Obs + Gynae II Flashcards
Crown rump length required for diagnosis of miscarriage
> 7mm
At <7mm, may be too early to tell if pregnancy is viable but very early, or if it is non-viable
Foetal heartbeat expected once CRL >7mm
Repeat USS in potential miscarriage
If CRL <7mm without foetal heartbeat, scan repeated at least one week later to ensure heartbeat develops
CRL >7mm, without a foetal heartbeat, scan repeated one week later to confirm a non-viable pregnancy
If mean gestational sac diameter >25mm without a foetal pole, scan repeated after one week to confirm an anembryonic pregnancy
Measurements relevant in miscarriages
CRL = 7mm, foetal heartbeat expected once CRL >7mm
Mean gestational sac diameter = 25mm, foetal pole expected once diameter >25mm
Investigation/management in miscarriage <6 weeks
USS not useful, perform repeat urine pregnancy test after 7-10 days. Negative –> confirms miscarriage
Expectant management, unless bleeding continues, or pain occurs, or risk factors e.g. previous ectopic
Follow-up for low-grade cervical intraepithelial neoplasia (CIN 1)
Screen again at 12 months in the community
Most common type of vaginal cancer
Overall = secondary (metastatic cancer), usually from cervix, ovary or endometrium
Prumary cancer = squamous cell carcinoma
Features of vaginal cancer
Post-coital bleeding is common
May be followed by an offensive watery discharge
Follicular phase of menstrual cycle
Granulosa cells surround oocytes –> follicles
FSH stimulation –> further development of follicles
Granulosa cells secrete oestrogen as follicles grow –> negative feedback –> reduced FSH/LH secretion
Oestrogen –> cervical mucus is more permeable
Dominant follicle forms
LH surge –> dominant follicle release ovum
Luteal phase of menstrual cycle
After ovulation, follicle collapses –> corpus luteum –> secretes progesterone –> maintains endometrial lining, thickens cervical mucus
Also secretes some oestrogen
What happens to the corpus luteum when fertilisation occurs
Syncitiotrophoblast of the embryo secretes hCG –> maintain corpus luteum –> produces progesterone + oestrogen
What happens if no fertilisation occurs in menstrual cycle
No hCG production –> corpus luteum degenerates –> stops producing oestrogen + progesterone
This causes endometrium to break down + menstruation occurs
Stromal cells of endometrium release prostaglandins –> encourage breakdown of uterus + contraction
LH + FSH levels rise
Process of foetal descent through birth canal
Descent
Engagement (<2/5 palpable)
Flexion
Internal rotation
Crowning
Extension of presenting part
External rotation of head
Delivery (of shoulders and rest of body)
Management of asymptomatic bacteriuria in pregnancy
Confirm presence of bacteria with second culture (contamination of first sample possible)
Offer an immediate antibiotic prescription, taking into account urine culture + susceptibility
e.g. Nitrofurantoin (avoided at term), amoxicillin (if results available + susceptible), cefalexin
Diagnosis of polyhdramnios
Amniotic fluid index >24cm (or 2000ml+)
AFI >95th centile for gestational age
Diagnosis of oligohydramnios
Amniotic fluid index <5cm (or <200ml)
AFI <5th centle for gestational age
Timings of amniotic fluid
Increases steadily until 33 weeks gestation
Plateaus from 33-38 weeks
Declines –> approx 500ml at term
Causes of polyhdramnios
Idiopathic = 50-60% cases
Conditions preventing foetus from swallowing
Duodenal atresia
Anaemia
Foetal hydrops
Twin-to-twin transfusion syndrome
Genetic or chromosomal abnormalities
Macrosomia
Maternal diabetes
Maternal use of lithium
Viral infections
Management of polyhydramnios
No medical intervention required for majority
Aminoreduction if severe maternal symptoms (risk of infection + placental abruption)
Indomethacin –> enhance water retention –> reduce foetal output (premature closure of PDA so not used beyond 32 weeks)
Examine baby if idiopathic
Risks of polyhydramnios
Malpresentation
–> higher risk of cord prolapse
Postpartum haemorrhage
Causes of oligohydramnios
Preterm prelabour rupture of membranes
Placental insufficiency (blood flow to brain –> reduced foetal urine output)
Renal agenesis (Potter’s syndrome)
Non-functioning foetal kidneys
Obstructive uropathy
Genetic/chromosomal abnormalities
Viral infections
Management of oligohydramnios
Depends on underlying cause
P-PROM –> induction of labour if relevant, steroids for foetal lung development, antibiotics for infection
Placental insufficiency –> deliver before 36-37 weeks
Complication of oligohydramnios
Foetal muscle contractures due to inability to move limbs in utero
Points to remember for epilepsy in pregnancy
Risk of uncontrolled epilepsy > risk to foetus
Take 5mg folic acid per day prior to conception –> 12 weeks (risk of neural tube defects)
Aim for monotherapy
Epilepsy medications in pregnancy
Avoid sodium valproate (NTD)
Carbamazepine is least teratogenic of older antiepileptics
Phenytoin –> risk of cleft palate, given vitamin K in last month of pregnancy to prevent clotting disorders in newborn
Lamotrigine –> seems safe, may need increased dose
Most anti-epileptics safe in breastfeeding
Blood tests for hypothalamic/pituitary causes of secondary amenorrhoea
Low levels of gonadotrophins (FSH + LH)
Low levels of oestradiol (from ovaries)
FSH + LH should rise in response to low oestrogen –> hypothalamic dysfunction
What is postpartum thyroiditis
Changes in thyroid function within 12 months of delivery
Affects women without a history of thyroid disease
Can be hyper/hypothyroidism, or both
Typical pattern of postpartum thyroiditis
- Thyrotoxicosis (usually in first three months)
- Hypothyroid (usually from 3-6 months)
- Thyroid function gradually returns to normal (usually within 1 year)
Blood tests in postpartum thyroiditis
Thyrotoxicosis: Raised T3/T4, low TSH
Hypothyroidism: Low T3/T4, raised TSH
Thyroid peroxidase antibodies found in 90% patients
Management of thyrotoxic phase of postpartum thyroiditis
Propanolol for symptom control
Not usually treated with anti-thyroid drugs
Annual monitoring of TFTs
Management of hypothyroid phase of postpartum thyroiditis
Levothyroxine
Annual monitoring of TFTs
Risk factors for GDM
BMI >30
Previous macrosomic baby weighing 4.5kg+
Previous GDM
First degree relative with diabetes
Family origin with a high prevalence of diabetes e.g. South Asian
Indications for GDM screening
Any risk factor present
Large for dates foetus
Polyhydramnios
Glucose on urine dipstick
Cut-offs for GDM on OGTT
Fasting = 5.6 mmol/L
2 hours = 7.8 mmol/L
5, 6, 7, 8
Management of GDM
Fasting glucose <7: diet + exercise for 1-2 weeks, then metformin, then insulin
Fasting glucose >7: start insulin +/- metformin
Fasting glucose >6 + macrosomia/other complications: start insulin +/- metofmrin
Glibenclamide (sulfonylurea) can be used if decline insulin/cannot target metformin
Blood glucose targets for women with GDM
Fasting: 5.3 mmol/L
1-hour post-meal: 7.8 mmol/L
2 hours post-meal: 6.4 mmol/L
Avoid 4mmol/L or below
Management of pre-existing diabetes in pregnancy
Take 5mg folic acid from preconception to 12 weeks gestation
Weight loss for women with BMI >27
Stop oral hypoglycaemic agents (apart from metformin) and commence insulin
Retinopathy screening
Planned delivery 37-38+6 weeks gestation
Insulin use in labour
Sliding-scale insulin regime for T1DM
Dextrose + insulin infusion titrated to blood usgar levels
Also considered for women with GDM or T2DM with poorly controlled blood sugars
Postnatal care for GDM
Can stop diabetic medications immediately after birth
Test fasting glucose at least 6 weeks later
Regular BG checks for neonatal hypoglycaemia - aim >2mmol/L
Postnatal care for women with existing diabetes
Insulin sensitivity increases after birth, and with breastfeeding –> lower insulin doses + be aware of hypoglycaemia
Complications of diabetes in pregnancy
Neonatal hypoglycaemia
Polycythaemia
Jaundice
Congenital heart disease
Cardiomyopathy
Investigation for placenta praevia
Gold standard = transvaginal ultrasound, can be used to determine position of the placenta
Avoid digital vaginal examination as may provoke a severe haemorrhage
Contraception use in women who are menopausal (even if using HRT)
<50 years old: 2 years after last menstrual period
>50 years old: 1 year after last menstrual period
Appropriate methods: barrier, IUD/IUS, POP, Progesterone implant, sterilisation, depot injection (if <45)
- Depot can cause weight gain and reduce bone mineral density
NB: COCP can be used up to age of 50
Contraindications to HRT
Current or past breast cancer
Any oestrogen-sensitive cancer
Undiagnosed vaginal bleeding
Endometrial hyperplasia or cancer
Uncontrolled hypertension
VTE
Liver disease
Acive angina or MI
Pregnancy
Principles of HRT to reduce risks
Progesterone required in women who have a uterus, to avvoid endometrial hyperplasia and cancer associated with unopposed oestrogen
Patches > pills to avoid VTE risk
Non-hormonal treatments for menopausal symptoms
Lifestyle changes e.g. diet, exercise, weight loss, smoking cessation, alcohol/stress/caffeine reduction
CBT
Clonidine: lowers BP + reduces HR. Useful for vasomotor symptoms
SSRIs
Venlafaxine
Gabapentin
Indications for HRT
Premature ovarian insufficiency, even without symptoms
Reducing vasomotor symptoms
Improving symptoms e.g. low mood, decreased libido, poor sleep + joint pain
Reducing risk of osteoporosis in women <60
Risks of HRT
Increased risk of breast cancer (esp with combined HRT)
Endometrial cancer
VTE
Stroke + coronary artery disease (with long term use in older women)