endocrine disease pregnancy Flashcards
what are the physiological changes to the thyroid in pregnancy
Due to the increased metabolic state
Increase in serum thyroxine binding globulin TBG by oestrogen 2X in the liver
To maintain the same level T3 and T4 production increases
Stimulation of thyrotropin TSH by hcg
hcg and TSH are from the same family of glycoprotein hormones and share alpha subunit and unique B subunits but even their B subunit is very similiar
hcg has a weak thyroid activity
As hcg rises to peak at 12 weeks, so does total T3 and T4
The TSH can appear transiently suppressed
Iodine requirement in pregnancy
Increased because Increased T4 production requiring iodine + iodne transportation through the placenta and Increased renal excretion
Increase in blood volume means iodine concentration is less and thyroid increases its uptake of iodine
Thyroid cells are the only cells in the body which can absorb iodine. These cells combine iodine and the amino acid tyrosine to make T3 and T4.
Severe deficicency - permanent brain injury, neurologic creatinism - deaf mutism, spatic motor disorder, hypothyroid
maternal overt hypothyroid in pregnancy
Fetal risk - prematurity and perinatal mortality, miscarriage developmental delay
Maternal risks PET abruption Anaemia infertility PPH
maternal hyperthyroid in pregnancy
50% of woman have + FHx
95% graves disease - autoimmune disorder TSH receptor stimulating antibodies TRAb
Rarely toxic multinodular goitre usually improves in pregnancy
Can be related to inhibited ovulation and infertility
Increased rate FGR miscarriage PTL perinatal mortality
Antibodies can cross the placenta and cause neonatal thyrotoxicosis
Can be sick with tachycardia, SVT, AF HR
Tx carbimazole or PTU
Both cross the placenta - can cause fetal hypothyroidism - PTU safer
serial USS for growth, FHR, fetal neck
Risk factors for hyperglycaemia in pregnancy (8)
- Age Over or including 40
- Ethnicity - Asian, Indian, Pacific, Maori, Aboriginal, middle eastern
- Prev hyperglycaemia in pregnancy
- Prev elevated BSL
- FHx - first degree relative with DM or sister with GDM
- PCOS
- Pre preg BMI over 30
- Medications - steroids or antipyschotics
- prev Macrosomia
How is GDM screened for?
RANZCOG Guideline
Low risk - 26-28 weeks GTT
High risk - ‘earlier’ in pregnancy (HbA1c or GTT) then repeated at 24-28 weeks if previously negative
There should be no polycose
GTT is 75g of glucose
fasting tested and 2 hour BSL
RANZCOG cut offs 5.1, 8.5
Postnatal follow up for GDM
WHO guidelines
- risks
- screening
30% risk hyperglycaemia in future pregnancies
1.5-10% risk of developing diabetes each year
50% risk in 10-15 years
If considering future pregnancies should have a GTT annually
Low risk woman HbA1c or GTT every 1-2 years
High risk with possible T2DM then 3 monthly testing indicated
What does GDM increase the risk of?
Antenatal
GHTN or PET
Polyhydramnios unclear etiology ? fetal polyuria
Stillbirth
Intrapartum
Macrosomia
Accelerated growth may start from 20-28 weeks gestation
- excessive maternal weight gain doubles the risk of macrosomia
This increases the risk of
-operative delivery
- Adverse neonatal outcomes eg shoulder dystocia (brachial plexus injury, fractures, neonatal depression)
postnatal
Increased risk of IGT T1DM T2DM
Metabolic syndrome
Cardiovascular disease
Neonatal morbidity - hypoglycaemia, electrolyte abnormalities, respiratory distress, cardiomyopathy
Long term childhood obesity risk, IGT, metabolic syndrome
Postnatal management for GDM
LARC contraceptive + + pre pregnancy counselling is recommended
Breastfeeding should be encouraged
WHO Guideline 6-12/52 postpartum OGTT
30% risk hyperglycaemia in future pregnancies / CNP says ‘usually’ recurs
FU primary care
Type 2 diabetes:
1.5-10% risk of developing diabetes each year,
40-60% risk of developing T2DM in 10years
- this is significant as a change in weight may delay or prevent the onset of diabetes (the risk doubles every 4.5 kgs gained)
- Allow for ongoing screening and detection before microvascular complications have occurred
If considering future pregnancies should have a GTT annually
Low risk woman HbA1c or GTT every 1-2 years
High risk with possible T2DM then 3 monthly testing indicated
Lean caucasian woman with no family history may have evolving Type 1 and should be screened for anti glutamic acid decarboxylase antibodies
Fetal risk of T2DM
Double risk of congenital abnormalities
4% (from baseline 2%)
3-4X increased risk NTD and cardiac defects – also increase in skeletal abnormalities
Sacral agenesis is rare but pathopneumonic
Perinatal mortality increased 5-10X
Perinatal mortality 3%
maternal ketoacidosis related to high perinatal mortality
RDS
PTB
Macrosomia / shoulder dystocia
Polyhydramnios / PPROM /Cord prolapse
If T1DM
Offspring risk if maternal 2-3% paternal 4-5%
What are the maternal risks in pregnancy of T2DM
Increased miscarriage
3-4X increased risk PET (more so if renal disease and HTN) - related to glycaemic control
Anaemia – normochromic, normocytic
Oedema- proteinuria and hypoalbuminaemia
Infections – endometritis, respiratory, endometrial, wound
LSCS rate 65%
How does pregnancy affect diabetes?
increasing insulin requirement rapidly from 28-32 weeks
Deterioration of nephropathy (renal function + proteinuria) - more so if HTN or Cr >125
2X increase risk of deteriorating retinopathy - (risk factors for this are high diastolic BP, renal disease, anaemia, poor metabolic control are severe baseline retinopathy)
Hypoglycaemia is more common
Risk of ketoacidosis in relation to hyperemesis, infection, steroids
Autonomic neuropathy and gastric paresis experience a deterioration in sx
How to manage diabetes in pregnancy ?
Importance of normoglycaemia
Increase frequency of home testing
Targets fasting 3.5-5.9
Post prandial targets <7.8
T1
Increasing doses insulin (although can fall in T1)
Increase in hypoglycaemic attacks
Pts need to be warned about sx
Partners need to be taught to administer glucagon (this must be followed up with a sugary drink as short acting)
No evidence a pump or continuous infusion is better then bolus dosing
Woman should have ketone testing strips if they are unwell / hyperglycaemia
T2
Metformin +/- insulin
Most need insulin in pregnancy
If refusing insulin metformin is better then nothing
Avoid the newer thiazolidinediones
Strict low sugar low fat high fibre diet
Screening for complications
Retinal
Retinal screen at 28 weeks if the last one was normal
16 weeks if abnormal
Laser photocoagulation can be used in pregnancy to prevent or treat proliferative retinopathy
Not a contradiction for tighter BSL control of VB
If severe – needs post partum FU
Renal
Renal involvement if severe imapirment Cr >120 / protein 2g/day
Regular PCR and Cr assessment
30% will have HTN – 75% HTN by the end of pregnancy
HTN
Strict control of HTN prevents ongoing renal damage
Low threshold for antihypertensive therapy is needed
Why give aspirin and ca to diabetics?
Aspirin from 12 weeks – 36 weeks
Some evidence better if taken later in the day
NNT 90
15% reduction in PET
Calcium
At least 1 g daily
Reduces PET risk by over 50- 80%
Physiological changes to the adrenals in pregnancy
3-8x ↑ in cortisol secondary to increased CRH & ACTH from placenta
↑ androstenedione and total testosterone
↓ DHEAS and free testosterone
4x ↑ in plasma renin activity from 8/40 to 20/40- then plateau
3x ↑ angiotensin II (due to ↑renin & angiotensinogen) 4x ↑aldosterone (due to ↑renin & angiotensinogen) by 8/40 then continued rise to 10x higher levels by term
No change in catecholamine secretion in pregnancy
