Revise Notes Obg Flashcards
Amenorrhoea
Background
Amenorrhoea is the absence of menstruation. It is classified into primary & secondary:
Primary amenorrhoea - the failure to commence menstruation by the age of expected menarche
Usually 15 yrs if otherwise normal sexual development or..
13 years if no secondary sexual characteristics
Secondary amenorrhoea - the cessation of menstruation in a women with previous menses for 3 months (or 6 months if Hx oligomenorrhoea)
Causes of Amenorrhoea
Primary amenorrhoea
If normal secondary sexual characteristics, amenorrhoea can be caused by:
❤️Constitutional delay - usually a family history
Endocrine - Thyroid dysfunction, hyperprolactinaemia, Cushing’s
❤️Androgen insensitivity syndrome
If the patient has no secondary sexual characteristics (e.g. breast development), amenorrhoea can reflect:
❤️Primary ovarian insufficiency - commonly Turner’s syndrome (46XO)
Suggested by short stature, shield chest, wide carrying angle, scoliosis, web neck
❤️Hypothalamic dysfunction - e.g. stress/ excess weight loss/exercise (e.g. in endurance athletes/eating disorders)
Secondary amenorrhea
Secondary amenorrhoea
If there is hyperandrogenism (e.g. hirsutism/acne), causes include:
❤️PCOS
❤️Cushing’s syndrome
If there is no evidence of hyperandrogenism:
❤️Physiological - pregnancy/lactation, menopause
❤️Premature ovarian insufficiency
FSH > 20 in a F < 40 yrs is suggestive of ovarian failure
❤️Hypothalamic dysfunction as above
❤️Pituitary causes - Prolactinoma
❤️Thyroid dysfunction
Investigating Amenorrhoea
Assessment of Primary Amenorrhoea
Referral to a specialist is recommended. Investigations may include:
❤️Pelvis US - to r/o absent uterus / abnormal development of genital organs
❤️Serum prolactin - if > 1000 invx for prolactinoma
❤️TFTs
❤️FSH and LH - if elevated, can suggest primary ovarian failure - Turner’s syndrome
❤️Total testosterone - if evidence of hyperandrogenism (acne, hirsutism etc.)
—If elevated can suggest androgen insensitivity syndrome
—If moderately increased, can support a diagnosis of PCOS
Assessment of Secondary Amenorrhoea
Investigations may include
❤️FSH/LH
—-Elevated FSH/LH are suggestive of premature ovarian insufficiency in women < 40 yrs
—-If FSH is normal, and LH is moderately increased - can suggest PCOS
—-If FHS/LH are low/normal - can suggest a hypothalamic cause (e.g. weight loss)
❤️Prolactin levels
❤️TFTs
❤️Testosterone
❤️US - to investigate for polycystic ovaries (12 or more follicles / volume > 10cm3)
Turner Syndrome
Pathophysiology
Genetics 45 X,O
1/2500 females
Clinical features
Short stature – growth rate falters after 3-5yrs (skeletal dysplasia)
Broad ‘webbed’ neck;
Wide carrying angle at elbows (cubitus valgus)
Shield chest with widely-spaced hypoplastic nipples
Primary amenorrhoea
Hypothyroidism - approximately 1/3rd of patients develop Hashimoto’s thyroiditis
Associated abnormalities
CHD – coarctation of the aorta ; VSD
Renal – horseshoe kidney / unilateral agenesis
Hypoplastic ‘streak’ ovaries – primary amenorrhoea and infertility
Diagnosis & Management
Diagnosis: Karyotyping
Management
S/C HGH +/- anabolic steroids
Oral oestrogen – induce puberty
Polycystic Ovarian Syndrome [PCOS]
A very common disorder affecting an estimated 5-15% of the population.
Pathology: Multifactorial, involving insulin resistance, hyperinsulinemia and hormonal imbalance (elevated LH & androgens)
Clinical features
Oligo/amenorrhoea
Impaired fertility - so often present with difficulty conceiving
Evidence of hyperandrogenism - hirsutism, acne
Evidence of insulin resistance:
Acanthosis nigricans
Obesity
Investigations
Bloods:
Increased LH:FSH ratio
Moderately elevated testosterone levels
Sex hormone binding globulin levels are low
Pelvis USS - ovarian cysts
Diagnosis
The Rotterdam criteria - a diagnosis of PCOS can be made if 2/3 criteria are present:
Olgio/amenorrhoea
Hyperandrogenism - acne, hirsutism, biochemical evidence
Cysts - 12 or more follicles in at least one ovary OR > 10cm3 total ovarian volume
Management
Hirsutism + acne
1st line - COCP
Infertility
Weight loss
Clomifene - most effective measure, can be complicated by multiple pregnancies
Metformin
The Menstrual Cycle (Follicular vs Luteal)
The menstrual cycle can be divided into 4 core phases. The duration of each phase varies between individuals
Phase 1: Menstruation
Menstruation occurs between DAY 1- 4
Phase 2: The Proliferative (Follicular) Phase – DAY 5-13
Ovarian changes
During the proliferative phase, the ovarian follicles develop.
One follicle becomes the ‘dominant’ follicle.
Endometrial changes
The endometrial tissue proliferates
Hormonal changes
Follicle stimulating hormone (FSH) increases – this stimulates follicle development
The developing follicles secrete increasing amounts of oestradiol
When the dominant follicle has matured, there is a significant increase in OESTRADIOL which TRIGGERS AN ACUTE INCREASE IN LUTEINIZING HORMONE (LH).
The acute rise in LH TRIGGERS OVULATION (LH surge)
Cervical mucus:
Initially thick, but prior to ovulation becomes clear, thin and ‘stretchy’
Basal body temperatures decreases just before ovulation occurs.
The Menstrual Cycle (Follicular vs Luteal)
The menstrual cycle can be divided into 4 core phases. The duration of each phase varies between individuals
Phase 3: Ovulation – DAY 14
Phase 4: The Secretory (luteal) Phase – Day 15-28
Ovarian changes:
An ovarian follicle forms into the CORPUS LUTEUM after the release of the oocyte during ovulation
The corpus luteum SECRETES PROGESTERONE
Endometrial changes
Progesterone stimulates changes to the endometrium to form a ‘secretory’ lining.
Hormonal changes:
If fertilisation does NOT occur, the corpus luteum degenerates, resulting in a FALL IN PROGESTERONE (as well as an increase in oestradiol) – this leads to menstruation
Uterine prolapse mng
Management
❤️Pelvic Floor Muscle Training
💕Kegel Exercises: Pelvic floor exercises to strengthen the levator ani and associated muscles.
💕Physiotherapy: Pelvic floor rehabilitation guided by a specialist physiotherapist.
❤️Pessary Device
💕Ring Pessary: A non-surgical device inserted into the vagina to provide structural support to the prolapsed uterus.
❤️Surgical Management
💕Colporrhaphy: Vaginal wall repair to reinforce the vaginal fascia and improve support.
💕Uterine suspension procedures: Sacrospinous fixation, uterosacral ligament suspension, or sacrohysteropexy using native tissue or synthetic mesh.
💕Hysterectomy: Vaginal or abdominal removal of the uterus, often combined with pelvic floor repair procedures.
Uterine Prolapse
Descent of the pelvic organs into the vagina as a result of weakness of the muscles of the pelvic floor and supporting ligaments
❤️Pathophysiology
Pelvic organ prolapse (POP) occurs when the pelvic floor muscles, ligaments, and connective tissue lose their integrity.
❤️Contributing factors include
vaginal deliveries,
ageing (post-menopausal) and
chronic intra-abdominal pressure (obesity, chronic cough, or heavy lifting).
Clinical Features
❤️A chronic dragging sensation or pelvic heaviness.
Patients often report a sensation of a vaginal mass or “something coming down,” which may be visible on physical examination.
❤️Urinary Symptoms - stress incontinence, urgency, frequency, and incomplete voiding due to bladder outlet obstruction.
❤️Bowel Symptoms - Constipation, straining, incomplete evacuation.
❤️Sexual Dysfunction - dyspareunia, reduced sexual sensation, and difficulty with coitus
Antenatal Care
Gestational Diabetes
The second most common complication of pregnancy (after hypertension), affecting approximately 1 in 40 pregnancies.
Risk factors
💕Ethnicity (Asian, African-Carribean)
💕Obesity - BMI > 30
💕Previous macrosomia (newborn >4.5kg)
💕Previous gestational diabetes
💕1st relative with diabetes
Investigations
💕Screening
💕Patients without risk factors should be screened with the Oral Glucose Tolerance Test (OGTT)
at 24-28 weeks
💕Patients who have any of the above risk
factors should be screened for GDM with an OGTT at booking AND at 24-28 weeks.
💕Diagnosis
Fasting BM > 5.6
OGTT > 7.8
Tip: GDM - 5, 6, 7, 8
BM targets for GDM/DM during pregnancy
Fasting target - 5.3
1 hour post-meal target 7.8
2 hour post-meal target 6.4
Gestational Diabetes
The second most common complication of pregnancy (after hypertension), affecting approximately 1 in 40 pregnancies.
Mng
Management
Management if fasting BM < 7
❤️If fasting BM is < 7 - trial diet and exercise for 2 weeks
💕If BM is still too high (see targets below), add metformin
💕If BM remains too high despite metformin, treat with insulin, metformin and diet/exercise
❤️Management if fasting BM > 7 (or FBM 6.1-6.9 and complicated pregnancy (macrosomia, hydramnios etc.))
Commence insulin as first step
❤️Management of Pre-existing diabetes in pregnancy
💕Diabetic control:
All oral hypoglycaemics should be stopped
Continue metformin
Start insulin
Additional measures
💕Prescribe high dose folic acid 5mg OD until 12 weeks (high risk of neural tube defects)
💕Aspirin 75mg OD from 12 weeks (high risk of pre-eclampsia)
💕Detailed anomaly scan at 20 weeks + 4 chamber echo.
Antenatal Care
Imaging
Dating scan - Ultrasound at 11-14 weeks
Fetal anomaly scan - 18-21 weeks
Combined test
💕10-13 weeks - nuchal lucency and blood tests for PAPP &
b-hcg levels - the value of these 3 markers gives the
💕estimated risk of Down syndrome (trisomy 21), Edwards Syndrome (trisomy 18), Patau syndrome (trisomy 13)
Further investigations
If combined test result is > 1:150 risk = ‘higher chance’ - offer women the following:
Further investigations
❤️If combined test result is > 1:150 risk = ‘higher chance’ - offer women the following:
❤️Non-invasive prenatal testing (blood test)
Measures DNA released from placenta into maternal bloodstream. Quantifies DNA from chromosome 21, 18, 13
Results: Low chance or High chance - then offer diagnostic testing
❤️Chorionic villus sampling at < 13 weeks
❤️Amniocentesis at > 15 weeks
The additional risk of misscarriage following CVS or amniocentesis is likely to be < 0.5%
Booking and 28 week appointment
❤️Booking appointment
💕Screen for GDM if RFs (as above)
Screen for pre-eclampsia (if high risk - aspirin from 12 weeks)
💕Check blood pressure and urine dip (for proteinuria)
Recheck at each appointment thereafter
💕Check FBC, blood group and Rh status
❤️28 week appointment
💕Offer anti-D prophylaxis to rhesus-negative women
💕Repeat at 31-34 weeks if following 2 dose regimen
Supplements
Supplements
💕Folic acid - to reduce risk of neural tube defects - take for at least first 12 weeks of pregnancy
💕Most women should take 400 micrograms OD
💕For women at high risk of NTDs (previous child with NTD,
AEDs, diabetes,
coeliac,
sickle/thalassaemia,
BMI > 30) -
take 5 milligrams per day
💕Advise all women to take 10mcg Vit D OD throughout pregnancy
💕Avoid vitamin A supplementation - birth defects
Secondary amenorrhea
Secondary amenorrhoea
If there is hyperandrogenism (e.g. hirsutism/acne), causes include:
❤️PCOS
❤️Cushing’s syndrome
If there is no evidence of hyperandrogenism:
❤️Physiological - pregnancy/lactation, menopause
❤️Premature ovarian insufficiency
FSH > 20 in a F < 40 yrs is suggestive of ovarian failure
❤️Hypothalamic dysfunction as above
❤️Pituitary causes - Prolactinoma
❤️Thyroid dysfunction
Screening test
UK National Cancer Screening Programmes
Key learning
UK National Cancer Screening Programmes:
💕Cervical Cancer:
Women aged 24.5-64.
Ages 25-49: Every 3 years; Ages 50-64: Every 5 years.
Screening via cervical smear and HPV test.
Abnormal results lead to cytology, colposcopy, and treatment or rescreening.
💕Breast Cancer:
Women aged 47-73, every 3 years.
Mammography for most, MRI for high-risk young women.
Triple assessment for abnormal results. DCIS treated as cancer.
💕Bowel Cancer:
Ages 60-74, every 2 years.
Faecal occult blood test (FOBT); abnormal results lead to colonoscopy.
💕Abdominal Aortic Aneurysm
Men aged 65 - ultrasound to measure abdominal aortic diameter