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Obstetrics > thyroid disease in pregnancy > Flashcards

thyroid disease in pregnancy Flashcards

1
Q

Should we screen for subclinical thyroid disease

A

Screening for subclinical hypothyroidism or TPO antibodies, and subsequent treatment with thyroxine is not recommended in pregnancy

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2
Q

What are the main causes of hypothyroid disease in NZ

What are other causes

A

affects 1% of pregnancy woman
Hashimotos thyroiditis
Autoimmune disorder
Associated T1DM / pernicious anaemia / vitiligo

Other causes are post treatment - radioactive iodine, radiation, removal for nodules or malignancy

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3
Q

What is the Physiology of thyroid hormone production in pregnancy

A

ßHCG is structurally similar to TSH and provides weak thyroid stimulating activity , and so the normal
increase in ßHCG in early pregnancy may cause a small transient increase in free T4 (FT4) with
subsequent TSH suppression.

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4
Q

When does the fetuses thyroid start working?

A

The fetus is reliant on transplacental transfer of maternal thyroid hormone until the fetal thyroid
starts to become functional from 12 weeks. The fetus and the fully breastfed infant are dependent on
maternal iodine for thyroid hormone synthesis.

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5
Q

How does pregnancy affect normal ranges for thyroid function?

A

TSH - local pregnancy ranges should be used
If not available 4mU/l upper range for pregnancy
or
T1 0.5 mU/L less then non pregnant range.
T2/3 the same

T4
FT4 concentrations also change with increasing gestation. As there is no single international method
for standardisation of free thyroid hormone tests, method specific reference intervals are necessary
for free thyroid hormone assays.

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6
Q

What is overt vs subclinical hypothyroidism

A

Overt hypothyroidism is defined as increased serum TSH and decreased FT4,
or,
TSH >10mIU/L with FT4 within the normal range.

Subclinical hypothyroidism is defined as serum TSH above the reference range, and FT4 within the
normal range.

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7
Q

What does overt hypothyroidism cause?

A

miscarriage
anovulation

Adverse pregnancy outcomes
PET Abruption
anemia
PPH 
PTB
LBW
perinatal mortality 
reduced IQ and developmental delay 
Adequately tx hypothyroidism is not at increased risk
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8
Q

Who should get TFTs to screen for overt hypothyroidism?

A

Thyroid function testing with serum TSH should be performed in early pregnancy for women with
symptoms of thyroid disease or a personal history of thyroid disease

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9
Q

How does dosing for thyroxine change in pregnancy?

How often testing?

Treatment aim?

A

Often 30-50% increase in dosing from early pregnancy

Levels should be done at least once / trimester to assess adequacy of replacement

Treatment goal should be TSH in lower half of trimester specific ranges

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10
Q

does subclinical hypothyroidism need to be treated?

A

nope
Some suggestive studies but meta analysis didnt agree
no population wide screening

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11
Q

Shall we screen for and treat woman with TPO antibodies?

A

no

There is no substantive evidence to support alteration in TSH
targets or benefits from thyroxine treatment based on TPO antibody status and so universal or
targeted screening for thyroid autoantibodies is not recommended in pregnancy

also not enough evidence it increases the risk of miscarriage and that thyroxine helps so not currently recommended

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12
Q

What are the sx of hypothryroidism

A

Most sensitive in pregnancy
Cold intolerance
slow pulse
delayed relaxation of the tendon

Common
Constipation
weight gain
lethargy
hair loss 
dry skin carpal tunnel
fluid retention
goitre
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13
Q

What does severe iodine deficiency cause?

A

neurological creastinisn
Deaf mutism
Spastic motor disorder
hypothyroid

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14
Q

neonatal hypothyroidism

A

1:180 000
TSH receptor blocking antibodies transplacentally cross to fetus
more with atrophic then hashimotos
suspect if fetal goitre - dx on guthrie card

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15
Q

What is the incidence of post partum thyroiditis?

A

Variable depending on screening and iodine intake

but average 7% (numbers range from 1-17%

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16
Q

Who is at risk for post partum thyroiditis

A

Woman with a family hx of hypothyroid
Woman with thyroid peroxidase (antimicrosomal) antibodies - 50% of whom develop post partum thyroiditis have antibodies
85% of patients have antibodies
more common in T1DM
25% have a FHx of autoimmune thyroid disease

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17
Q

When does post partum thyroiditis present?

How does it present?

A

Many asymptomatic

usually 3-4 months post partum - can be up to 6 months

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18
Q

What are the ways post partum thyroiditis can present?

With what sx?

A

Monophasic or biphasic

monophasic
40% transient hypothyroid (lethary, tired, depression)
40% transient hyperthyroid (palpitations and fatigue)

20% biphasic
Hyperthyroid then hypothyroid lasting 4-8 months

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19
Q

What is the pathogenesis of post partum autoimmune thyroiditis ?

What does a FNA show?

any other test to differentiate it?

A

It is a destructive autoimmune thyroiditis causing first a release of preformed thyroxine from the thyroid (not a hyperfunctional gland)
And then hypothyroid as stores are deplete

FNA shows lymphocytic thyroiditis

It could be a rebound after the immunosuppressive affects of pregnancy

Radioactive iodine will show low uptake (Graves shows high uptake)

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20
Q

Management of post partum thyroititis

Who needs managing?
How to manage it?

A

Most woman recover spontaneously and dont require treatment
need for treatment is determined by symptoms
Hyperthyroid sx should be treated by B blockers (its not a synthesis problems it a release problem)
Hypothyroid with thyroxine
Withdraw threatment after 6-8 months and assess if spont recovery has occurred
96% will not need ongoing treatment

21
Q

Post partum thyroiditis recurrence

A

10-20% suffer recurrence
20-30% who had + Antibodies have hypothyroidism within 4 years - recommend annual TFTs

Woman with positive thyroid antibodies have increaesed risk of postnatal depression

22
Q

What are the physiological changes of the thyroid in pregnancy

A

Thyroid binding globulin synthesis in the liver increases
T4 and T3 increase to compensate
T4 levels fall a little in the second and third trimester
TSH rises and falls in T1 - then is higher then normal in T2/3
Levels of Free T3/4 lower in T2/3
Hyperemesis gives high free T4 and suppressed TSH in 60% of cases
(hcg has a TSH like activity)

State of iodine deficiency
fetal requirements
Increased excretion
Uptake in the thyroid increases - it can hypertrophy to trap any iodine there

23
Q

Incidence of thyrotoxicosis

What is the biggest risk factor

A

1:500 pregnancies

50% of woman have a FHX of autoimmune thyroid disease

24
Q

What are the sx of thyrotoxicosis in pregnancy?

What are the most obvious sx in pregnancy?

A 
head intolerance 
tachycardia
palpitations
palmar erythema
emotional lability
vomiting
goitre
Most discriminatory
weight loss
tremor
tachycardia
lid lag
exophthalmos
50% of people with graves have ophthalmopathy  and can present before hypothyroidism
25
Q

What is the cause of hyperthyroid in pregnancy?

How to diagnose?

A

95% of hyperthyroid in pregnancy is Graves
TSH receptor stimulating antibodies

Rare other causes are toxic nodular goitre, toxic adenoma subacute thyroiditis, or iodine, amiodarmone or lithium therapy

High T4 suppressed TSH

26
Q

How does pregnancy affect graves

A

As with other autoimmune disease - it often improves in pregnancy in a relative state of immunosuppression
There may be a first trimester exacerbation due to hcg affect
no change to ophthalmopathy
30% stop meds at end of pregnancy

post natal relapses
test 3 months post partum

27
Q

How does thyrotoxicosis affect pregnancy

A

inhibits ovulation and fertility
if untreated
increased miscarriage, FGR, PTL Perinatal mortality
Can leave to AF, SVT, tachycardia
If poorly controlled can develop a thyroid storm
with heart failure

Rarely retrosternal goitre extensions cause tracheal obstruction
thyroid stimulating antibodies can cause fetal or neonatal thyrotoxicosis

28
Q

How to manage thyrotoxicosis in pregnancy

What are the 2 drugs as proc and cons of each

A

Onset delayed 3-4 weeks as preformed hormone is depleted. Aggressive tx 4-6 weeks
total tx 18 months but relapse high
aim to quickly control then maintain on lowest dose possible

both cross placenta PTU + carbimazole
Typically people stay on what they are on

PTU 150-400mg
Risk 0.01 % liver failure
Less cross into placenta and breast milk
First line

Carbimazole 15-40 mg
Risk of aplasia cutis - loss of skin over fetal skull in T1

no role for block and replace in pregnancy as the anti thyroid is TF across placenta and makes the baby hypothyroid but the thyroxine doesnt cross

29
Q

How to manage relapses?

A

more medication long term
Surgery
radioactive iodine

30
Q

SE of anti thyroid drugs

A

1-5% develop a rash from anti thyroid drugs
- should promptly switch
Can cause neutropenia and agranulocytosis
Should report infection / sore throat
liver impairment 1:10 000 on PTU

31
Q

Plan pregnancy management if on anti thyroid drugs

A

See monthly

32
Q

is breastfeeding safe on anti thyroid mediation?

A

small amounts are transferred in breast milk
so ok to breast feed at ow doses PTU less then 150 mg / day - 0.07% dose TF to baby
carbimazole -0.5% of dose TF

Check fetal TFT on umbilical blood andat regular intervals / at regular intervals if breastfeeding on high doses

33
Q

What is the role for B blockers?

A

symptomtic tx of tachycardia
Also reduce T4 to T3 conversion
Often used short term until the anti thyroid drugs kick in - usually 3 weeks

34
Q

Can you perform a thyroidectomy in pregnancy?

A 
Rarely indicated
can be done in T2
Usaully if large goitre causing stridor or dysphagia
Close FU for hypothyroid
Hypocalcaemia in 1-2% of cases
35
Q

Can radioactive iodine be used in pregnancy?

A

nope as also taken up by fetal thyroid

Dx radioiodine also contraindicated although can be used in breastfeeding if pump and dump for 24 hours

Pregnancy should be avoided for 4 months after treatment- theoretical risk chromosomal damage

36
Q

What are TSIs?
Thyroid stimulating antibodies?
What is the risk?
How to manage that?

A

antibodies in graves disease
can cross the placenta
Can cause fetal thyrotoxicosis - Occurs in 1% babies with current or past hx graves - more so with active disease

Can predict by TSI levels
test in T1 to predict fetal thyrotoxicosis
USS - FGR, tachycardia, goitre
mortality 25%
neonatal TFTs on cord blood
In utero treatment - anti thyroid drugs (and thyroxine if needed)

Neonatal antibodies last 4 months
Maternal treatment can last 1-7 days
So can present in first week of life with weight loss, tachycardia, irritability, poor feeding, goitre, hepatospenomegaly
Mortality 15%

37
Q

How common is a thyroid nodule in pregnancy?

A

1-2% of woman

up to 40% are malignant

38
Q

What are concerning features of a thyroid lump in pregnancy ?

A 
prev RT to head or neck
Fixation of the lump
rapid growth
lymphadenopathy
vice change
horners
39
Q

What are the first tests to do after finding a thyroid nodule ?

A

TFT
Thyroid antibodies
(exclude a toxic nodule or hashimotos)
USS (solid or cystic)

40
Q

How does the parathyroid change in pregnancy?

A

increased demand for Calcium (pregnancy and lactation)
Increased urinary loss
Calcium absorption is increased X2
Vit D requirements are increased 50-100%
Total fall in albumin, calcium and free ionized calcium

41
Q

Hyperparathyroidism

What is the incidence

A

Nearly 1:10 000
It may be parathyroid adenoma or hyperplasia

Can be no sx, or fatigue, thirst, hyperemesis, constipation, depression
HTN, pancreatitis, renal calculi

Difficult to dx in pregnancy

42
Q

How does pregnancy affect hyperparathyroidism

How does hyperparathyroidism affect pregnancy

A

hypercalcaemia can be improved in pregnancy due to increased Ca demand

Increased risk of miscarriage, IUD, PTB,
If severe fetal mortality 40%
25% HTN or PET

Neonatal risk is hypocalcaemia due to suppression of fetal PTH due to high maternal Ca
can be a prompt to dx the mother

Tx is surgery
OR high fluid, oral phosphate

43
Q

Hypoparathyroid

Causes?
Diagnosis?

A

Autoimmune
post thyroidectomy 1-2%

Dx - low Ca and PTH levels

44
Q

What is the affect of hypoparathyroidism on pregnancy?

A

Low Ca increases risk T2 miscarriage, fetal hypocalcaemia and secondary hypoparathyroidism
bone demineralisation
neonatal rickets
Can be dx with neonatal seizures

45
Q

How to treat hypoparathyroidism?

A

Vit D and Ca supplements
Vit D doses will need to be increased 2-4 X

Check Ca and albumin monthly

46
Q

What is the incidence and risk factors of vitamin D deficiency ?

A 
Pigmented skin
obesity
vegans
covered woman
several pregnancies with a short interpregnancy interval
malabsorption (coeliac)
AEDs / highly active ART
renal or liver disease
alcohol abuse
47
Q

What are maternal consequences of Vit D deficiency

A 
Bone loss
reduces weight gain
hypocalcaemia
osteomalacia
myopathy
gestational diabetes
HTN PET SGA
Increased risk LSCS
48
Q

Fetal risks for low vit D

A

Adverse skeletal development
reduces neonatal calcium - seizures
subsequent atopy, asthma

49
Q

NICE guideline for Vit D supplementation for all pregnancy woman

A

400 U / day - part of a pregnancy multivit

Obstetrics (41 decks)

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