Obstetrics and gynaecology Flashcards
How is gestation estimated? What is the most accurate method?
Ultrasonography within the first 13 6/7 weeks of gestation is most accurate method to establish/confirm gestational age
Using LMP:
Expected date of delivery = 280 days (40 weeks) from 1st day of last menstrual period
Naegele’s rule
EDD = LMP + 1 year and 7 days - 3 months
If IVF - days since oocyte retrieval or co-incubation + 14 days
Physical examination:
After 20 weeks - pubic symphysis to fundal height in cm should correlate with week of gestation
Describe the normal process of fertilisation and implantation in pregnancy
Fertilisation in fallopian tube
Transportation of embryo along tube
Implantation in endometrium occurs approximately 6 days post-fertilisation
Describe the hormonal changes which occur in normal early pregnancy
HCG rises exponentially from 4-12 weeks gestation, then falls and levels off at 24 weeks until birth
Progesterone and oestrogen rise from early gestation until birth, initially progesterone higher then oestrogen higher
Describe the normal physiological changes which occur in the respiratory system in pregnancy and the clinical consequences of these changes
Diaphragm pushed up so decreased expiratory reserve volume, giving the sensation of SOB (increased tidal volume balances out so sensation only)
Reduced CO2 (to draw CO2 out of baby’s blood) so reduced bicarb = compensated respiratory alkalosis
Increased respiratory rate
Increased laryngeal oedema - difficult intubation
Describe the normal physiological changes which occur in the cardiovascular system in pregnancy and the clinical consequences of these changes
Reduced systemic and pulmonary vascular resistance, BP can fall in 2nd trimester and rise slightly in late pregnancy
Cardiac output and stroke volume peak by week 16 - highest risk if pre-existing CVD
Drop in BP causes RAAS activation, leading to sodium and water retention - blood volume increased, physiological (dilutional) anaemia
Constriction of peripheral circulation - Raynaud’s
Can have ejection systolic murmur/third heart sound
ECG’s look different due to different position of heart
Increased risk varicose veins
Describe the normal haematological changes which occur during pregnancy
Increased plasma volume - dilutional anaemia
EPO release - increased RBC but haemoglobin still low
Modest leukocytosis
High demand for additional iron - serum iron falls, transferrin and total iron binding capacity rise
Describe the normal physiological changes which occur in the urinary tract during pregnancy and the clinical consequences they have.
Increased blood volume and cardiac output - increased renal blood flow - increased GFR - increased excretion (frequent urination), reduced levels of urea, creatinine, urate and bicarbonate
Mild glycosuria/proteinuria as increase in GFR can exceed ability for reabsorption
Increased water retention, reduction in plasma osmolality
Smooth muscle of renal pelvis and ureter relaxes and dilates, kidneys increase in length and ureters become longer, more curved (increased risk UTI) and increase in residual urine volume
Bladder smooth muscle relaxes, increased capacity, increased risk UTI
Mechanical pressure of uterus on bladder - increased urination
Describe the normal physiological changes in the GI tract during pregnancy and the clinical consequences these have
Relaxation of smooth muscle - decreased LOS pressure, decreased gastric peristalsis, delayed gastric emptying, increased small and large bowel transit times, reduced gallbladder contraction
= GORD, nausea and vomiting, constipation, gallstones
Describe the normal physiological changes which occur in the skin during pregnancy and the clinical consequences these can have
Hyperpigmentation of umbilicus, nipples, abdominal midline (linea nigra) and face
Hyperdynamic circulation and high levels oestrogen - spider naevi and palmar erythema
Striae gravidarum (stretch marks)
Describe the normal physiological changes in the musculoskeletal system which occur during pregnancy and the clinical consequences these can have
Increased ligament laxity due to relaxin contribute to back pain and pubic symphysis dysfunction
Shift in posture with exaggerated lumbar lordosis - typical gait of pregnancy
Define the terms:
Miscarriage
Stillbirth
Livebirth
Miscarriage - any pregnancy loss before 24 weeks
Stillbirth - any fetus born dead at or after 24 weeks gestation
Livebirth - a fetus which shows signs of life after delivery at any gestation
Define these types of miscarriage:
Threatened
Inevitable
Incomplete
Complete
Delayed/missed/early embryonic demise
Septic
Recurrent
Threatened - painless bleeding with continuing intrauterine pregnancy, before 24 weeks, cervix closed
Inevitable - bleeding with non-continuing intrauterine pregnancy, cervix may be open
Incomplete - retained products of conception remain in uterus
Complete - full miscarriage has occurred, no products of conception left in uterus
Delayed/missed/early embryonic - fetus died in-utero prior to 24 weeks gestation, no symptoms
Septic - miscarriage complicated by intrauterine infection
Recurrent - 3 or more consecutive miscarriages
Describe the methods for estimation of gestational age by US in each trimester
First trimester - crown-rump length
Second trimester - head circumference, femur length
Third trimester - head circumference, femur length
List causes and risk factors for miscarriages
Spontaneous usually due to embryonic abnormalities - chromosomal abnormalities, placental defects
No cause found in 50% of recurrent miscarriages
Causes of recurrent:
Thrombophilic abnormalities - factor V leiden mutation, prothrombin gene mutation
Immunological abnormalities - antiphospholipid syndrome
Anatomical/structural - uterine abnormalities (bicornuate or arcuate uterus), cervical abnormalities (cervical incompetence)
Genetic abnormalities
Endocrinological - PCOS, hyperprolactinaemia, thyroid disease, poorly controlled DM
Infective causes - bacterial vaginosis
Risk factors
Maternal age
Previous miscarriages
Occupational/environmental factors - pesticides, radiation
Advanced paternal age
Lifestyle - stress, obesity, smoking
Describe the clinical presentation of miscarriage
Pregnant - positive pregnancy test or symptoms of pregnancy (amenorrhoea, missed period, breast tenderness)
Vaginal bleeding (brown spotting to heavy +/- tissue), lower abdominal cramping or backache
Can be asymptomatic
What is the differential diagnosis for miscarriage?
Ectopic pregnancy
Molar pregnancy - heavy, prolonged bleeding, uterus large for dates
Pregnancy related:
Ruptured ovarian corpus luteal cyst
Adnexal torsion
Pregnancy-related degeneration of a fibroid
Non-pregnancy related:
Cervicitis, cervical ectropion, cervical polyps
Cancer of cervix, vagina, vulva
Haemorrhoids
Urethral bleeding, UTI
Vaginitis
MSK pain
Constipation
IBS
PID
Appendicitis
Renal colic
Bowel obstruction
Adhesions
Ovarian cyst - torsion, rupture, bleeding
Torsion of fibroid
Pelvic vein thrombosis
Describe assessment/investigations for suspected miscarriages
A-E - haemodynamically stable?
Removal of POC (speculum)
US - transabdominal, transvaginal (investigation of choice for diagnosis)
Examination of POC
Serum HCG tracking
Assess FBC, group and save/crossmatch
Describe the ultrasound findings used to diagnose miscarriages
No fetal heart activity with crown-rump length >7mm on transvaginal scan - repeat scan after 1 week to confirm non-viable pregnancy
Empty sac (no fetal pole) when gestational sac diameter >25mm on transvaginal scan - repeat scan after 1 week to confirm anembryonic pregnancy
Retained tissue seen in incomplete miscarriage
Empty uterus - complete passage of tissue (complete miscarriage), pregnancy too early to visualise or ectopic pregnancy
What are the options for management of miscarriages? When is each option appropriate?
Expectant management - give 1-2 weeks for miscarriage to occur spontaneously
Used if <6 or >6 weeks gestation if no pain and no other complications or risk factors
Medical/surgical - if increased risk of haemorrhage/infection, previous adverse experience of pregnancy (e.g. stillbirth, miscarriage)
Medical management - misoprostol (oral or vaginal)
Surgical - misoprostol to soften cervix then manual or electric vacuum aspiration
Describe the mechanism of action and side effects of misoprostol
Prostaglandin analogue - binds and activates prostaglandin receptors
Prostaglandins soften cervix and stimulate uterine contractions
Side effects:
Heavier bleeding
Pain
Vomiting
Diarrhoea
Describe the methods of surgical management of miscarriages and when they are appropriate
Manual vacuum aspiration - local anaesthetic applied to cervix, syringe through cervix into uterus and aspiration of contents of uterus
Electric vacuum aspiration - general anaesthetic, cervix dilated and products of conception removed through cervix using electric-powered vacuum
Manual - <10 weeks gestation, parous
If products of conception retained or ongoing symptoms after expectant/medical management
Definite indications - infection of retained tissue, haemodynamic instability, gestational trophoblastic disease
When is anti-rhesus prophylaxis required in miscarriages? When is it not required?
Rhesus negative women
Surgical management of miscarriage <12 weeks
Any potential sensitising event >12 weeks
Not required:
Threatened or complete miscarriage
Medical management of miscarriage
How is an incomplete miscarriage managed? Why?
Medical management - misoprostol
Surgical management - evacuation of retained products of conception (dilation of cervix and removal through vacuum aspiration and curettage)
Retained product are infection risk
What is a key complication of evacuation of retained products of conception?
Endometritis
Describe the success rates of different management options for miscarriages
Expectant - 60%
Medical - 80-90%
Surgical - 97%
How should women be followed up after expectant management of miscarriage?
Return if bleeding continues or pain develops
Repeat urine pregnancy test after 7-10 days, return if positive, if negative miscarriage confirmed
List risk factors for ectopic pregnancy
Previous ectopic pregnancy
Damage to fallopian tube - PID, tube surgery
History of infertility
Assisted reproduction techniques - IVF
Smoking
Maternal age >35
Multiple sexual partners
Contraception - if contraception failure higher risk of ectopic pregnancy with IUD, POP, sterilisation compared to other methods of contraception
Describe the clinical presentation of ectopic pregnancy
Positive pregnancy test or symptoms of pregnancy (missed period etc.)
Usually presents 6-8 weeks gestation
Can be asymptomatic
Lower abdominal/pelvic pain
Can have referred shoulder tip pain (peritonitis)
Vaginal bleeding - brown spotting to heavy
Pain with opening bowels/urination
Cervical motion tenderness
Collapse/hypovolaemic shock
How is a suspected ectopic pregnancy investigated?
Transvaginal US is investigation for diagnosis
Serum hCG
Assess FBC, group and save/crossmatch
Describe US findings in ectopic pregnancies
Gestational sac with fetal pole in fallopian tube
May just be non-specific mass in tube - blob/bagel/tubal ring sign
Empty uterus
Fluid in uterus - pseudogestational sac
How are serial hCG measurements used to dictate management of pregnancy of unknown location?
Measure 48 hours apart
Used if PUL on US and patient stable
Increase >66% - likely intrauterine pregnancy, US to determine location 7-14 days later, if hCG >1,500 should be visible
<66% increase or <50% decrease - ectopic, requires close monitoring/management
> 50% decrease - failing PUL, repeat pregnancy test in 2 weeks to confirm miscarriage
Describe emergency and non-emergency management of ectopic pregnancies
Emergency:
A-E resuscitation
Early involvement from gynaecology, anaesthetics, haematology (+ blood)
Theatre to remove source of bleeding and stabilise
Non-emergency:
Conservative
Medical - methotrexate
Surgical
When is conservative management of ectopic pregnancy appropriate? What does this involve?
Size <35mm
Unruptured
Asymptomatic
No fetal heartbeat
hCG <1,000
Compatible if another intrauterine pregnancy
Closely monitor patient over 48 hours, if hCG levels rise or symptoms manifest need to intervene
When is medical management of ectopic pregnancy appropriate? What does it involve?
Size <35mm
Unruptured
No significant pain
No fetal heartbeat
hCG <5000
Not suitable if intrauterine pregnancy
Able to return for follow up
No medical contraindications - anaemia, renal/hepatic impairment, UC, peptic ulcer
Methotrexate
When can a patient become pregnant again after medical management of ectopic pregnancy? Why?
12 weeks after hCG <5
Need to replenish folic acid
What are the key risks and side effects of medical management of ectopic pregnancy?
7% risk fallopian tubal rupture
Side effects
Vaginal bleeding
Nausea and vomiting
Abdominal pain
Stomatitis
When is surgical management of ectopic pregnancy appropriate?
Size >35mm
Rupture
Pain
Visible fetal heartbeat
HCG >5,000
Compatible with another intrauterine pregnancy
Describe the options for surgical management of ectopic pregnancy
Laparoscopy or laparotomy depending on clinical situation
1st line - salpingectomy (if no other risk factors for infertility)
Salpingotomy if risk factors for infertility e.g. contralateral tube damage
1 in 5 need further treatment - methotrexate or salpingectomy
Which women need Anti-D in management of ectopic pregnancy? Which don’t?
Rhesus negative, surgical management - need anti-D
Conservative or medical management - don’t need anti-D
Describe the risk of recurrence of ectopic pregnancies
18.5% risk recurrence after ectopic pregnancy
Define gestational trophoblastic disease
A group of conditions characterised by abnormal proliferation of trophoblastic tissue with production of HCG
Includes:
Pre-malignant conditions (more common) - partial molar pregnancy and complete molar pregnancy
Malignant conditions (rarer) - invasive mole, choriocarcinoma, placental trophoblastic site tumour, epithelioid trophoblastic tumour
What is a hyatidaform mole?
Pre-malignant tumour within uterus arising from an abnormality in chromosomal number during fertilisation
Partial molar pregnancy - one ovum with 23 chromosomes fertilised by two sperm, each with 23 chromosomes, resulting in cells with 69 chromosomes (triploidy), may exist with viable fetus (triploid placenta only)
Complete molar pregnancy - one ovum without any chromosomes is fertilised by one sperm which duplicates or by two different sperm, leading to 46 chromosomes of paternal origin
Describe the malignant types of gestational trophoblastic disease - tissue of origin, common presentations
Choriocarcinoma - malignancy of trophoblastic cells of placenta, commonly co-exists with molar pregnancy, metastasises to lungs
Placental site trophoblastic tumour - malignancy of intermediate trophoblasts, normally responsible for anchoring placenta to uterus, can occur after normal pregnancy (most commonly), molar pregnancy or miscarriage
Epithelioid trophoblastic tumour - malignancy of trophoblastic placental cells, can be difficult to distinguish from choriocarcinoma, mimics cytological features of squamous cell carcinoma
List risk factors for gestational trophoblastic disease
Maternal age <20 or >35
Previous gestational trophoblastic disease
Previous miscarriage
OCP use
Asian ethnicity
Describe the clinical features of gestational trophoblastic disease
Early pregnancy:
Vaginal bleeding
Abdominal pain
Larger uterus than expected for gestation with a soft, boggy consistency
Shedding of molar vesicles PV
Later symptoms:
Hyperemesis - increased bHCG
Hyperthyroidism - bHCG stimulates thyroid
Anaemia
Large for date uterus
How should suspected gestational trophoblastic disease be investigated?
Urine bHCG - confirm pregnancy
Blood bHCG - elevated at diagnosis, used to monitor
US - complete mole has granular/snowstorm appearance with central heterogeneous mass and surrounding multiple cystic areas/vesicles
Histological examination of POC
If metastatic spread - staging investigations e.g. MRI, CT, US
How is gestational trophoblastic disease managed?
Register with GTD specialist centre for follow-up and monitoring in future pregnancies
Molar pregnancy
Suction curettage more effective for complete and non-viable partial moles
Partial mole with fetal development - medial evacuation with urinary bHCG post-treatment
Histological assessment of POC
Malignant GTD - specialist centre treatment, chemotherapy +/- surgery
Why is medical management of molar pregnancies not recommended?
Theoretical risk of embolisation of trophoblastic tissue if managed with oxytocic agents
Is Anti-D required for gestational trophoblastic disease?
If mother Rh negative and surgical management
Define hyperemesis gravidarum. What causes it?
Persistent vomiting in pregnancy causing weight loss (more than 5% of body mass), dehydration and electrolyte imbalance
High bHCG levels - stimulates chemoreceptor trigger zone in brainstem
List risk factors for hyperemesis gravidarum
First pregnancy
Previous history hyperemesis gravidarum
Raised BMI
Multiple pregnancy
Gestational trophoblastic disease
How is the severity of hyperemesis gravidarum measured?
Pregnancy-Unique Quantification of Emesis (PUQE)
<7 - mild
7-12 - moderate
>12 - severe
When does nausea and vomiting of pregnancy typically occur? When should another diagnosis be considered?
4-7 weeks
Consider alternative if symptoms start after 10+6 weeks
How should hyperemesis gravidarum be investigated?
Weight
Urine dipstick - ketonuria
Mid-stream urine
FBC
U&Es - hypokalaemia, hyponatraemia, dehydration
Blood glucose - exclude diabetic ketoacidosis if diabetic
Exclude other causes e.g. LFTs, amylase, TFTs, ABG
US - confirm gestation, exclude multiple pregnancy/trophoblastic disease
How is hyperemesis gravidarum managed?
Mild - in community with oral antiemetics, hydration, dietary advice, reassurance
Moderate - ambulatory day care for IV fluids, parenteral antiemetics, thiamine, until ketonuria resolves
Severe - inpatient management
IV rehydration with electrolyte repletion as required (add potassium chloride)
H2 receptor antagonists/PPI for reflux, oesophagitis, gastritis
Thiamine - prevent Wernicke’s
Thromboprophylaxis
Which antiemetics are recommended for hyperemesis gravidarium?
First line - cyclizine, prochlorperazine, promethazine, chlorpromazine
Second line - metoclopramide (max. 5 days due to risk of EPS), domperidone, ondansetron
Third line - hydrocortisone IV (convert to prednisolone PO once symptoms resolve, reduce dose according to response)
Define infertility
Failure to achieve pregnancy after 12 months or more of regular unprotected sex between a man and a woman
Primary - couple never able to conceive
Secondary - couple cannot get pregnant again, despite previously having been able to without any difficulty
Describe the incidence of infertility in the UK
1 in 7 couples will struggle to conceive naturally
List causes of infertility in terms of basic reproductive physiology
FEMALE
Disorders of ovulation - hypothalamic-pituitary failure, hypothalamic-pituitary-ovulation dysfunction, ovarian failure, hyperprolactinaemia, pituitary tumours
Tubal causes - PID, sterilisation, endometriosis, pelvic surgery
Uterine/peritoneal causes - endometriosis, pelvic/cervical surgery, fibroids, Asherman’s syndrome
MALE
Oligospermia - <15 million sperm per ml
Teratospermia - <4% normal morphology
Asthenospermia - <32% sperm motility
Azoospermia - no sperm in ejaculate
Obstructive infertility - previous vasectomy, cystic fibrosis, ejaculatory duct obstruction, epididymal obstruction
Non-obstructive infertility - hormonal (hypogonadotropic hypogonadism, hyperprolactinaemia), varicocele, genetic causes (Klinefelter’s, androgen insensitivity syndrome, Kallmann syndrome), cryptorchidism, previous testicular trauma (e.g. torsion), malignancy
Coital infertility - ED, premature ejaculation, anejaculation (primary or secondary), retrograde ejaculation, penile deformities (Peyronie’s, hypospadies)
Who should be investigated for infertility?
Trying to conceive for 1 year after frequent (every 2-3 days) unprotected sexual intercourse
OR
Investigation after 6 months if:
Woman >36
Known cause of infertility
History of predisposing factors
What advice should be given to couples trying to conceive?
Regular (every 2-3 days) sexual intercourse throughout cycle
Preparation for pregnancy e.g. folic acid daily
Smoking cessation for men and women
Avoid drinking alcohol excessively (women should avoid entirely)
Women should aim for BM 19-25
Reduce stress
No need to time intercourse
How should infertility be investigated?
BMI
Chlamydia screening
Semen analysis
Female hormone testing - serum LH and FSH (day 2-5 of cycle), serum progesterone (day 21 or 7 days before end of cycle), anti-Mullerian hormone (ovarian reserve), TFTs, prolactin
Rubella immunity in mother
US pelvis - polycystic ovaries or structural abnormalities
Hysterosalpingogram - patency of fallopian tubes
Laparoscopy and dye test - patency of fallopian tubes, adhesions and endometriosis
Male genetic testing
Male US - structural abnormality
Male hormone analysis - testosterone, FSH, LH, prolactin
Describe management of female factor infertility
Medical - stimulate ovulation
Clomiphene - anti-oestrogen, increases GnRH, FSH and LH
Letrozole - aromatase inhibitor with anti-oestrogen effects
Gonadotrophins - if clomiphene resistant infertility
Pulsatile GnRH
Dopamine agonists - if secondary to hyperprolactinaemia
Ovarian drilling for PCOS
Surgery
Tubal surgery if mild tubal disease - catheterisation or cannulation
Uterine surgery for polyps, adhesions or structural abnormalities
How is male factor infertility managed?
Medical
Gonadotrophins for hypogonadotropic hypogonadism
Surgical
Correction of blockage in genital tract
List options for assisted conception
Surgical sperm retrieval - if blockage in male genital tract, collect sperm directly from epididymis
Intrauterine insemination - partner or donor sperm, injected into uterus during natural or stimulated cycles
In vitro fertilisation - used for more severe tubal disease with unexplained fertility, or other treatments unaffective
Intracytoplasmic sperm injection - low sperm count or sexual dysfunction
Donor inseminsation - persistent azoospermia
Oocyte donation - ovarian failure or absence of ovaries
Embryo donation
Define ovarian hyperstimulation syndrome, describe the cause and features
Complication of some infertility treatments - gonadotropin or hCG treatment (e.g. in IVF)
High levels of vasoactive substances (e.g. VEGF) with multiple luteinised cysts resulting in increased membrane permeability and loss of fluid from intravascular compartment
Features:
Mild:
Abdominal pain
Abdominal bloating
Moderate:
Nausea and vomiting
Ascites
Severe:
Oliguria
High haematocrit
Hypoproteinaemia
Critical:
Thromboembolism
Acute respiratory distress syndrome
Anuria
Tense ascites
Describe the process of egg retrieval for IVF. What are the potential side effects?
- GnRH analogue - down-regulation of pituitary
- FSH - stimulate ovulation
- hCG - egg maturation
- Egg retrieval - US guided needle through vagina
Risks/side effects - ovarian hyperstimulation syndrome, vaginal bleeding, cramps, multiple births, ectopic pregnancy
An ectopic pregnancy in which area of the fallopian tube is highest risk for rupture?
Isthmus
List the types of cysts which affect the ovaries and describe their malignant potential
Non-neoplastic (no malignant potential)
Functional:
Follicular cysts - developing follicle in first half of menstrual cycle
Corpus luteal cysts - luteal phase after corpus luteum is formed
Pathological
Endometrioma - chocolate cyst, in endometriosis
Polycystic ovaries - US appearance of >12 antral follicles in ovary or volume >10ml
Theca lutein cyst - due to raised hCG, resolves with normal hCG
Mullerian inclusion cyst - implantation of tubal epithelium in ovary at ovulation, can develop into epithelial ovarian cancer
List the cancers which affect the ovaries, if they are benign or malignant and the cells they originate from
Describe the incidence of ovarian cancer
6th most common cancer in women in the UK, 2nd most common gynaecological cancer
Highest incidence in 75-79 year olds
Poor prognosis if advanced - 10% survival stage IV
List risk factors and protective factors for ovarian cancer
Risk factors - more ovulations
Nulliparity
Age - peak 75
Early menarche
Late menopause
Oestrogen only HRT
Smoking
Obesity
Protective factors - less ovulations
Multiparity
Combined oestrogen and progesterone contraception
Breastfeeding
Genetic risk
Family history
BRCA1&2
Hereditary nonpolyposis colorectal cancer (Lynch II syndrome)
Describe the clinical presentation of ovarian cancer
Non-specific symptoms
GI symptoms - abdominal bloating, early satiety, loss of appetite, constipation or diarrhoea (change in bowel habit)
Pelvic pain - chronic or acute (ovarian torsion)
Mass effect - urinary symptoms (frequency, urgency), constipation, bowel obstruction, abdominal/pelvic mass, compression of obturator nerve (hip/groin pain)
Weight loss
Ascites
Rarely - paraneoplastic syndrome, pleural effusion (SOB)
PV bleeding
Describe the referral criteria for suspected ovarian cancer
2-week wait referral if:
Ascites
Pelvic mass (unless clearly due to fibroids)
Abdominal mass
Further investigations (initially CA125) in >50 with:
New symptoms of IBS/change in bowel habit
Abdominal bloating
Early satiety
Pelvic pain
Urinary frequency or urgency
Weight loss
Which investigations should be used in suspected ovarian cancer?
Initial investigations:
CA125 blood test (>35 significant)
Pelvic ultrasound
CT
Histology - CT guided biopsy, laparoscopy or laparotomy
Paracentesis (ascitic tap) - test ascitic fluid for cancer cells
<40 years with complex ovarian mass - check tumour markers for possible germ cell tumour:
Alpha-fetoprotein
HCG
Calculate risk of malignancy index (RMI)
What is the risk of malignancy index for ovarian cancer? How is it calculated?
Can be used as risk stratification tool in patients with suspected ovarian cancer
RMI = U (ultrasound score) x M (menopausal status) x CA125
Ultrasound score - 1 point if one feature from list, 3 points if 2 or more features from list:
Multilocular cyst
Solid areas
Metastases
Ascites
Bilateral lesions
Menopausal status
1 point - premenopausal
3 points - postmenopausal
RMI >200, refer for CT scan and MDT input
What causes raised CA125?
Glycoprotein antigen
Elevated in:
Malignancies - ovary, pancreas, breast, lung, colon
Benign - menstruation, endometriosis, PID, pleural/pericardial effusions, recent laparotomy
How are ovarian cancers staged?
FIGO staging
Stage IA - confined to one ovary, capsule intact, negative washings
Stage IB - both ovaries involved
Stage IC - 1 or both ovaries with surgical spill/capsule rupture/malignant cells in pleural fluid or washings
Stage IIA - extension to tubes +/- uterus
Stage IIB - extension to other pelvic tissues
Stage IIIA - positive retroperitoneal LNs +/- microscopic mets beyond pelvis
Stage IIIB - macroscopic, extra-pelvic, peritoneal mets <2cm
Stage IIIC - macroscopic, extra-pelvic, peritoneal mets >2cm
Stage IVA - pleural effusion with positive cytology
Stage IVB - hepatic/splenic mesenchymal metastasis, metastasis to extra-abdominal organs including inguinal nodes
Basically:
Stage 1 - confined to ovary
Stage 2 - spread past ovary but within pelvis
Stage 3 - spread past pelvis but inside abdomen
Stage 4 - spread outside abdomen (distant metastasis)
Describe the prognosis of ovarian cancer and the factors which affect prognosis
1 year survival - 70%
5 year survival - 46%
10 year survival - 35%
Affected by factors including:
Histological subtype
Grade
Stage
Co-morbidities
Residual disease at time of surgery
List the management options available for ovarian cancer
Surgery - staging laparotomy for those with high RMI and attempt to de-bulk tumour
Adjuvant/neoadjuvant chemotherapy - recommended for all except those with early, low grade disease, uses platinum-based compounds
Other options - biological therapy (anti-VEGF e.g. bevacizumab), hormonal therapy (tamoxifen/aromatase inhibitor, if platinum resistant)
What tests could be used for ovarian cancer screening? Why is this not done?
CA125 - false positive rate too high as raised in many other conditions and not sensitive enough
Transvaginal US - difficult to determine from scan if benign or malignant disease, would need to obtain biopsy to determine which would result in many unnecessary surgeries
Which women are high risk for ovarian cancer? How can this risk be reduced?
BRCA1(higher risk) or BRCA2 (lower risk), Lynch syndrome, Peutz-Jegher syndrome, Cowden syndrome
Recommended for age 35-40 for BRCA1 and 40-45 for BRCA2
Risk reducing surgery - prophylactic bilateral salpingo-oopherectomy, usually laparoscopic
Reduces risk of ovarian cancer by 96%, breast cancer by 53%
What is the most common kind of endometrial cancer?
Adenocarcinoma
List the types of cancer which affect the endometrium and their tissues of origin
Adenocarcinoma - glandular epithelium
Type 1 - oestrogen dependent, endometrioid most common (75%)
Type 2 - not oestrogen dependent, papillary serous (5%), clear cell (1%)
Sarcoma - muscular
Leiomyosarcoma most common
Uterine carcinosarcoma - rare, aggressive, mixed undifferentiated carcinoma and sarcoma
Describe the prevalence of endometrial cancer
Most common gynaecological cancer
13th most common cancer UK
65% increase since 1970s
Peak incidence in 70-75
Describe the aetiology of and list risk factors for endometrial cancer
Endometrial hyperplasia - precancerous condition, <5% progress to endometrial cancer (same aetiology and risk factors as type 1)
Type 1 adenocarcinoma - unopposed oestrogen (oestrogen without progesterone)
Causes of unopposed oestrogen:
Early menarche or late menopause
Low parity
PCOS
Oestrogen only HRT
Tamoxifen
Other risk factors:
Age
Obesity
Genetic factors - Lynch syndrome, family history
Type 2 diabetes
List protective factors against endometrial cancer
Increased progesterone:
Combined contraceptive pill
Mirena coil
Multiparity
Cigarette smoking - anti-oestrogenic so protective in post-menopausal women
How can the risk of endometrial cancer be reduced in women with PCOS?
Endometrial protection with:
Combined contraceptive pill
Intrauterine pill e.g. Mirena coil
Cyclical progestogens to induce withdrawal bleed
Maintain healthy BMI
Avoid diabetes
Describe the genetic pattern and clinical features of Lynch syndrome
Lynch I - site-specific colorectal cancer
Lynch II - autosomal dominant
Predisposition to colorectal, breast, ovarian, endometrial, gastric, hepatobiliary, brain, skin, upper urinary tract and small bowel cancers
How is Lynch syndrome diagnosed?
Amsterdam criteria:
Colorectal cancer in 3 or more relatives
Involves at least 2 generations
One case before age 50
Familial polyposis excluded
Describe the similarities and differences between FAP and Lynch syndrome in terms of genetics, clinical consequences and management
Both autosomal dominant and cause predisposition to colorectal cancer
FAP - mutation in APC gene
HNPCC - genetic alterations in DNA mismatch repair genes
FAP - colon, rectum, bones, eyes, duodenum affected
HNPCC - colon, endometrium, ovaries, upper urinary tract, skin, brain, stomach, hepatobiliary system affected
FAP - numerous (>100) benign polyps from young age, 100% cancerous transformation
HNPCC - few polyps, 50-70% cancerous transformation
Management:
FAP - prophylactic colectomy for all patients, regular endoscopic check of upper GI tract
HNPCC - no prophylactic surgery recommended, regular colonoscopic/gynaecologic examinations recommended
Describe the clinical presentation of endometrial cancer
Post-menopausal bleeding - >1 year after periods have stopped
Pre-menopausal - irregular, heavy or inter-menstrual bleeding
Post-coital bleeding
Rarely -
Clear/white vaginal discharge
Haematuria
Anaemia
Raised platelet count
Abdominal/pelvic mass
What is the differential diagnosis for post-menopausal bleeding?
Endometrial causes - endometrial cancer, endometrial hyperplasia without malignancy, benign endometrial polyps, endometrial atrophy
Vulval causes - vulval atrophy, vulval pre-malignant or malignant conditions
Cervical causes - cervical polyps, cervical cancer
What is post-menopausal bleeding?
Unexplained bleeding from the vagina >12 months after menstruation has stopped because of the menopause
How should a woman presenting with post-menopausal bleeding be assessed and investigated?
History:
Age
Timing of menopause
Parity
Risk factors for endometrial cancer - obesity, PCOS, tamoxifen use, T2DM, HRT, Lynch syndrome
Examination - whole lower genital tract including vulva, vagina and cervix, abdominal examination (masses), bimanual examination (size and axis of uterus)
Investigations
Transvaginal US - endometrial thickness
Thickness >3mm or >5mm in COCP/HRT users - endometrial biopsy
If high risk or unable to biopsy in clinic - hysteroscopy with biopsy
If malignancy confirmed - MRI/CT for staging
Describe the staging of endometrial cancer
FIGO staging:
Stage I: confined to uterus
A - <50% myometrial invasion
B - >50% myometrial invasion
Stage II: cervical stroma invasion but not beyond uterus
Stage III: tumour outside uterus but within pelvis
A - invades serosa or adnexa
B - vaginal/parametrial involvement
C1 - pelvic node involvement
C2 - para-aortic node involvement
Stage IV -
A - invasion into bowel/bladder mucosa
B - distant mets including abdominal mets or inguinal lymph nodes
Describe the prognosis and survival of endometrial cancer
1 year - 90% survival
5 year - 79% survival
10 year - 78% survival
25% present with stage 4 disease
Describe the referral criteria for suspected endometrial cancer
2-week wait for post-menopausal bleeding
Referral for TV US in >65 with unexplained vaginal discharge or visible haematuria plus raised platelets, anaemia or elevated glucose levels
Describe management of endometrial cancer by stage
Stage 1/2 - usually total abdominal hysterectomy with bilateral salpingo-oophorectomy, take peritoneal washings
Stage 2 - may have radical hysterectomy (vaginal tissue around uterus and supporting ligaments of uterus also removed, assessment and removal of pelvic LNs) +/- adjuvant radiotherapy
Stage 3 - maximal de-bulking surgery, chemotherapy, radiotherapy
Stage 4 - maximal de-bulking surgery although many have palliative approach with low-dose radiotherapy or high dose oral progestogens
List side effects of radiotherapy for endometrial cancer
Proctitis
Cystitis
Lethargy
Skin changes
Define endometrial hyperplasia, describe the types of endometrial hyperplasia and their malignant potential
Precancerous condition involving thickening of the endometrium
Types
Hyperplasia without atypia - 1-4% malignant potential
Atypical hyperplasia - 23% malignant potential
How is endometrial hyperplasia managed?
Progestogens:
IUS e.g. Mirena coil
Continuous oral progestogens e.g. levorgestrel, medroxyprogesterone
What is the most common type of cervical cancer? List other histological types of cervical cancer and their prevalence
70% squamous cell carcinoma
15% adenocarcinoma - mucinous or adenoma malignum
15% mixed type - adenosquamous carcinoma
Rarer - endometrioid, clear cell, serous, neuroendocrine
Describe the normal histology of the cervix
Inner surface (canal) lined by columnar epithelium
Outer surface lined by squamous epithelium
Junction is at transformation zone
Describe the incidence of cervical cancer by age
50% diagnosed <47, peak in 25-29 and second peak in 80s
Describe the aetiology and risk factors for cervical cancer
Usually a progression from cervical intraepithelial neoplasia (CIN)
Most caused by persistent HPV infection - risk factors for early HPV infection e.g. early sexual activity, increased numbers of sexual partners, sexual partners who have had more partners, not using condoms
Other risk factors:
Smoking
Other STIs
Long-term (>8 years) COCP use
Immunodeficiency e.g. HIV
Not engaging with cervical screening
Increased number of full-term pregnancies
Family history
Exposure to diethylstilbestrol during fetal development (used to prevent miscarriages before 1971)
Describe how HPV causes cancer
Produces E6 protein which inhibits p53 and E7 protein which inhibits pRb (p53 and pRb are tumour suppressor genes)
Which strains of HPV are associated with cancer? Which cancers are associated with HPV?
Type 16 and 18 responsible for 70% of cervical cancers
HPV also associated with anal, vulval, vaginal, penis and head and neck cancers
Describe the clinical presentation of cervical cancer
Often asymptomatic in early stages and detected through screening
Abnormal vaginal bleeding - post-coital, intermenstrual or post-menopausal
Vaginal discharge - blood-stained, foul smelling
Dyspareunia
Pelvic pain
Weight loss
Pelvic masses
Abnormal appearance of cervix - ulceration, inflammation, bleeding, visible tumour
Advanced disease
Oedema
Loin pain
Rectal bleeding
Radiculopathy
Haematuria
Obstructive renal failure, hydronephrosis
Describe the investigation of women presenting with suspected cervical cancer
Pre-menopausal
Test for chlamydia - if positive treat, if symptoms persist refer for colposcopy and biopsy, if negative usually require colposcopy and biopsy
Post-menopausal - urgent colposcopy and biopsy
Colposcopy - colposcopy used to view cervix, acetic acid stain to show dysplastic areas, biopsy taken (punch biopsy or large loop excision of transformation zone)
If diagnosis confirmed, further investigations:
CT chest/abdomen/pelvis - metastases
+/- examination under anaesthesia with further biopsies
How should a woman with suspected cervical cancer be assessed?
History
Smear history
Risk factors - smoking, family history, immunocompromised
Previous colposcopy or cervical treatments
Examination
Abdominal examination including PR - masses, rectal bleeding, hydronephrosis
Bimanual examination - pelvic masses
Speculum examination - evidence of bleeding, discharge and ulceration (early cervical changes may not be visible)
How is dysplasia graded based on colposcopy appearance of the cervix? What is the prognosis of each grade?
Cervical intraepithelial neoplasia - grading system for level of dysplasia in cells of cervix (premalignant change)
CIN I - mild dysplasia, affects 1/3 thickness of the epithelial layer, likely to return to normal without treatment
CIN II - moderate dysplasia, affects 2/3 thickness of epithelial layer, likely to progress to cancer if untreated
CIN III - severe dysplasia, very likely to progress to cancer if untreated (cervical carcinoma in situ)
Describe the process and side effects of large loop excision of the transformation zone
Performed with local anaesthetic usually during colposcopy procedure
Uses loop of wire with diathermy to removal abnormal epithelial tissue on cervix
Side effects:
Bleeding
Abnormal discharge
Infection - avoid intercourse and tampon use to reduce risk
Preterm labour risk depending on depth of tissue removed from cervix
How is cervical intraepithelial neoplasia managed? What are the main risks of this?
Cone biopsy - sent to histology for analysis
Under GA
Pain
Bleeding
Infection
Scar formation - stenosis of cervix
Increased risk miscarriage and premature labour
How is cervical cancer staged?
FIGO staging:
Stage 0 - carcinoma in-situ
Stage 1 - confined to cervix
A - only identifiable under microscopy
B - gross lesions, clinically identifiable
Stage 2 - beyond cervix but not pelvic sidewall/involves upper 2/3 vagina
A - no parametrial involvement
B - obvious parametrial involvement
Stage 3 - extends to pelvic sidewall/involves lower 1/3 vaginal/hydronephrosis not explained by other cause
A - no extension to sidewall, lower 1/3 vagina only
B - extension to sidewall and/or hydronephrosis
Stage 4 -
A - spread to adjacent pelvic organs (bladder, rectum)
B - spread to distant organs
Describe the prognosis of cervical cancer
1 year 83%
5 years -
Overall 70%
Stage 1 - 95%
Stage 2 - 55%
Stage 3 - 38%
Stage 4 - 5%
10 years 63%
List options for management of cervical cancer by stage
MDT input for all
Options - surgery, radiotherapy, chemotherapy
Depends if fertility preservation is desired
Gold standard for stage 1b - 3 = chemoradiotherapy
Surgery:
Stage 1a - radical trachelectomy if fertility preservation is priority, laparoscopic hysterectomy with pelvic lymphadenectomy if not
Stage 1b/2a - radical (Wertheim’s) hysterectomy is curative
Stage 4a or recurrent disease - anterior/posterior/total pelvic extenteration
Describe the surgical options for management of cervical cancer
Early stage:
Trachelectomy - fertility preserving, removal or cervix and upper vagina
Radical hysterectomy - removal of uterus, vagina and parametrial tissues up to pelvic sidewall + lymphadenectomy
Late stage/recurrent disease:
Anterior/posterior/total pelvic extenteration - removal of all pelvic adnexae plus bladder (anterior), rectum (posterior) or both (total)
Describe palliative options for management of cervical cancer
Chemotherapy - cisplatin-based
Single dose radiotherapy for heavy bleeding
Bevacizumab - targets VEGF-A, used in metastatic/recurrent disease
May need nephrostomy/ureteric stents
Who receives the HPV vaccine? When? What strains does it protect against?
Offered to every 12-13 y/o (previously only girls)
Also available for MSM <45 at sexual health clinics
Now use 9-valent HPV vaccine - protects against:
6 and 11 - genital warts
16 and 18 - cervical cancer
and 31, 33, 45, 52, 58
Describe the current cervical screening programme in Scotland
Offered to those between 25-64, every 5 years
Cytological sample - tested for high risk HPV, if positive cells examined for dyskaryosis, if negative return to routine screening schedule
Results:
If high risk HPV but no dyskaryosis - repeat screening in 12 months to check HPV cleared
If high risk HPV and dyskaryosis - refer for colposcopy
Smear only done if normal cervical appearance - if not refer for colposcopy
List the possible results from cervical screening cytology
Inadequate
Normal
Borderline
Low-grade dyskaryosis
High-grade dyskaryosis - moderate
High-grade dyskaryosis - severe
Possible invasive squamous cell carcinoma
Possible glandular neoplasia (adenocarcinoma)
Can also identify infections e.g. BV, candidiasis, trichomoniasis
Acetinomyces-like organisms - often with IUS, do not require treatment unless symptomatic, if symptomatic may need to remove IUS
Describe the incidence of vulval cancers
Rare compared with other gynae cancers
Used to be only older women (80s - 90s), but HPV has increased prevalence in young women
What is the most common histological type of vulval cancer? List the other histological types of vulval cancer.
Most common is squamous cell carcinoma (90%)
Other types:
Malignant melanoma
Adenocarcinoma
BCC
Sarcoma
Metastatic
Describe the aetiology and risk factors associated with vulval cancers
HPV
Inflammation due to chronic skin conditions - lichen sclerosus, lichen planus
Advanced age (>75)
Immunosuppression
Describe the precancerous condition associated with vulval cancer
Vulval intraepithelial neoplasia
VIN 1 - not a precursor for 2/3, low grade squamous intraepithelial lesion, caused by low-risk HPV, usually resolve without treatment
VIN 2/3 - high grade squamous intraepithelial lesion, caused by ongoing infection with high-risk HPV, usually requires treatment, usually in 35-49 year olds, smokers, immunocompromised
Differentiated VIN - 50-60 years, not usually linked to HPV, found in lichen sclerosus, higher risk of malignant transformation, usually requires surgery
Describe the clinical presentation of VIN
Pruritus most common
Pain
Ulceration
Leukoplakia - thickened, white areas
Lump/wart
20% asymptomatic, often identified at cervical screening
Describe the malignant potential of VIN
9% malignant transformation if untreated
Differentiated and symptomatic have higher malignant potential
What are the management options for VIN?
Observation - watch and wait with close follow-up
Wide local excision
Laser ablation
Imiquimod cream
Describe the clinical features of vulval cancer
Lump
Ulceration
Bleeding
Pain
Itch
Lymphadenopathy in groin
Lower limb lymphoedema
Mostly occurs on labia majora (can also be clitoris, perineum)
How is suspected vulval cancer investigated?
Biopsy:
Incisional - preferred, original lesion used to plan treatment
Excisional
Under LA as outpatient
Local regional LN assessment - US, MRI, CT
Describe the staging of vulval cancer
FIGO
Stage I - confined to vulva
A <2cm
B >2cm
Stage II - involvement of lower 1/3 of vagina, urethra or anus
Stage III - extends to upper 2/3 of vagina or urethra or invasion to bladder or rectal mucosa or lymph nodes (non-ulcerated)
Stage IV - ulcerated LNs, disease fixed to pelvic bone or distant mets
Describe the prognosis of vulval cancer
5 year - 64%
10 year - 53%
Stage 1 - 80%
Stage 2 - 60%
Stage 3 - 40%
Stage 4 - 15%
List options for management of vulval cancer
Surgery is gold standard
Early stage
Wide local excision and groin lymphadenectomy (node surgery important for decreasing mortality)
Advanced stage
Radical vulvectomy with resection of bilateral inguinofemoral LNs
Post-op radiotherapy to pelvis and groin
List the types of surgeries used for vulval cancers
Wide local excision - small cancers
Partial radical vulvectomy - if unilateral or anterior/posterior only
Complete radical vulvectomy - if covering a large area
Lymphadenectomy
Often also require reconstructive surgery with flaps/grafts
List potential complications of groin lymphadenectomy
Wound dehiscence
Infection
Lymphocyst formation
Lymphoedema
Immobility
Prolonged hospitalisation
Define gravidity
Sum of all pregnancies regardless of outcome - includes live birth, pregnancies terminated at <6 months and those which did not result in live birth
Define parity
Number of births (including live and stillbirths) where pregnancies reached viable gestational age (24 + 0 in the UK)
Multiple pregnancy e.g. twins still counted as one
Calculate gravidity and parity for these scenarios:
- Patient is currently pregnant; had two previous deliveries
- Patient is not pregnant, had one previous delivery
- Patient is currently pregnant, had one previous delivery and one previous miscarriage
- Patient is not currently pregnant, had a live birth and a stillbirth
- Patient is not pregnant, had a twin pregnancy resulting in two live births
- G3 P2
- G1 P1
- G3 P1+1 (+1 refers to pregnancy not carried to 24+0)
- G2 P2
- G1 P1
List the main parts of a gynaecological history
Presenting complaint
History of presenting complaint - SOCRATES
Gynaecological symptoms - abdominal/pelvic pain, post-coital/inter-menstrual/post-menopausal bleeding, vaginal discharge, dyspareunia, vulval skin changes/itching, systemic symptoms (fatigue, fever, weight loss)
Menstrual history - frequency, duration, volume, date of LMP, dysmenorrhoea, age at menarche, menopause
Reproductive plans - are they considering having children in the future or currently trying to fall pregnant
Past medical history
Pregnancies - births/miscarriages/abortions/ectopics, means of delivery, age of child and birth weight, obstetric complications
Cervical smear - date of last smear, result
Surgical history
Previous gynaecological problems
Previous STIs
Drug history
Contraception
HRT
Other medications
Allergies
Family history
Breast/ovarian/endometrial cancer
Diabetes
Bleeding disorders
Social history
Occupation
Living situation
Smoking and alcohol
Systemic enquiry
Define LMP
Last menstrual period - date of first day of last menstrual period
Describe the main hormones of the hypothalamic-pituitary-ovarian axis involved in the menstrual cycle
Gonadotropin releasing hormone (GnRH) from the hypothalamus stimulates luteinising hormone (LH) and follicular stimulating hormone (FSH) release from the anterior pituitary
FSH - binds to granulosa cells to stimulate follicule growth, convert androgens from theca cells to oestrogens and stimulate inhibin secretion
LH - acts on theca cells to stimulate production and secretion of androgens
Controlled by feedback loops:
Moderate oestrogen levels exert negative feedback on HPG axis
High oestrogen levels (without progesterone) positively feedback on HPG axis
Oestrogen in the presence of progesterone exerts negative feedback on the HPG axis
Inhibin selectively inhibits FSH secretion from anterior pituitary
List the phases of ovarian activity during the menstrual cycle
Follicular phase - days 1-14
Ovulation - day 14
Luteal phase - days 14-28
Describe the hormonal changes which occur during the menstrual cycle and the effects they have on the ovaries
Follicular phase:
Follicles begin to mature independently of steroid or gonadotropin hormones
Due to low steroid and inhibin levels there is little negative feedback on HPG axis so increased FSH and LH levels, which stimulate follicle growth and oestrogen production
As oestrogen rises, negative feedback reduces FSH levels so all follicles except one regress
Follicular oestrogen becomes high enough to cause positive feedback to HPG axis, increases levels of GnRH and LH (FSH inhibited by inhibin)
Ovulation:
LH surge causes follicle rupture, oocyte migrates to fallopian tube for 24 hours viable for fertilisation
Follicle secretes oestrogen and progesterone, exerts negative feedback to HPG axis - pauses cycle for fertilisation
Luteal phase:
Corpus luteum formed, produces oestrogens, progesterone and inhibin to maintain conditions for fertilisation and implantation
In absence of fertilisation corpus luteum spontaneously regresses after 14 days, fall in hormones, HPG axis resets ready to begin cycle
If fertilisation occurs embryo produces HCG which maintains corpus luteum
Describe the hormonal changes which occur during the menstrual cycle and the effect they have on the endometrium
Proliferative phase (follicular phase):
Oestrogen causes thickening of endometrium, production of thin alkaline cervical mucus
Secretory phase (luteal phase):
Progesterone causes thickening of endometrium into glandular secretory tissue, thick acidic cervical mucus production (prevent polyspermy)
Menses:
Occurs in absence of fertilisation once corpus luteum breaks down, internal lining of uterus is shed due to lack of progesterone
Define menarche. What is the average age of menarche in the UK?
First menstrual period
Average age 12 Caucasian, 4-8 months later in Afro-Caribbean
Which placental abnormality is associated with IVF?
Placenta praevia
Define menopause. What is the average age of menopause in the UK? What is premature menopause?
Retrospective diagnosis - permanent end to menstruation, diagnosed after no periods for 12 months
Average age UK = 51, usually between 45-55
Premature menopause - <40
Define climacteric
Stage in life starting from decline in ovarian activity to end of ovarian function, including peri-menopause, menopause and post-menopause
Gradual loss of cyclical ovarian activity due to declining numbers of ovarian primordial follicles
What causes premature menopause?
Premature ovarian insufficiency - follicular dysfunction or early loss of eggs
90% idiopathic
Can also be due to:
Autoimmune disease e.g. T1DM, pernicious anaemia, Addison’s, Hashimoto’s
Genetic disorders e.g. Turner’s, Fragile X
Chemo/radiotherapy
Pelvic surgery - oophorectomy, hysterectomy without oophorectomy
Smoking
List the criteria for diagnosis of premature ovarian insufficiency
Amenorrhoea
Hypergonadotropism
Hypoestrogenism
Describe the changes in the HPO axis which lead to menopause
Reduction in circulating oestrogen due to reduced sensitivity of ovary to circulating FSH and LH - less follicles so less binding sites
Reduced oestrogen leads to more anovulatory cycles
Levels of FSH and LH increase during menopause as less negative feedback from oestrogen and less inhibin from follicles
In anovulatory cycles there is no corpus luteum to produce progesterone so endometrial lining not supported and frequently breaks down leading to breakthrough bleeding, as frequent as every two weeks
What risks are associated with early menopause?
Infertility
Osteoporosis
Ischaemic heart disease
Pelvic organ prolapse
Urinary incontinence
Higher endometrial cancer risk
How is menopause/perimenopause diagnosed?
If >45 can diagnose perimenopause based on typical vasomotor symptoms and menstrual history (irregular periods), menopause if not had period for 12 months
If <45 or >45 with atypical symptoms should measure FSH and consider genetic testing
What FSH level is diagnostic of menopause in <45s?
Consistently >30mIU/ML (not a one-off value) and no menstrual period for >12 months
List symptoms associated with the menopause
Irregular menstrual cycle
Vasomotor symptoms - hot flushes, night sweats, can be associated with sweating, palpitations, anxiety
Cognitive impairment and mood disorders - anxiety, mood swings, irritability, sleep disturbance, low mood, poor concentration and memory
Urogenital symptoms - vulvovaginal irritation, discomfort, burning, itching, dryness, dyspareunia, reduced libido, dysuria, urinary frequency/urgency, recurrent UTIs, prolapse
Joint and muscle pains
Headaches
Fatigue
Loss of bone density - increased risk fragility fractures
Ischaemic heart disease
Describe the hormonal changes which cause symptoms and clinical consequences of the menopause
Vasomotor changes - pulsatile LH influences central temperature control
Urogenital changes - lower circulating oestrogen causes atrophy of vagina, thinning of vaginal walls and dryness, atrophy of bladder and urethra causes urinary symptoms
Bone density - lower circulating oestrogen causes increased bone reabsorption by osteoclasts
Ischaemic heart disease - oestrogen reduces levels of LDL cholesterol and raises HDL cholesterol, less oestrogen causes reversal of this process
What are the indications for HRT?
Premature menopause even without symptoms
Reducing vasomotor symptoms
Improving symptoms such as low mood, decreased libido, poor sleep and joint pain
Reducing risk of osteoporosis in women under 60
Describe the different preparations of HRT available
Oestrogen:
Oral
Transdermal - patches or gels
Progesterone:
Cyclical or continuous
Oral
Transdermal - patches
IUS - Mirena coil
Combined -
Cyclical, continuous oestrogen with progesterone added at specific periods during cycle:
Oral
Patches
What are the risks associated with HRT? How can these risks be minimised?
Generally in under 60s, the benefits outweigh the risks - more significant in older women
Increased risk breast cancer, particularly with combined HRT (oestrogen-only has lower risk, risk increases with length of use and returns to normal once stopped for 5 years)
Increased risk endometrial cancer (oestrogen-only higher risk)
Increased risk VTE (2-3x background risk with oral HRT, no difference in risk with patches)
Increased risk stroke and CAD with long term use in older women (no risk with oestrogen-only HRT, risk only if >10 years post-menopausal)
Inconclusive evidence about risk of ovarian cancer, minimal increased risk if any
List side effects of HRT (not risks)
Oestrogenic:
Bloating
Breast tenderness
Nausea
Headaches
Leg cramps
Progestogenic:
Mood swings
Bloating
Fluid retention
Weight gain
Acne, greasy skin
List resources for information about HRT risks
British Menopause Society
Royal College of Obstetricians and Gynaecologists
Menopause matters website
List contraindications for HRT
Undiagnosed abnormal bleeding
Endometrial hyperplasia or cancer
Breast cancer
Uncontrolled hypertension
Venous thromboembolism
Liver disease
Active angina or myocardial infarction
Pregnancy
How should HRT formulation be chosen?
Step 1 - do they have local or systemic symptoms?
Local - topical e.g. oestrogen cream, pessary
Systemic - go to step 2
Step 2 - do they have a uterus?
No uterus - continuous oestrogen-only HRT
Uterus - add progesterone (combined HRT), go to step 3
Step 3 - have they had a period in the past 12 months?
Perimenopausal - cyclical combined HRT
Postmenopausal - continuous combined HRT
Why is it important to give combined HRT to women with a uterus?
Addition of progesterone greatly decreases the incidence of endometrial hyperplasia and endometrial cancer
Describe fertility and contraceptives in peri/postmenopausal women
HRT is not contraception
Recommended to use effective contraception until:
12 months after the last period in women > 50 years
24 months after the last period in women < 50 years
Examples of contraceptive options:
Mirena Coil
Progesterone only pill in addition to HRT
Good contraceptive options:
Barrier methods
Mirena or copper coil
Progesterone-only pill
Progesterone implant
Progesterone depot injection (<45)
Sterilisation
List non-hormonal options for management of vasomotor symptoms in menopause and describe the evidence for their efficacy
Prescribed - good evidence for efficacy:
Clonidine
SSRI/SNRI - paroxetine, venlafaxine, fluoxetine
Gabapentin
Non-prescribed:
Black cohosh - Small RCTs show reduction in mild-moderate hot flushes
Vitamin E - no benefit
Evening primrose oil - no benefit
Phytoestrogens - may reduce severity
CBT - improved vasomotor symptoms and mood
Alternative:
Acupuncture
Lifestyle - avoid triggers, light clothing etc.
Stellate ganglion blockade - potentially efficacious
Describe the mechanism of action of clonidine in reducing vasomotor symptoms of the menopause
Alpha-2 adrenergic receptor and imidazoline receptor agonist
Lowers BP, reduces heart rate
List common side effects of clonidine
Dry mouth
Headaches
Dizziness
Fatigue
Sudden withdrawal - rapid increase in BP, agitation
List potential adverse effects of alternative remedies used to manage vasomotor symptoms of menopause
Black cohosh - liver damage
Dong quai - bleeding disorders
Red clover - oestrogenic effects, concerning in oestrogen sensitive cancers
Evening primrose oil - significant drug interactions, linked with clotting disorders and seizures
List non-hormonal therapies used for urogenital symptoms of the menopause
Vaginal moisturisers/lubricants
Urinary incontinence - weight reduction, supervised pelvic floor training, bladder training, antimuscarinics
List non-hormonal therapies used for management of osteoporosis of the menopause
Calculate FRAX to determine if high, medium or low-risk
Lifestyle - smoking cessation, exercise
Calcium and Vitamin D supplementation
Bisphosphonates
Define heavy menstrual bleeding
Technically >80ml blood loss during menstruation - not measured in practice
Self-reported excessive menstrual loss which interferes with quality of life
Also defined as - need to change menstrual products every 1-2 hours, passage of clots greater than 2.54cm
List causes of heavy menstrual bleeding
PALM-COPEEIN
PALM - structural causes
Polyp
Adenomyosis
Leiomyoma (fibroid)
Malignancy and hyperplasia
COPEEIN - non-structural causes
Coagulopathy - anticoagulants, Von Willebrand
Ovulatory dysfunction
Pelvic inflammatory disease
Endometrial - endometriosis, endometrial cancer, endometrial hyperplasia
Endocrine - PCOS, diabetes, hypothyroidism
Iatrogenic - copper coil
Not yet classified
Describe the clinical assessment of a patient with heavy menstrual bleeding
History:
Nature of bleeding and impact on QOL
Symptoms of anaemia
Age at menarche
Cycle length, days menstruating, variation
Intermenstrual and post-coital bleeding
Contraceptive history
Sexual history
Possibility of pregnancy
Plans for future pregnancies
Cervical screening history
Migraines with or without aura
PMH, DH, SH, FH
Examination:
Abdominal palpation - palpable uterus or pelvic mass
Speculum - cervical excitation, inflamed cervix, cervical polyp/tumour, vaginal tumour
Bimanual examination - smooth or irregular uterus (fibroids), bulky uterus (adenomyosis)
Investigations:
Bloods - FBC, TFTs, hormone testing if clinically suspicious (e.g. of PCOS)
Coagulation screening, test for VWD if suspicious of clotting disorder
Biopsy - endometrial cancer
US - structural abnormalities
Cervical smear - no need if up to date
High vaginal and endocervical swabs - infection
What are the options for management of heavy menstrual bleeding?
If does not want contraception:
Treatment during menstruation for symptomatic relief - tranexamic acid (no associated pain), mefenamic acid (associated pain)
If contraception is wanted/acceptable:
Levonorgestral-releasing IUS (Mirena coil) - first-line
Combined oral contraceptive pill
Cyclical oral progestogens e.g. norethisterone (does not work as contraceptive)
Progesterone-only contraception - pill, depot, implant
If medical management failed:
Endometrial ablation
Hysterectomy - partial or total
Describe the mechanism of action of non-hormonal pharmacological management options for heavy menstrual bleeding
Tranexamic acid - antifibrinolytic, inhibits plasminogen activator reducing fibrinolytic activity in endometrium
Mefenamic acid - NSAID, prostaglandin synthase inhibitors, reduces pain, and bleeding
Describe the mechanism of action of hormonal management options for heavy menstrual bleeding
Pseudo-pregnancy - endometrial decidualization and necrosis:
Mirena coil
COCP
Progestogens
Pseudomenopause:
GnRH analogues - suppress FSH and LH, can be used short-term, improve Hb, shrink fibroids
Progesterone receptor modulators:
Esmya - ullipristal acetate
Act directly on endometrium, induce amenorrhoea, shrink fibroids
Describe the surgical options for management of heavy menstrual bleeding
Endometrial ablation:
Local or general anaesthetic
Ablation of endometrium to myometrium
For those who do not wish to conceive - will need to continue using contraception after
Hysterectomy:
Only definitive treatment - guaranteed amenorrhoea
Abdominal or laparoscopic
Associated morbidity and mortality
Partial - uterus removed only (not cervix)
Total - cervix and uterus removed
Total with bilateral salpingo-oophorectomy only if ovaries are abnormal
Define primary amenorrhoea
Failure to menstruate by 13 with no evidence of pubertal development
Failure to menstruate by 15 with signs of puberty e.g. breast bud development
Define secondary amenorrhoea
Cessation of periods for >6 months after menarche (after excluding pregnancy)
Or >12 months if previous oligomenorrhoea
Define oligomenorrhoea
Cycle persistently longer than 35 days, menses less frequently than every 35 days
(less than 9 periods per year)
List the most common causes of primary amenorrhoea
Physiological delay
Weight loss/dieting/heavy exercise
PCOS
Imperforate hymen
List causes of primary amenorrhoea
Normal secondary sexual characteristics:
Physiological - constitutional delay, pregnancy
Genito-urinary malformations - imperforate hymen, transverse septum, absent vagina or uterus
Endocrine disorder - hypothyroidism, hyperthyroidism, hyperprolactinaemia, Cushing’s syndrome, PCOS
Androgen insensitivity syndrome
No secondary sexual characteristics:
Primary ovarian insufficiency - genetic (Turner’s, gonadal agenesis), chemo/radiotherapy, autoimmune disease
Hypothalamic dysfunction - excessive exercise/weight loss, chronic systemic illness, hypothalamic or pituitary tumours, cranial irradiation, infection or head injury, Kallman’s syndrome, empty sella symdrome, Laurence-Moon-Biedl syndrome, Prader-Willi syndrome
Causes of ambiguous genitalia - 5-alpha reductase deficiency, androgen-secreting tumour, congenital adrenal hyperplasia
Define hypogonadotropic hypogonadism and list examples
Deficiency of LH/FSH leading to deficiency of sex hormones (oestrogen)
Hypopituitarism
Radiation/surgical damage to hypothalamus or pituitary
Chronic conditions
Excessive exercise or dieting
Kallman’s syndrome - reduced/absent sense of smell
Define hypergonadotropic hypogonadism and list examples
Gonads fail to respond to stimulation from LH/FSH, so increased amounts of FSH/LH produced (lack of negative feedback)
Damage to ovaries
Congenital absence of ovaries
Turner’s syndrome
Describe causes of amenorrhoea in terms of the HPO axis
Hypothalamic causes:
Functional disorders - exercise, eating disorders
Severe chronic conditions
Kallman syndrome - failure of migration of GnRH cells
Pituitary causes:
Prolactinomas or other pituitary tumours e.g. acromegaly, Cushing’s syndrome
Sheehan’s syndrome
Destruction of pituitary - radiation, surgery, autoimmune disease
Post-contraception amenorrhoea - Depo-Provera highest risk
Ovarian causes:
PCOS
Turner’s
Premature ovarian failure
Adrenal causes:
Congenital adrenal hyperplasia
Genital tract abnormalities:
Ashermann’s syndrome - instrumentation of uterus damages basal layer of endometrium, causes intrauterine adhesions which fail to respond to oestrogen
Imperforate hymen, transverse vaginal septum
Mayer-Rokitansky-Kuster-Hauser syndrome - agenesis of Mullerian duct system, congenital absence of uterus and upper 2/3 of vagina
How are secondary sexual characteristics in females assessed?
Tanner staging
List causes of secondary amenorrhoea
Physiological:
Pregnancy
Lactation
Menopause
Premature ovarian insufficiency
Chemotherapy
Radiotherapy
Autoimmune disease
Hypothalamic causes:
Hypothalamic dysfunction due to stress, excessive exercise, and/or weight loss
Chronic systemic illness
Cranial irradiation, infection or head injury
Pituitary causes:
Prolactinoma, other hormone-secreting tumours
Head injury, cranial irradiation
Hypopituitarism
Sheehan’s syndrome
Sarcoidosis
TB
Uterine causes:
Cervical stenosis
Asherman’s syndrome
Thyroid disease
Iatrogenic:
Contraceptive
Drugs e.g. antipsychotics (hyperprolactinaemia), illicit drug use
Surgery - hysterectomy, endometrial ablation, ovarian surgery
With androgen excess:
PCOS
Cushing’s
Late-onset congenital adrenal hyperplasia
Androgen-secreting tumours of the ovary or adrenal gland
Describe the diagnostic criteria for PCOS
Rotterdam criteria - 2/3 of:
Oligo- and/or anovulation
Clinical and/or biochemical signs of hyperandrogenism
Polycystic ovaries on imaging (>12 developing follicles in one ovary), or ovarian volume >10
List features of hyperandrogenism in PCOS
Clinical:
Hirustism
Acne
Male pattern hair-loss
Biochemical:
Raised testosterone
Low SHBG
Raised LH
Normal FSH
Low progesterone
May have mildly elevated prolactin
List the clinical features and complications of PCOS
Oligomenorrhoea or amenorrhoea
Infertility
Hirsutism
Obesity
Chronic pelvic pain
Depression
Acne
Acanthosis nigricans - insulin resistance
Male pattern hair-loss
Obesity
Hypertension
Insulin resistance and diabetes
Hypercholesterolaemia
Endometrial hyperplasia and cancer
Obstructive sleep apnoea
Sexual problems
How is PCOS managed?
Reduce risk of cardiovascular disease and diabetes: lifestyle (weight loss, exercise, smoking cessation), antihypertensives and statins where indicated
Reduce risk of endometrial cancer - Mirena coil (continuous protection), inducing withdrawal bleed at least 3-4 monthly with cyclical progestogens or COCP
Manage infertility - weight loss, clomifene, metformin, letrozole, laparoscopic ovarian drilling, IVF
Manage hirsutism - weight loss, COCP, topical eflornithine, other options e.g. electrolysis, laser hair removal, spironolactone, finasteride, flutamide, cyproterone acetate
Manage acne - COCP, topical retinoid, topical antibiotics, topical azelaic acid, oral tetracycline antibiotics
COCP used for hirsutism/acne = cyprindiol, anti-androgenic but increased risk VTE
Define primary and secondary dysmenorrhoea
Dysmenorrhoea = painful cramping, usually in the lower abdomen often radiating to legs and back, occurs shortly before and/or during menstruation
Can be accompanied by GI symptoms and malaise
Primary = idiopathic, no identifiable underlying pelvic pathology
Secondary = caused by underlying pelvic pathology
Describe the features of primary vs secondary dysmenorrhoea
Primary:
Usually young females, 6-12 months after menarche once cycles are regular
Pain most severe on day of or prior to start of menstruation
Secondary:
Usually starts many years after menarche after long period of painless periods
List common causes of secondary dysmenorrhoea
Endometriosis/adenomyosis
Fibroids
PID
Ovarian cancer
Cervical cancer
IUD insertion
How should a woman presenting with dysmenorrhoea be assessed?
Need to consider and rule out causes of secondary before diagnosing primary - diagnosis of exclusion
Examination -
Abdominal - masses
Pelvic (not appropriate in adolescents who are not sexually active) - speculum, bimanual, swabs
Investigations - may not be needed if no features of secondary
US - fibroids, adnexal pathology, endometriosis, IUS
High vaginal and endocervical swabs
Pregnancy test
How is primary dysmenorrhoea managed?
Reassurance
Smoking cessation
Pharmacological:
Analgesia (first-line) - NSAIDs (ibuprofen, naproxen, mefenamic acid), inhibit prostaglandins
Paracetamol
3-6 month trial of hormonal contraception (second-line) - monophasic COCP, IUS (Mirena), depo-Provera
Non-pharmacological:
Local application of heat
TENS
Define intermenstrual bleeding
Bleeding between periods
Define post-coital bleeding
Bleeding after intercourse
List causes of inter-menstrual bleeding, post-coital bleeding and post-menopausal bleeding in terms of anatomical site
Uterine:
Polyp
Cancer
IUS
Fibroids
Infection
Pregnancy
Cervix:
Cancer
Ectropion
Infection
Cervical erosion
Vagina:
Atrophic vaginitis
Cancer
Trauma
Vulval:
Cancer
Describe the assessment of inter-menstrual bleeding and post-coital bleeding
Cervical smear history - do not take if not due
Speculum and bimanual examination - urgent colposcopy referral if suspicious of cancer
STI screen and treat +/- GUM referral if appropriate
Urine pregnancy test
Which patients should be urgently/routinely referred for inter-menstrual/post-coital bleeding?
Urgent:
>35 with persistent (>4 weeks) post-coital or inter-menstrual bleeding
Routine:
<35 with post-coital or inter-menstrual bleeding for >12 weeks
Single heavy episode of post-coital or inter-menstrual bleeding at any age
Reassurance:
<35 with normal findings and results
Define chronic pelvic pain
Intermittent or chronic pain in the lower abdomen or pelvis for >6 months, not occurring exclusively with menstruation or intercourse and not associated with pregnancy
List causes of pelvic pain in terms of anatomical location
Vulva:
Bartholin abscess
Lichen sclerosus
Herpes
Cancer
Vulvodynia
Uterus:
Fibroids - degeneration or torsion causes acute pain
Endometriosis
Adenomyosis
Cancer
Fallopian tubes:
Pelvic inflammatory disease
Hydrosalpinx
Ovaries:
Ovarian cysts - torsion, haemorrhage, rupture (acute)
Cancer
GI system:
IBS
Urinary system:
Interstitial cystitis
MSK pain
General:
Adhesions
Pelvic organ prolapse
Nerve entrapment e.g. post C-section
Psychological and social issues
Chronic pelvic pain syndrome
List ovarian cyst accidents and describe their presentation
Rupture - sudden onset pelvic pain, can have acute peritonism, shock or be asymptomatic
Haemorrhage - sudden onset pelvic pain, pelvic mass, bloating, vaginal spotting/bleeding, may be asymptomatic
Torsion - common gynaecological emergency, usually sudden onset severe unilateral pelvic pain which gets progressively worse, associated with nausea and vomiting, or can be mild or intermittent pain. Localised tenderness, may have palpable mass.
Describe the investigation of pelvic pain where an ovarian cyst event is suspected
Pregnancy test
MSU - rule out UTI
Vaginal/cervical swabs - ?PID
FBC + CRP
CA125
Transvaginal US - ‘whirlpool sign’, free fluid in pelvic and oedema of ovary seen in torsion
Definitive diagnosis - laparoscopic surgery
How are ovarian cysts managed?
Depends on type of cyst
If ovarian cancer suspected - two-week wait to gynaecological oncology specialist
Dermoid cysts - ?surgery
Simple ovarian cysts
Pre-menopausal - <5cm will likely resolve on their own, do not need management or follow-up scan, 5cm-7cm require routine referral to gynaecology and yearly US monitoring, >7cm consider MRI or surgical evaluation
Post-menopausal - measure CA125, if raised two-week wait referral, if normal and <5cm may be monitored with US 4-6 monthly
Persistent/enlarging cysts - surgical intervention, usually laparoscopic, ovarian cystectomy +/- oophorectomy
Define pelvic inflammatory disease
Ascending infection of the upper genital tract, spreads from endocervix to cause one or more of:
Endometritis - endometrium
Salpingitis - fallopian tubes
Parametritis - parametrium (connective tissue around uterus)
Oophoritis - ovaries
Tubo-ovarian abscess - adnexa
Pelvic peritonitis - peritoneal membrane
What are the most common causes of pelvic inflammatory disease?
STIs:
Chlamydia trachomatis
Neisseria gonorrhoea
Mycoplasma genitalium
Other:
Gardnerella vaginalis
Haemophilus influenzae
E. Coli
Streptococcus agalactiae
Can commonly be pathogen-negative
List complications of pelvic inflammatory disease
Ectopic pregnancy
Infertility
Tubo-ovarian abscess
Chronic pelvic pain
Fitz-Hugh-Curtis syndrome - RUQ pain, peri-hepatitis, especially associated with chlamydia
Describe the presentation of pelvic inflammatory disease
Can be asymptomatic
Lower abdominal/pelvic pain
Deep dyspareunia
Menstrual abnormalities e.g. menorrhagia, dysmenorrhoea, intermenstrual bleeding
Post-coital bleeding
Dysuria
Abnormal vaginal discharge - purulent, malodorous
If advanced - severe lower abdominal pain, fever, nausea and vomiting
On examination
Tenderness of uterus/adnexae or cervical excitation
Palpable mass in lower abdomen
Abnormal vaginal discharge
How should suspected pelvic inflammatory disease be investigated?
NAAT swab for gonorrhoea, chlamydia, mycoplasma genitalium
HIV test
Syphilis test
High vaginal swab for bacterial vaginosis, candidiasis and trichomoniasis
Microscopy of vaginal/endocervical swabs - pus cells, absence is useful for excluding PID but presence is not specific for PID diagnosis
Pregnancy test - exclude ectopic pregnancy
ESR/CRP
MSU - exclude UTI
Transvaginal US if tubo-ovarian abscess is suspected
Laparoscopy if diagnosis uncertain or no improvement after initial management
How is PID managed?
Antibiotics - 14-day course, broad spectrum with good anaerobic coverage
Start immediately, before swab results are available
Options for Abx:
Doxycycline + ceftrixone + metronidazole
Ofloxacin + metronidazole
Analgesics e.g. paracetamol
Avoid sexual intercourse until Abx course complete and partner(s) are treated
Referral to GUM - contact tracing, test all sexual partners from previous 6 months
More severe - admission for IV antibiotics
Pregnant (including ectopic), signs of sepsis/pelvic peritonitis, unresponsive to oral Abx
Define endometriosis
Chronic condition with growth of ectopic endometrium-like tissue outside the uterus
Describe the aetiology of endometriosis
Several theories:
Retrograde menstruation - endometrial cells flow from uterine cavity through fallopian tubes and out into pelvic cavity where they implant on tissues and seed and grow
Lymphatic or circulatory dissemination - endometriotic tissue travels through lymphatic system or in bloodstream to ectopic sites
Genetic predisposition - well documented, no specific genes identified
Metaplasia - cells in pelvis and abdominal area change into endometrial-type cells of the germinal epithelium
Embryonic cells - embryonic cells remain outside uterus during development and later develop into ectopic endometrial tissue
Environmental factors
Immune dysfunction - those with endometriosis seem to have reduced immunity to other conditions, unknown if this is a contributor or consequence
List sites for endometriosis to develop
Pelvic most common:
Ovaries
Pouch of Douglas
Uterosacral ligaments
Pelvic peritoneum
Rectum
Sigmoid colon
Bladder
Distal ureter
Extra-pelvic sites rarer:
Bowel
Diaphragm
Umbilicus
Pleural cavity
Describe the clinical presentation of endometriosis
Can be asymptomatic
Cyclical pelvic pain - occurs during menstruation
May be constant pain if adhesions have formed
Dysmenorrhoea
Dyspareunia
Dysuria
Dyschezia (painful defecating)
Subfertility
Urinary symptoms
Bowel symptoms
Examination:
Fixed, retroverted uterus
Uterosacral ligament nodules
Endometrial tissue visible in vagina
General tenderness
Describe the assessment and investigations of women with suspected endometriosis
Examination - abdominal and pelvic examination (speculum and bimanual)
Gold standard for diagnosis = laparoscopy
Typical findings - chocolate cysts, adhesions, peritoneal deposits, powder burn lesions
Biopsy of lesions
Can also be used as treatment - remove endometriomas, divide adhesions
Pelvic US should be done before surgery - determine severity of endometriosis
List potential complications of endometriosis
Endometriomas - rupture, torsion
Fertility problems - mechanism not clear
Adhesion formation - chronic pelvic pain
Bowel obstruction
Chronic pain without visible disease
Reduced quality of life
?Link between endometriosis and ovarian cancer - evidence not clear
List management options for endometriosis
Initial management:
Analgesia as required for pain - NSAIDs and paracetamol first line (follow analgesic ladder)
Hormonal management:
COCP
Progesterone only pill
Depo-provera
Nexplanon implant
Mirena coil
GnRH agonists (induce menopause-like state)
Surgical management:
Laparoscopic surgery to excise or ablate endometrial tissue + adhesiolysis (relapses likely, may need repeated surgery)
Hysterectomy + bilateral salpingo-oophorectomy
Define adenomyosis
Endometrial tissue inside the myometrium
How is the position of the fetal head determined in labour? What is the normal orientation of the head during labour?
Orientate using position of fontanelles - posterior fontanelle is triangle shaped, anterior is diamond shaped
Begins in right or left occipitotransverse at pelvic brim
When head reaches pelvic floor, rotates to occipitoanterior
Shoulders deliver in AP diameter, head follows in external rotation (restitution)
Describe the mechanism of action, side effects and contraindications of uterotonic drugs
Describe the inheritance of rhesus status
D antigen gene (positive) is dominant, d (lacking D antigen so negative) is recessive
If mother is negative (homozygous) and father is positive (heterozgous) child has 50% chance of being positive, if father is positive (homozygous) child has 100% chance of being positive
List pharmacological anti-hypertensive agents used in pregnancy, describe their mechanism of action and common side effects
