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THYROID DISEASES IN
PREGNANCY
Physiological changes of thyroid
 Thyroid Function in Pregnancy
 Increased TBG
 Increased total thyroxine, and T3
 Free T4 and T3 remain unchanged
 BMR increases 15-20% above normal
 TSH is lower in first trimester (HCG effect)
 TSH does not cross the placenta
 Relative iodine deficiency
 Increase absorption of iodine
 In pregnancy thyroid function is tested by free T4 and TSH , total T3 T4 not to be used
Hypothyroidism
 CAUSES OF HYPOTHYROIDISM :
Hypothyroidism
clinical picture
Hypothyroidism in pregnancy
 Incidence of 1 %
 Subclinical is more than overt (2 % vs 0.2 % )
 Most common cause worldwide is iodine deficiency
 Most common cause In developed countries is autoimmune thyroiditis
(hashimotos )
 Treatment is needed for overt cases and maybe some subclinical cases with
positive antibodies
 Serial thyroid function test is needed for hypothyroid cases in pregnancy every 4-
6 months using TSH and FREE T4
 Aim of treatment is TSH less than 4 mmol/L
Possible complications of hypothyroidism
Subclinical hypothyroidism
seems to has no effect unless
antibodies are positive
(TPO positive ) where TSH is
high but free T3 T4 is normal
Treatment by L-thyroxine
 Most widely prescribed treatment
 Category A
 25-300 mcg
 If newly diagnosed in pregnancy started @ 1-2µg/kg/d or 100-150µg/d
 If previously hypothyroid dose increased by 25-40%
 Postpartum:
• Decrease dose by 30% (if newly diagnosed)
• Breast feeding is not contraindicated
Hyperthyroidism
 Incidence of 0.2 %
 Types :
• Subclinical- low TSH normal FT3, FT4
• Overt- low TSH high FT4, FT3
• Physiological and Gestational hyperthyroidism (in cases where there is an excessive HCG )
 Symptoms: Palmar erythema, emotional lability, vomiting, goiter, heat intolerance, exophthalmos, fail
to gain weight
 Only overt needs treatment
Causes of hyperthyroidism
 Most common cause in child bearing age is GRAVES disease (autoimmune )
 INTRINSIC THYROID DISEASE
• Grave’s
• Toxic nodule
• Subacute thyroiditis
 EXOGENOUS THYROID HORMONE
• Factitious
• Therapeutic
GESTATIONAL THYROTOXICOSIS (increased
HCG)
•Hyperemesis
•GTD
•Hydatidiform mole
•Multiple gestations
•Hydrops
RARE
•TSH producing pituitary tumour
•Iodine deficiency
•Struma ovarii
Symptoms
Complications of hyperthyroidism
Antenatal treatment of new cases
 Detected in 1st trim- observe
 Persists in 2nd trim- t/t
 THIONAMIDES:
1. Propylthiouracil
• Less readily crosses placenta
• 50-150mg TDS
• Category D
• Side effects-
m/c rash
Fetal hypothyroidism
Transient leukopenia (10%)
Agranulocytosis (0.3-0.4%) discontinue t/t
Hepatotoxicity (0.1-0.2%)
Vasculitis
2. Methimazole or carbimazole
• 5-20mg BD
• Crosses placenta readily
• Category D
• Methimazole embryopathy- Esophageal atresia, choanal atresia, cutis aplasia
 FETAL MONITORING:
• 10% hypothyroidism
• Clinical exam
• USG
• Cordocentesis
• Selective Fetal blood sampling
 treatment aims to maintain maternal fT3 and fT4 levels in the high/normal
range
 Subtotal thyroidectomy rarely (retrosternal goiter causing airways
obstruction , suspicion of malignancy )
 Radioactive iodine ablation is contraindicated
 While Using drugs regular checks of maternal white cell count are necessary
 Both drugs cross placenta and present in breast milk (use the least effective
dose )
Postpartum management
 Immunosuppression disappears postpartum
 Graves Relapse postpartum in 70 % (improve in late pregnancy )
 TSH & freeT4 test at 6weeks post partum
 Lactating mother-
• PTU & methimazole excreted in breast milk
• PTU protein bound. Safer
• Methimazole only at low doses (10-20mg/d)
Thyroid storm
 life-threatening (20-50 % mortality if untreated )
 Acute exacerbation of hyperthyroidism, life threatening, hypermetabolic state
 Rare in pregnancy
 precipitated by sepsis, preeclampsia & anemia and labor
 Excessive sweating, pyrexia, tachycardia, atrial fibrillation, hypertension,
hyperglycemia, vomiting, agitation and cardiac failure
Postpartum thyroiditis
 lymphocytic infiltration of gland
 High chances if high titers of Antibodies
 Phases-
 Hyperthyroid (1/3 will go into the second phase )
 Hypothyroid (1/3 will have permeant hypothyroidism )
 Hyperthyroidism usually doesn’t need treatment as its transient but hypothyroid
phase needs thyroxine therapy )
Fetal thyroid disease
 Hypothyroidism or thyrotoxicosis can occur due to passage of maternal antibodies
to the fetus
 over treatment of maternal hyperthyroidism by antithyroid drugs can lead to fetal
hypothyroidism
 Fetal hyperthyroidism is more common and fetal monitoring to detect goiter ,
tachycardia or hydrops and IUGR is needed for women having antibodies even if
euthyroid (women with positive antibodies who had ablation or total thyroidectomy
before )

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Lecture 14 Thyroid diseases in pregnancy

  • 2. Physiological changes of thyroid  Thyroid Function in Pregnancy  Increased TBG  Increased total thyroxine, and T3  Free T4 and T3 remain unchanged  BMR increases 15-20% above normal  TSH is lower in first trimester (HCG effect)  TSH does not cross the placenta  Relative iodine deficiency  Increase absorption of iodine  In pregnancy thyroid function is tested by free T4 and TSH , total T3 T4 not to be used
  • 3. Hypothyroidism  CAUSES OF HYPOTHYROIDISM :
  • 5. Hypothyroidism in pregnancy  Incidence of 1 %  Subclinical is more than overt (2 % vs 0.2 % )  Most common cause worldwide is iodine deficiency  Most common cause In developed countries is autoimmune thyroiditis (hashimotos )  Treatment is needed for overt cases and maybe some subclinical cases with positive antibodies  Serial thyroid function test is needed for hypothyroid cases in pregnancy every 4- 6 months using TSH and FREE T4  Aim of treatment is TSH less than 4 mmol/L
  • 6. Possible complications of hypothyroidism Subclinical hypothyroidism seems to has no effect unless antibodies are positive (TPO positive ) where TSH is high but free T3 T4 is normal
  • 7. Treatment by L-thyroxine  Most widely prescribed treatment  Category A  25-300 mcg  If newly diagnosed in pregnancy started @ 1-2µg/kg/d or 100-150µg/d  If previously hypothyroid dose increased by 25-40%  Postpartum: • Decrease dose by 30% (if newly diagnosed) • Breast feeding is not contraindicated
  • 8. Hyperthyroidism  Incidence of 0.2 %  Types : • Subclinical- low TSH normal FT3, FT4 • Overt- low TSH high FT4, FT3 • Physiological and Gestational hyperthyroidism (in cases where there is an excessive HCG )  Symptoms: Palmar erythema, emotional lability, vomiting, goiter, heat intolerance, exophthalmos, fail to gain weight  Only overt needs treatment
  • 9. Causes of hyperthyroidism  Most common cause in child bearing age is GRAVES disease (autoimmune )  INTRINSIC THYROID DISEASE • Grave’s • Toxic nodule • Subacute thyroiditis  EXOGENOUS THYROID HORMONE • Factitious • Therapeutic GESTATIONAL THYROTOXICOSIS (increased HCG) •Hyperemesis •GTD •Hydatidiform mole •Multiple gestations •Hydrops RARE •TSH producing pituitary tumour •Iodine deficiency •Struma ovarii
  • 12. Antenatal treatment of new cases  Detected in 1st trim- observe  Persists in 2nd trim- t/t  THIONAMIDES: 1. Propylthiouracil • Less readily crosses placenta • 50-150mg TDS • Category D • Side effects- m/c rash Fetal hypothyroidism Transient leukopenia (10%) Agranulocytosis (0.3-0.4%) discontinue t/t Hepatotoxicity (0.1-0.2%) Vasculitis
  • 13. 2. Methimazole or carbimazole • 5-20mg BD • Crosses placenta readily • Category D • Methimazole embryopathy- Esophageal atresia, choanal atresia, cutis aplasia  FETAL MONITORING: • 10% hypothyroidism • Clinical exam • USG • Cordocentesis • Selective Fetal blood sampling
  • 14.  treatment aims to maintain maternal fT3 and fT4 levels in the high/normal range  Subtotal thyroidectomy rarely (retrosternal goiter causing airways obstruction , suspicion of malignancy )  Radioactive iodine ablation is contraindicated  While Using drugs regular checks of maternal white cell count are necessary  Both drugs cross placenta and present in breast milk (use the least effective dose )
  • 15.
  • 16. Postpartum management  Immunosuppression disappears postpartum  Graves Relapse postpartum in 70 % (improve in late pregnancy )  TSH & freeT4 test at 6weeks post partum  Lactating mother- • PTU & methimazole excreted in breast milk • PTU protein bound. Safer • Methimazole only at low doses (10-20mg/d)
  • 17. Thyroid storm  life-threatening (20-50 % mortality if untreated )  Acute exacerbation of hyperthyroidism, life threatening, hypermetabolic state  Rare in pregnancy  precipitated by sepsis, preeclampsia & anemia and labor  Excessive sweating, pyrexia, tachycardia, atrial fibrillation, hypertension, hyperglycemia, vomiting, agitation and cardiac failure
  • 18.
  • 19. Postpartum thyroiditis  lymphocytic infiltration of gland  High chances if high titers of Antibodies  Phases-  Hyperthyroid (1/3 will go into the second phase )  Hypothyroid (1/3 will have permeant hypothyroidism )  Hyperthyroidism usually doesn’t need treatment as its transient but hypothyroid phase needs thyroxine therapy )
  • 20. Fetal thyroid disease  Hypothyroidism or thyrotoxicosis can occur due to passage of maternal antibodies to the fetus  over treatment of maternal hyperthyroidism by antithyroid drugs can lead to fetal hypothyroidism  Fetal hyperthyroidism is more common and fetal monitoring to detect goiter , tachycardia or hydrops and IUGR is needed for women having antibodies even if euthyroid (women with positive antibodies who had ablation or total thyroidectomy before )