thyroid disorders in pregnancy.pptx

1. Anatomy of thyroid gland

2. Anatomical location
✓ Located in the anterior neck from C5-T1 vertebrae.
✓ Consists of two lobes connected by a central isthmus.
✓ Wrapped around the cricoid cartilage and superior rings of the trachea.

3. Anatomical relations
✓ Anteriorly: infrahyoid muscles
✓ Laterally: carotid sheath
✓ Medically: larynx, pharynx, trachea, oesophagus, external laryngeal nerve
and recurrent laryngeal nerve

4. Blood supply
• Arterial supply
✓ Superior thyroid artery: arises as the first branch of external carotid artery
✓ Inferior thyroid artery: arises from the thyrocervical trunk
• In small proportion of people (10%) there is an additional artery present-
thyroid ima artery, which arises from the brachiocephalic trunk and supplies
the anterior surface and isthmus of the thyroid gland.

5. • Venous supply
✓ Superior, middle and inferior thyroid veins which form a venous plexus around
the thyroid gland.
✓ Superior and middle veins drain into the internal jugular vein and the inferior
vein empties into the brachiocephalic vein.

6. Nerve supply
✓ Innervated by branches derived from the sympathetic trunk
✓ These nerves do not control the secretory function of the gland- the release of
thyroid hormones is regulated by the pituitary gland.
• Lymphatic drainage
✓ Lymphatic drainage of the thyroid is to the paratracheal and deep cervical
nodes.

7. Physiology of thyroid gland

8. Synthesis of thyroid hormones

9. ✓ Iodide transport: iodide is transported into the follicular cell via Sodium- iodide
symporter(NIS). This is actually a secondary active transport, and the sodium
gradient driving it is maintained by a Sodium-Potassium ATPase.
✓ Thyroglobulin: a large protein rich in tyrosine, is formed in follicular ribosomes and
placed into secretory vesicles.
✓ Exocytosis: of thyroglobulin into the follicle lumen, where it is stored as colloid.
✓ Iodisation: of thyroglobulin. Iodide is made reactive by the enzyme thyroid
peroxidase.
✓ Coupling: of MIT and DIT gives the triiodothyronine (T3) and coupling of DIT and
DIT gives the tetraiodothyronine (T4) or thyroxine.
✓ Endocytosis: of iodinated thyroglobulin back into the follicular cell which then
undergoes proteolysis to release free T3 and T4.

10. Regulation of thyroid hormones synthesis
• TRH from hypothalamus stimulates the anterior pituitary. Anterior pituitary
releases TSH.

11. • Action of TSH on thyroid gland:
• Increases vascularity
• Increases iodide trapping
• Increases thyroid hormone synthesis

12. T3 T4
• Most potent less potent
• Active: responsible for physiological effects less active
• Rapid action slow acting
• Short half life long half life
• Circulating level is less circulating level more

13. Actions of thyroid hormone
• Increases basal metabolic rate
• Physiological uncouplers of electron transport chain
• Catabolic in nature (increase blood glucose, free fatty acids, protea lysis and
decrease blood cholesterol level)
• Important in growth of brain(myelination in cns) and growth of bone
• Increases responsiveness of heart to circulating catecholamines like
norepinephrine
• Thermogenesis

14. EFFECT OF PREGNANCY ON
THYROID

15. • Pregnancy has goitrogenic effect on thyroid because increased
demand of thyroid hormones to maintain increased maternal
hormonal levels and additional requirement of foetus.
• The production of T3 and T4 increase nearly by 50% due to increased
thyroxin binding globulin (TBG) , which is increased in early pregnancy
to reach to reach twice the non pregnant level by 16 to 20 weeks and
an increase in plasma volume.
• Increase in TBG occurs as a result of increased synthesis under the
influence of oestrogen and reduced clearance.
• This two factors result in increase in Total T4 although the pre
hormone level remain unchanged

16. • Iodine requirement in pregnancy increase by 50%
• Thyroid hormones are transferred to the foetus in the first trimester,
later iodine is transferred once the foetus starts manufacturing its own
thyroid hormones.
• Iodine excretion in urine increases in pregnancy due to increase in GFR
, plasma clearance and decreased renal tubular reabsorption.
• Iodine sufficient women with intra thyroidal store cope with this
demand ,however women with borderline or iodine deficient reserve ,
the thyroid hormone levels fall stimulating TSH leads to goitre
formation in the mother as well as fetus.

17. Effect of iodine deficiency in pregnancy outcome
• Severe iodine deficiency leads to increased rate of miscarriage , still
birth , perinatal and infant mortality rate.
• Cretinism in baby.
• Urinary iodine level used to asses the iodine status
• According to WHO guidelines median urinary iodine levels for pregnant
women should be 149 to 249 µgm/ litre.
• To prevent goitre formation, women in the reproductive age should
have adequate daily intake of iodine atleast 150 µgm/ day.
• During pregnancy and lactation ,WHO recommends daily intake should
be 250 µgm/ day.

19. HYPERTHYROIDISM
IN PREGNANCY
Incidence of hyperthyroidism in pregnancy varies between 0.4
and
1.7 % of births
(WILLIAMS 26TH EDITION)

20. PREGNANCY OUTCOME IN THYROTXICOSIS

21. CLINICAL FEATURES
It is due to supraphysiological levels of TSH causing
hypermetabolism and hyperactivity
• Nervousness,Irritability,Tremors,Tachycardia that
exceeds that usually seen with normal pregnancy
• Heat intolerance,Facial flushing,Failure to gain
weight despite adequate food intake
• Insomnia,Exopthalamos,Diplopia
• Thyromegaly,diffuse swelling which moves with
deglutination
If the serum TSH level is found to be supressed by
less than 0.1mIU/L in first trimester free t3 free t4
measurement should be done in all the patients

22. CAUSES OF HYPERTHYROIDISM IN PREGNANCY
1. GRAVES DISEASE(most common
pathological cause)
2. GESTATIONAL TROPHOBLASTIC
DISEASE
3. TRANSIENT THYROTOXICOSIS IN
PREGNANCY
4.THYROID STORM AND THRYOTOXIC
HEART FAILURE

23. It is an organ specific autoimmune
disease associated with thyroid
stimulating TSH receptor antibodies.
Women with graves disease should be
stably euthyroid before attempting
pregnancy

24. MANAGEMENT OF GRAVES DISEASE IN NON
PREGNANT FEMALES
• Antithyroid drugs,radioactive iodine ablation,thyroidectomy
• After radioactive ablation pregnancy should be avoided for 6
months
• Women on ANTIthyroid drugs are counselled regarding
possiblity of teratogenic side effects.

25. MANAGEMENT OFGRAVES DISEASE DURING
PREGNANCY
• THIONAMIDE DRUGS , reduce the production of thyroid hormones by
selectively inhibiting thyroid peroxidase .PTU(PREFFERED AS IT PARTIALLY
INHIBITS CONVERSION OF T4 TO T3 AND CROSSES THE PLACENTA LESS
READILY THAN METHIMAZOLE)>METHIMAZOLE
1. PROPYLTHIOURACIL- DOSE 50 TO 150 MG ORALLY THREE TIMES A DAY
DAILY
SIDE EFFECTS :TRANSIENT LEUCOPENIA –It has an acute onset so serial
leucocyte count during pregnancy is not helpful , it doesn’t require
cessation of therapy,it is not dose related
If women develops agranulocytopenia,sore throat,fever only then cessation of
therapy is done and a complete blood count is to be done.

26. MEDICAL MANAGEMENT
2.METHIMAZOLE- DOSE INITIAL HIGHER DAILY DOSE OF 10 TO 20 MG/DAY TO
MAINTENANCE DOSE OF 5 TO 10MG/DAY
SIDE EFFECTS-Methimazole associated embryopathy characterised by aplasia
cutis,choanal atresia,esophageal atresia,hepatotoxicity
SURGICAL MANAGEMENT :1)SUBTOTAL THYROIDECTOMY in females with non
compliance to medical management or the drug therapy has toxic side
effects.Complications of thyroidectomy include injury to reccurent laryngeal
nerve,inadvertent resection of parathyroid gland leading to hypocalcemia.
2)THYROID ABLATION with radioactive iodine is contraindicated in pregnancy(women
are advised to avoidgetting pregnant during first 6 months of radioablative therapy

27. GESTATIONAL TRANSIENT THYROTOXICOSIS
• Seen in early pregnancy ,resulting from TSH receptor
stimulation from HCG,May be associated with hyperemesis
gravidarum,multiple pregnancy,molar pregnancy and
choriocarcinoma.
• It is not associated with adverse pregnancy outcome.
• Antithyroid drugs are not needed,normalises by midpregnancy

28. THYROID STORM AND THYROTOXIC HEART FAILURE
• Hypermetabolic state in the setting of thyrotoxicosis leading to
systemic decompensation that is cardiac failure
• It is reversible
• Since pregnant women has minimal cardiac reserve
decompensation is usually precipitated by
preeclampsia,anaemia,sepsis

29. MANAGEMENT OF THYROID STORM

30. POSTPARTUM THYROIDITIS
It is an autoimmune disorder.,It has triphasic pattern thyrotoxicosis in
first 6 months followed by features of hypothyroidism,later euthyroid
by 10 to 12 months.
• Risk of recurrence is almost 70%,it has strong association with
antiTPOantibodies,postpartum depression,hence females with
postpartum depression are to be screened for it.
• Tsh screening to be done 2 monthly upto one year,later TSH
screening anually.
• Neonatal assesment is done at 5 to 10 days of age , it is self limiting
and supportive treatment is required upto a period of six weeks until
antibodies have been cleared from the system of neonate.

31. HYPOTHYROIDISM

32. • Incidence in India - 13%
• Overt or symptomatic hypothyroidism complicates between 0.2 and
1.2 % of pregnancies.
• Clinical findings include - fatigue, constipation, cold intolerance,
muscle cramps and weight gain.
Visible goitre, edema, dry skin and hair loss.
Overt hypothyroidism –high TSH, low free t4.
Subclinical hypothyroidism-high TSH, Normal t4.

33. OVERT HYPOTHYROIDISM
• Mcc in pregnancy is Hashimoto thyroiditis.(anti TPO antibodies)
• Hashimoto thyroiditis characterized by glandular destruction from
autoantibodies,particularly anti-TPO antibodies.
• Other cause is post ablative Grave’ disease.
Whom to evaluate- past history, family history, type 1 DM, patient with
symptoms.
Severe hypothyroidism during pregnancy is uncommon, probably
because it is often associated with infertility and higher miscarriage
rates.
Outcomes:

35. • Treatment :oral levothyroxine-1-2microgram/kg/day(100microgram)
• Surveillance is with TSH levels measured at 4 week intervals in the first half
of pregnancy and atleast once in the third trimester(28 week).
• Target TSH - <2.5mU/L.
• IF patient is already on treatment increase dose by 25%.
• FOGSI +Indian Thyroid Society –TSH levels at
1. T1 -2.5m IU/L
2. T2 -3m IU/L
3. T3-3m IU/L

36. SUBCLINICAL HYPOTHYROIDISM
• Raise TSH with normal t4.
• 1/3rd will become normal in 5 year, 2/3rd will become overt hypothyroidism.
• Routine screening for low risk pregnancy is not required.
• ACOG 2020 - screen patient with greater risk.
• CATS(controlled antenatal thyroid screening study) Study- ANC thyroid screening
and randomized treatment of subclinical hypothyroidism and isolated maternal
hypothyroxinemia (normal TSH with low t4) shows offspring IQ was same at the
end of 3 yr of treatment and untreated patient.
• TREATMENT- 50-100 microgram/day(if TSH >10m IU/L or TSH 4-10 m IU/L + TPO
Antibody positive).
• Treatment can be considered if TSH 4-10mIU/L with TPO negative or TSH 2.5-
4mIU/L with TPO ab positive.

37. EUTHYROID AUTOIMMUNE THYROID DISEASE
• Autoantibodies to TPO and thyroglobulin(2-17% of pregnant women)
• Most who test positive for such antibodies, however, are euthyroid.
• No need to screen antibody in all patient.(ACOG 2020)
• Antibodies associated with early pregnancy loss and preterm birth.
• Levothroxine reduces the preterm birthfrom 22 to 7 %(Negro 2006)

38. Iodine defeciency
• Dietery iodine requirements are higher during pregnancy due to augmented
thyroid harmone productions,increased renal losses, and fetal iodine
requirments.
• Mild defeciency –supplementation does prevent fetal goiter and had no
effect on child neurodevelopment.(stagnaro-green,2012b)
• Moderate deficiency- supplement studies shows inconsistent findings with
regard to psychomotor development(Bell 2016).
• Severe defeciency – frequently associated with endemic cretinism, and
benefits of universal salt iodization or supplementation have been
confirmed(alexander,2017).
• Regarding daily iodine intake,American thyroid association recommends an
average iodine intake of 250 microgram in pregnancy.

39. Postpartum thyroiditis
• It includes hyperthyroidism, hypothyroidism, or both.
• Presentation- 2 clinical phase
1. Destruction induced thyrotoxicosis –excessive release of harmone
from glandular disruption, abrupt onset, small and painless goiter.
Symptoms include fatigue and palpitations, if severe beta blocking
agent may be given.
2. Hypothyroidism from thyroiditis-between 4-8 months postpartum,
levothyroxine replacement at doses of 25 to 75 microgram/day is
typically given for 6-12 months.

40. Nodular thyroid disease
• Palpable thyroid nodules can be found in up to 5% of reproductive-
aged women (Angel,2019).
• Evaluation of thyroid nodules during pregnancy should be similar