55.
Menopause: no periods for 12 mnths. Average age 52
Premature: <40
Lack of ovarian follicular function, oocytes lost due to aging, ↓oestrogen + progesterone ↓hypothalamic inhibition > ↑bursts of GnRH > ↑FSH + LH. But still no oestrogen, endometrium doesn’t develop, anovulation, irregular menstrual cycle + amenorrhea
Sx of menopause?
Hot flushes, night sweats. Diaphoresis, palpitations.
Emotional liability or mood. Anxiety + depression, diff concentrating.
Premenstrual synd
Joint pains, muscle pain
Heavier/lighter periods, change in length of periods
Vaginal dryness + atrophy.
STM impairment
↓libido
UT dysfunction: dysuria, urinary urgency, freq.
Complications of menopause?
Atrophic vaginitis: post-menopausal, vaginal dryness, dyspareunia, occasional spotting. Vagina may appear pale + dry
CVD + stroke
Osteoporosis #
Pelvic organ prolapse
UI: GU atrophy
↓risk of breast cancer
Late menopause ↑ risk of endometrial cancer
Unopposed oestrogen ↑risk of endometrial Ca if woman still has uterus.
Investigations of menopause?
FSH: <40 suspected prem menopause, 40-45 menopausal Sx or change in cycle. Cessation of menses <45. Perimenopause Sx <45, + iatrogenic amenorrhoea (hysterectomy, POC, endometrial ablation). Women on POC>50 + wishes to stop
No need for bloods: >45yrs menopausal Sx + irregular periods. No period for 12 mnths, not on contraception, hysterectomised with Sx, difficult in women on hormonal Tx for HMB, can’t use FSH if on CHC or high dose progestogen.
Transdermal preferred in women at risk of VTE.
Unscheduled vaginal bleeding common in 1st 3/12.
Management of menopause?
Contraception in: <50 2yrs after LMP, >50 1yr after
Reg exercise, WL, ↓stress, smoking, alcohol, caffeine
Sleep hygiene: avoid late evening exercise
Vasomotor: resolve in 2-5 yrs w/o Tx. Avoid triggers eg hot drinks, spicy food, maintain cool ambient temp, lighter clothing. HRT, fluoxetine, citalopram, venlafaxine
HRT: ↑endometrial + breast ca, VTE, small ↑ CVD/stroke. ↓CRC + osteoporosis. Oestrogen HRT may ↓risk of CVD
HRT CI: current/past breast ca, oest-sensitive ca, undiagnosed vaginal bleeding, untreated endometrial hyperplasia, VTE/DVT unless on anticoag, active/recent arterial disease eg anginal/MI, uncontrolled BP, acute liver disease/ abnormal LFTs, porphyria, pregnancy, Dubin-Johnson/ Rotor (close monitoring)
Clonidine: agonist of α adrenergic receptors.
Psychological Sx: self help groups, CBT, antidepressants
Urogenital atrophy: vaginal oest. Moisturisers + lubricants.
Altered sexual function: HRT, testosterone. Gel eg testogel. Patch > intrinsa, tibolone.
What is premature ovarian failure?
defined as the onset of menopausal symptoms and elevated gonadotrophin levels before the age of 40 years.
Follicles stop responding to LH + FSH, disrupted ovulation, ↓oest, progest, androstenedione > amenorrhoea, hypogonad, hypoestrogenism
It occurs in around 1 in 100 women.
Causes of premature ovarian failure?
idiopathic
> the most common cause
> there may be a family history
bilateral oophorectomy
> having a hysterectomy with preservation of the ovaries has also been shown to advance the age of menopause
radiotherapy
chemotherapy
infection: e.g. mumps
autoimmune disorders
resistant ovary syndrome: due to FSH receptor abnormalities
genetic - Turner’s, fragile X synd, BRCA1 mutation > gonadal dysgenesis.
Features of premature ovarian insufficiency?
climacteric symptoms: hot flushes, night sweats
infertility
secondary amenorrhoea
raised FSH, LH levels
> e.g. FSH > 40 iu/l
> elevated FSH levels should be demonstrated on 2 blood samples taken 4–6 weeks apart
low oestradiol
> e.g. < 100 pmol/l
Management of premature ovarian insufficiency?
hormone replacement therapy (HRT) or a combined oral contraceptive pill should be offered to women until the age of the average menopause (51 years)
it should be noted that HRT does not provide contraception, in case spontaneous ovarian activity resumes
IVF Tx
Investigations for premature ovarian insufficiency?
USS: shrunken ovaries
↓oestrogen, ↑LH, FSH (2 blood samples 4-6 wks apart)
If AI: test for steroid cell antibodies/ STCAs
Genetic testing: karyotype, chr abnormalities, evaluate for genetic disease.
What is menorrhagia?
what the woman considers to be excessive and aims to improve quality of life measures.
Causes of menorrhagia?
dysfunctional uterine bleeding: this describes menorrhagia in the absence of underlying pathology. This accounts for approximately half of patients
anovulatory cycles: these are more common at the extremes of a women’s reproductive life
uterine fibroids
hypothyroidism
intrauterine devices* (copper coil)
pelvic inflammatory disease
bleeding disorders, e.g. von Willebrand disease
Fibroids, endometriosis, adenomyosis, polyps,
malig (endometrium, cervical, ovarian)
endometrial hyperplasia
Sx of menorrhagia?
Dx on Sx not vol: changing pads every 1-2 hrs, >7 days, passing large clots.
Normal 40ml, XS >80ml
Speculum + bimanual palp
Swabs: infection
Investigations of menorrhagia?
FBC: iron studies, ferritin.
Pelvic + transvaginal USS: palpable pelvic mass (large fibroids) pelvic pain + tenderness on exam (adenomyosis), obesity (exam difff) if Sx suggest structural or histological abnormality.
Outpt hysteroscopy: submucosal fibroids, endometrial pathology (Ca or hyperplasia).
Management of menorrhagia?
1st: mirena coil
COCP
Tranexamic acid 1g or mefenamic acid.
Long-acting progestogens eg Depo Provera
Endometrial ablation
Hysterectomy
What are fibroids?
Benign tumours of smooth muscle of uterus
Common in black women
Oest sensitive: grow
Intramural: in myometrium.
Subserosa: just below outside layer of uterus. Grow out + become very large, filling abdo cavity
Submucosal: just below lining of uterus (endometrium)
Pedunculated: on stalk
Sx of fibroids?
Asymptomatic.
Rare before puberty
Heavy menstrual/ prolonged bleeding
Abdo pain, lower, cramping, worse on menstruation
Dyspareunia
Bloating or feeling full in abdo
Abdo + biman may reveal palpable mass or enlarged, firm, non-tender uterus
Complications of fibroids?
Generally regress after menopause
Iron def anaemia
Urinary/ bowel Sx due to pressure or fullness, constipation
↓fertility
Polycythaemia 2° to production EPO
Miscarriages, prem labour, obstructive labour
Urinary outflow obstruction
UTIs
Torsion of fibroids
Malig changes: rare, leiomyosarcoma
Investigations of fibroids?
TVUS
Hysteroscopy: visualise fibroids
Pelvic USS: larger fibroids.
MRI: before surgery, info needed about size, shape, blood supply.
Management of fibroids?
Asymptomatic: no Tx, periodic review
GnRH agonists: goserelin or leuprorelin. ↓size of fibroid before surgery. Induce menopause like state, used in ST.
Mifepristone
Menorrhagia: mirena coil, NSAIDs (mefenamic acid), tranexamic acid, COCP, progestogen.
Myomectomy - abdominally, laparoscopically or hysteroscopically
Endometrial ablation
Uterine a embolism
Hysterectomy
What is red degeneration of fibroid?
haemorrhage into tumour - commonly occurs during pregnancy
Fibroid rapidly enlarges in preg outgrow blood supply, or kinking in BVs as uterus changes shape + expands in preg. ischaemia, infarction, necrosis of fibroid.
Sx of red degeneration of fibroid?
Preg woman with Hx of fibroids
Severe abdo pain + low grade fever
↑HR. vomiting.
Large fibroids >5cm
2nd/3rd trim of preg
Management of red degeneration of fibroid?
Supportive
Fluids
Rest
Analgesia
Should resolve within 4-7 days
What is dysmenorrhoea?
characterised by excessive pain during the menstrual period. It is traditionally divided into primary and secondary dysmenorrhoea.
Summary of primary dysmenorrhoea?
primary dysmenorrhoea there is no underlying pelvic pathology. It affects up to 50% of menstruating women and usually appears within 1-2 years of the menarche. Excessive endometrial prostaglandin production is thought to be partially responsible. Begins due to onset of ovulatory cycles
Features
- pain typically starts just before or within a few hours of the period starting
- suprapubic cramping pains which may radiate to the back or down the thigh
- V/N/D
- fatigue
- headache
- 1st 2 yrs of menarche
Investigations
- Transabdo USS to rule out pathology.
Management
- NSAIDs such as mefenamic acid and ibuprofen are effective in up to 80% of women. They work by inhibiting prostaglandin production
- combined oral contraceptive pills are used second line
Summary of secondary dysmenorrhoea?
Secondary dysmenorrhoea typically develops many years after the menarche and is the result of an underlying pathology. In contrast to primary dysmenorrhoea the pain usually starts 3-4 days before the onset of the period.
Features:
- May worsen as progresses.
- Heavy/ irreg bleeding, discharge, dyspareunia
Causes include:
- endometriosis
- adenomyosis
- pelvic inflammatory disease
- intrauterine devices* - copper coils
- fibroids
- congenital uterine abnormalities
- cervical stenosis
- ovarian pathology
Clinical Knowledge Summaries recommend referring all patients with secondary dysmenorrhoea to gynaecology for investigation.
What is endometriosis?
a common condition characterised by the growth of ectopic endometrial tissue outside of the uterine cavity. Around 10% of women of a reproductive age have a degree of endometriosis.
Cause unknown
Retrograde menstruation: endometrial lining flow back through fallopian tubes + seed around pelvis + peritoneum.
Embryonic cells destined to become endometrial tissue remain in areas outside uterus in development.
Spread of endometrial cells through lymphatic system
Metaplasia: cells outside uterus change to endometrial cells.
Iatrogenic implantation
Features of endometriosis?
chronic pelvic pain - localised bleeding + inflam > adhesions. Sharp, stabbing, pulling, nausea.
asymptomatic in some cases
secondary dysmenorrhoea
> pain often starts days before bleeding. dull, heavy, burning pain
deep dyspareunia
subfertility
non-gynaecological: due to deposits in bladder/bowel > urinary symptoms e.g. dysuria, urgency, haematuria. Dyschezia (painful bowel movements), PR bleed
on pelvic examination reduced organ mobility, tender nodularity in the posterior vaginal fornix and visible vaginal endometriotic lesions may be seen
Investigation for endometriosis?
laparoscopy is the gold-standard investigation
there is little role for investigation in primary care (e.g. ultrasound)- if the symptoms are significant the patient should be referred for a definitive diagnosis
Pelvic/transvaginal USS: large endometriomas (endometrial tissue) + chocolate cysts (ovary).
Often unremarkable. Uterus generally not enlarged. Nodules in bladder or rectovaginal septum.
Management of endometriosis?
Depends on clinical features
1st - NSAIDs and/or paracetamol are the recommended first-line treatments for symptomatic relief
2nd - if analgesia doesn’t help then hormonal treatments such as the combined oral contraceptive pill or progestogens e.g. medroxyprogesterone acetate should be tried
3rd - If analgesia/hormonal treatment does not improve symptoms or if fertility is a priority the patient should be referred to secondary care. Secondary treatments include:
> GnRH analogues - leuproelin, goserelin - said to induce a ‘pseudomenopause’ due to the low oestrogen levels
> drug therapy unfortunately does not seem to have a significant impact on fertility rates
> Immediate fertility desired: clomifene (oestrogen receptor modulator), letrozole (aromatase inhib), menotrophin (highly purified gonadotropins), follitropin alfa. IVF.
> surgery: some treatments such as laparoscopic excision and laser treatment of endometriotic ovarian cysts may improve fertility, hysterectomy
Complications of endometriosis?
↓fertility: adhesions, block release of eggs, kinking fallopian tubes, damage eggs if deposits in ovaries.
Anaemia
Ectopic preg
Fibrous adhesions, strictures, entrapment of organs. Intestines (C/D, obstruction, ileus, intussusception) ureter (urine retention)
↑risk ovarian Ca
What is adenomyosis?
Endometrial tissue in myometrium.
More common in later reproductive yrs + in multiparous women.
Can occur alone or alongside endometriosis + fibroids.
Hormone dependent
Features of adenomyosis?
Dysmenorrhoea
Menorrhagia
Infertility
Dyspareunia
Pregnancy related complications
Asymptomatic
Exam: enlarged, boggy tender uterus. Feel softer than uterus containing fibroids.
Complications of adenomyosis?
Pregnancy: poor outcomes, infertility, miscarriage, preterm birth, SGA, preterm PROM, malpresentation, C-section, PPH.
Investigations for adenomyosis?
Transvaginal USS
MRI + transabdo USS if transvaginal USS not suitable
Gold standard: histological exam of uterus after hysterectomy
Management for adenomyosis?
Contraception: mirena, COP, POP/implant/depot
If not wanting contraception: tranexamic acid if no pain, mefenamic acid when pain.
GnRH agonists
Endometrial ablation. Uterine artery embolization.
Hysterectomy
