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Thyroid disorders in pregnancy obgy topic
- 1. Thyroid disorders in pregnancy Dr.OMKAR KALANE JR2 OBGY
- 2. ➢Changes during pregnancy ➢Hyperthyroid ➢Hypothyroid ➢Postpartumthyroid disease ➢Thyroid cancer ➢Euthyroid with autoimmune thyroid disease
- 3. ❖Increase in thyroid-bindingglobulin ➢secondary to an estrogenic stimulation of TBG synthesis and reduced hepatic clearance of TBG ; two to threefold ➢levels of bound proteins, total thyroxine, and total triiodothyronine are increased and resin triiodothyronine uptake (RT3U) is decreased ➢begins early in the first trimester, plateaus during midgestation, and persists until shortly after delivery decrease in its hepatic clearance, estrogen-induced sialylation ❖free T4 and T3 increase slightly during the first trimester
- 4. ❖Human chorionic gonadotropin(hCG) •intrinsic thyrotropic activity •begins shortly after conception, peaks around gestational week 10,declines to a nadir by about week 20 •directly activate the TSH receptor partial inhibition of the pituitary gland •transient decrease in TSH between Weeks 8 and 14 mirrors the peak in hCG concentrations • 20% of normal women, TSH levels decrease to less than the lower limit of normal
- 6. ➢0.2% of pregnancies ➢prevalence0.1% to 0.4%, with 85% Graves’ disease • Single toxic adenoma, multinodular toxic goiter, and subacute thyroiditis • gestational trophoblastic disease,viral thyroiditis and tumors of the pituitary gland or ovary (struma ovarii) ➢TSH is depressed and fT4 and fTI are increased. ➢The RT3U that normally is decreased in pregnancy is increased in hyperthyroidism.
- 7. ➢serum TSH value<0.01 mU/L and also a high serum free T4 value ➢may be difficult to determine the cause • thyroid radionuclide imaging is contraindicated in pregnant women. ➢Measurement of thyrotropin receptor antibody (thyroid stimulating immunoglobulins) Graves' disease during pregnancy ➢Transient hyperthyroidism in hyperemesis gravidarum and gestational transient thyrotoxicity (GET)
- 8. ➢Severe maternal hyperthyroidism -increasedrisk of stillbirth -preterm delivery -intrauterine growth restriction -Preeclampsia -heart failure -spontaneous abortion -Fetal thyroid hyperfunction or hypofunction caused by TSHRAbs -Fetal goiter from excessive antithyroid drug treatment -Neonatal thyrotoxicosis -Increased perinatal and maternal mortality -Decreased IQ of offspring because of excessive use of antithyroid drugs
- 9. Hyperemesis gravidarum •severe nauseaand vomiting •absence of goiter and ophthalmopathy, and absence of the common symptoms and signs of hyperthyroidism •Normalization of T4 levels by midgestation. •Treatment is supportive care
- 10. -First trimester -Related tohCG stimulation of the thyroid gland -Symptoms of hyperthyroidism and elevated free T4 levels. -The thyroid gland usually is not enlarged -Resolution of symptoms parallels the decline in hCG levels -Usually resolves spontaneously by 20 weeks’
- 11. ❖Hydatidiform mole &choriocarcinoma. ❖High serum hCG concentrations and abnormal hCG isoforms ❖ 55 to 60 percent had clinically evident hyperthyroidism normal thyroid gland and few symptoms of thyroid hormone excess. ❖ A diffuse goiter ophthalmopathy is not present ❖Nausea and vomiting may predominate
- 12. ❖Associated with osteoporosis,cardiovascular morbidity, and progression to overt thyrotoxicosis and thyroid failure. ❖Not associated with adverse pregnancy outcomes ❖Does not warrant treatment.
- 13. ❖ Activity levelfluctuate during gestation, with : exacerbation during the first trimester gradual improvement during the latter half. exacerbation shortly after delivery ❖Clinical scenarios: • stable Graves’ disease receiving thionamide therapy with exacerbation during early pregnancy. •in remission with a relapse of disease. • without prior history diagnosed with Graves’ disease de novo during pregnancy.
- 14. ❖Diagnosis •difficult :hypermetabolic symptomsin normal pregnancy •thyroid examination: goiter suppressed serum TSH level and usually elevated free and total T4 serum concentrations. ❖ Complications related to the duration and control of maternal hyperthyroidism ❖Autoantibodies mimic TSH can cross the placenta and cause neonatal Graves’ disease
- 15. ❖Pregnancy outcome inGraves’ Disease -preterm labor -preeclampsia -stillbirth -small for gestational age -congenital malformations unrelated to thionamide therapy -Mother may have thyroid-stimulating hormone- binding inhibitory immunoglobulin (TBII) -Neonatal Thyrotoxicosis
- 16. •obstetric emergency •extreme metabolicstate •10% of pregnant women with hyperthyroidism •high risk of maternal cardiac failure. •fever, change in mental status, seizures, nausea, diarrhea, and cardiac arrhythmias. •inciting event (eg, infection, surgery, labor/delivery) and a source of infection •treatment immediately, even if serum free T4, free T3, and TSH levels are not known. •untreated thyroid storm can be shock, stupor, and coma.
- 17. ❖Thionamides ❖Beta blockers ❖Iodides ❖Surgery Subtotal thyroidectomy: Second trimester, before gestational week 24 prepared with a β-adrenergic blocking agent and a 10 to 14 day course of potassium iodide.
- 18. ❖Elevated serum TSHconcentration:2.5% of pregnancies ❖ In iodine-sufficient environment Hashimoto’s thyroiditis prior radioactive iodine treatment surgical ablation of Graves’ disease
- 19. Diagnosis ❖Symptoms masked bythe hypermetabolic state of pregnancy. ❖ 20% to 30% overt hypothyroidism develop symptoms : weight gain, lethargy,decrease in exercise capacity, and intolerance to cold,constipation,hoarseness, hair loss,brittle nails, dry skin, goiter, or delay in the relaxation phase of the deep tendon reflexes ❖Elevated serum TSH concentration
- 20. Pregnancy outcome ❖ Dependson the severity of disease and adequacy of treatment ❖Gestational hypertension in overtly hypothyroid women ❖Overt hypothyroid vs subclinical disease: •increased use of cesarean section because of fetal distress •placental abruption, anemia, andpostpartum hemorrhage increased rates of miscarriage, preeclampsia,placental abruption, growth restriction,
- 21. CLINICALLY: ❖TSH can beelevated with or without suppressed levels of free T4. ❖antithyroid autoantibodies are present ❖ elevated creatine phosphokinase, cholesterol, and liver function tests. ❖5% to 8% prevalence of hypothyroidism in type I diabetes mellitus and women who have type I diabetes have a 25% risk of developing postpartum thyroid dysfunction
- 22. ❖normal free T4level ❖elevated TSH above the upper limit of reference range (4.5–10.0mIU/L) ❖TSH in the first half of pregnancy is 3.0 mIU/L ❖Prevalence of subclinical hypothyroidism 2–5% ❖Increased risk of placental abruption and preterm birth ❖2–5% progress to overt hypothyroidism each year
- 23. ❖Normal TSH ❖Free T4below 0.86 ng/dl. ❖In the first half of pregnancy,prevalence 1.3%. ❖Not associated with adverse perinatal outcome
- 24. 1. For newlydiagnosed hypothyroid women, initial levothyroxine dosage is based on severity of hypothyroidism. 2. For overt hypothyroidism, administer 2 mcg/kg/d. If TSH is < 10 mU/L, initial dose of 0.1 mg/d may be sufficient. 3. For previously diagnosed hypothyroid women, monitor serum TSH every 3–4 weeks during first half of pregnancy and every 6 weeks thereafter. 4. Adjust levothyroxine dosage to maintain serum TSH ≤ 2.5 mU/L. 5. Monitor serum TSH and total T4 levels 3–4 weeks after every dosage adjustment. When
- 25. ❖Autoimmune disorder witha self-limited hyperthyroid phase within one year after parturition. ❖Presentations •Transient hyperthyroidism alone •Transient hypothyroidism alone •Transient hyperthyroidism followed by hypothyroidism and then recovery. ❖ Can also occur after spontaneous or induced abortion 3 to 16 percent.
- 26. Distinguished from Graves' hyperthyroidism, ❖hyperthyroidism in postpartum thyroiditis is usually mild (both clinically and biochemically), ❖Thyroid enlargement is minimal ❖Graves' ophthalmopathy is absent. ❖ By re-evaluation in three to four weeks: postpartum thyroiditis improved
- 27. Antithyroids :no role. Hypothyroid:may require treatment and some significant rate of residual hypothyroidism Recommend: maintain thyroxine until childbearing is complete, with an attempt to wean off medication 1 year after the last delivery
- 28. ❖60% Graves’ diseasein the reproductive years; postpartum onset ❖Euthyroid patients with Graves’ disease with TSI ▪ Increased risk of developing recurrent Graves’ disease if antithyroid medication was withheld ❖TSIs differentiate postpartum Graves’ disease from postpartum thyroiditis with a hyperthyroid component.
- 29. ❖Thyroid tumors ;mostcommon endocrine neoplasms. ❖Thyroid cancer accounts for 1% of all cancers. ¾ women; 1/2 reproductive years. ❖Diagnosis :biopsy ,Serum TSH and free T4 levels,ultrasonography & Fine needle aspiration . Radionucleotide scanning is contraindicated during pregnancy. ❖Malignant or suspicious for papillary cancer, surgery at the earliest safe period ❖No evidence that pregnancy causes a reactivation of
- 31. ❖Increased risk forspontaneous miscarriage, subclinical hypothyroidism, and postpartum thyroiditis ❖Increase in serum TSH levels ❖Presence of antithyroid antibodies Lack of thyroidal reserve in response to the stimulatory effects of pregnancy.
- 32. 1. Recommend initiatinglevothyroxine therapy in women with antithyroid antibodies before pregnancy, if TSH level is greater than 2.5 mU/L. 2. Serum TSH should be monitored throughout pregnancy in all antithyroid antibody–positive women 3. Maintain the TSH concentration at 2.5 mU/L or less.