6. Obs and Gyn 3 Flashcards
When do women require contraception after giving birth?
Day 21
What is endometrial hyperplasia and give the pathophysiology, and a risk factor.
Abnormal proliferation of the endometrium.
It develops due to presence of unopposed oestrogen; oestrogen stimulates endometrial growth whilst progesterone stimulates shedding of this tissue.
Tamoxifen has pro-oestrogenic effects on endometrium (though it has anti-oestrogenic effects on breast)
Risk factors for endometrial carcinoma (7).
Excess oestrogen e.g. nulliparity, late menopause, early menarche, unopposed oestrogen e.g. HRT
Metabolic syndrome e.g. obesity, DM, PCOS
Tamoxifen
HPNCC
Third stage of labour is measured from the birth of the baby to the expulsion of placenta and membranes. Why is active management of this stage recommended and what does it involve (3 things)?
Reduce PPH and need for blood transfusion post delivery.
Lasts <30 minutes, involves uterotonic drugs, deferred clamping and cutting of cord (1 min < x < 5 mins) and controlled cord traction after signs of placental separation.
What is an amniotic fluid embolism, and give some signs and symptoms a patient may present with.
Fetal cells / amniotic fluid enter the mother’s bloodstream and stimulate a reaction.
Shivering, chills, sweating, anxiety, coughing.
Cyanosis, hypotension, tachycardia, dyspnoea, arrhythmias, MI
Supportive management in a critical care setting.
What is the intervention used in obstetric cholestasis that prevents stillbirth, and also give 4 other management strategies for symptom relief.
Elective induction from 37 weeks.
Ursodeoxycholic acid
Vitamin K
Emollients
Chlorphenamine
What are the 3 types of oestrogen, where and when are they produced?
E1 = ESTRONE; post menopause, converted from androgens in peripheral tissues.
E2 = OESTRADIOL; premenopausal, from ovaries.
E3 = ESTRIOL; produced from the placenta, weakest of them all. Maintains uterine lining and supports fetal development.
Describe the histological types of endometrial cancer.
Endometrioid type = 80%. Split into mostly endometrioid adenocarcinoma, + some others inc mucinous carcinoma.
Non-endometrioid type = 20%. Split into clear cell, serous and mixed adenocarcinoma.
State some contraindications to HRT.
History of unprovoked / recurrent VTE
Oestrogen sensitive malignancy
Undiagnosed PV bleeding
Untreated hypertension
Liver dysfunction
Untreated endometrial hyperplasia
What is adenomyosis, and give 3 clinical features of it.
Endometrial tissue present in the myometrium. More common in multiparous women at the end of their reproductive years.
Dysmenorrhoea
Menorrhagia
Enlarged, boggy uterus
What is the first line investigation for adenomyosis?
TVUS
What specific levels are measured in the combined screening and the quadruple screening tests offered in pregnancy, and when are they offered?
Combined at 11-13+6 weeks. Nuchal translucency, PAPP-A, b-hCG.
Quadruple at 15-20 weeks. Inhibin A, unconjugated estriol, AFP, hCG.
What are the diagnostic thresholds for gestational diabetes?
Fasting glucose >/= 5.6 mmol/L
2-hour glucose >/= 7.8mmol/L
If <7mmol fasting at diagnosis then diet and exercise should be encouraged, if not then metformin and insulin added in later.
If >7mmol at presentation then insulin should be started. If borderline but evidence of complications such as macrosomia or polyhydramnios then offer insulin as well.
What is the mnemonic used to remember the process for reading a CTG?
DR - define risk
C - contractions
BRa - baseline rate
V - variability
A - accelerations
D - decelerations
O - overall impression
When should fetal movements be established by?
24 weeks
Quickening usually occurs between 18-20 weeks, and increase until 32 weeks and then plateaus.
What is considered as RFM and therefore warrants further investigation in a patient after 28 weeks?
<10 recognised movements in 2 hours
Late decelerations begin at the peak of a uterine contraction and recover after the contraction ends. What does this type of deceleration indicate, and give 3 causes.
Late decels indicate insufficient blood flow to uterus and placenta.
This can lead to fetal hypoxia and acidosis.
Causes:
Maternal hypotension
Pre-eclampsia
Uterine hyperstimulation
Early decelerations occur at the start of a uterine contraction and recover quickly once it ends. What is the physiology behind this?
Early decels indicate increased fetal ICP and increased vagal tone during a contraction, and quick recovery indicates return to normal ICP post contraction.
A sinusoidal pattern on a CTG is rare but very concerning. What does it look like and what 3 things could it indicate?
Smooth, regular wave pattern, around 2-5 cycles per minute.
Severe fetal hypoxia
Severe fetal anaemia
Fetal / maternal haemorrhage
What is a normal baseline rate for a fetal heartbeat on a CTG?
110-160 bpm
What are variable decelerations usually caused by, and give the mechanism.
Umbilical cord compression
Acceleration is caused by umbilical vein compression.
Rapid deceleration during artery compression.
When pressure on the cord is reduced, baseline rate returns.
What does the ‘shoulders of deceleration’ refer to, and what does their presence / absence indicate?
Occurs in variable decelerations.
Shoulders indicate fetus is not hypoxic and is adapting to reduced blood flow. Reassuring.
Absence of shoulders may indicate hypoxia.
What is classed as prolonged deceleration?
> 2 mins
Non-reassuring = 2-3 minutes
Abnormal = >3 minutes
Give 3 features of a CTG that would be reassuring.
110-160 bpm rate
Variability of 5-25 bpm
None or early decels, or variable decels with no concerning features for <90 mins
https://geekymedics.com/how-to-read-a-ctg/