hyperthyroidism, thyrotoxicosis, grave disease, thyroid storm, pregnancy, high risk pregnancy, pregnancy complications, management of thyrotoxicosis and thyroid storm in pregnancy
A normal pregnancy results in a number of important reversible physiological and hormonal changes that alter thyroid structure and more importantly function.
Understanding these change are important to interpreting, identifying and managing of thyroid disease in pregnancy.
The document discusses the effects of pregnancy on thyroid physiology and function. It notes that thyroid stimulating hormone (TSH) levels are initially suppressed in the first trimester due to increased human chorionic gonadotropin (hCG) but become a reliable indicator again later in pregnancy. It provides references ranges for TSH, free T4, and total T4 in pregnancy and discusses screening and treatment of hypothyroidism. Maternal hypothyroidism can impact both maternal and fetal health outcomes.
1. Thyroid disorders are common in pregnancy, affecting 1-2% of pregnant women. Optimal management is important for pregnancy outcomes.
2. Hypothyroidism and hyperthyroidism can cause complications for both mother and fetus if not treated properly. Levothyroxine is the treatment of choice for hypothyroidism. Antithyroid drugs are used to treat hyperthyroidism.
3. Factors like hCG and estrogen increase thyroid function in pregnancy, requiring adjustments to diagnosis and treatment of thyroid disorders compared to non-pregnant individuals. Monitoring of thyroid levels is important during and after pregnancy.
The document discusses thyroid physiology and function during pregnancy. It notes that the hypothalamus-pituitary-thyroid axis is regulated by negative feedback, with TRH and TSH levels inversely related to T3 and T4 levels. During pregnancy, thyroid function is impacted due to increases in TBG, TT4, and TT3 to support fetal development. The document outlines screening recommendations for hypothyroidism in pregnancy, treatment with levothyroxine to maintain normal TSH levels, and potential complications of untreated maternal hypothyroidism such as preterm birth, low birth weight, and impaired neurodevelopment.
Over the past several years it has been proved that maternal thyroid disorder influence the outcome of mother and fetus, during and also after pregnancy. The most frequent thyroid disorder in pregnancy is maternal hypothyroidism. It is associated with fetal loss, placental abruptions, pre-eclampsia, preterm delivery and reduced intellectual function in the offspring.1 In pregnancy, overt hypothyroidism is seen in 0.2% cases2 and sub clinical hypothyroidism in 2.3% cases3. Fetal loss, fetal growth restriction, pre-eclampsia and preterm delivery are the usual complications of overt hyperthyroidism (low TSH and high T3, T4) seen in 2 of 1000 pregnancies whereas mild or sub clinical hyperthyroidism (suppressed TSH alone) is seen in
1.7% of pregnancies and not associated with adverse outcomes4. Autoimmune positive euthyroid pregnancy shows doubling of incidence of miscarriage and preterm delivery. Worldwide more than 20 million people develop neurological sequel due to intra uterine, iodine deprivation5. Other problems of thyroid disorders in pregnancy are post partum thyroiditis, thyroid nodules and cancer, hyper emesis gravidarum etc. Debates and disputes persist regarding several protocol and management plan in this specific spectrum of diseases.
THYROID DISEASES IN PREGNANCY BY DR SHASHWAT JANIDR SHASHWAT JANI
This document discusses thyroid disorders in pregnancy. It provides information on thyroid physiology changes during pregnancy, screening and management of thyroid dysfunction. Key points include: thyroid hormones play a key role in fetal development; pregnancy causes changes in thyroid binding globulin, placental conversion of T4 to reverse T3, and increased renal clearance of thyroid hormones; screening is recommended for high risk women and with a TSH cutoff of 2.5 mIU/L in the first trimester. Management involves treatment of hypothyroidism and hyperthyroidism to prevent complications of each condition for both mother and fetus.
1. Thyroid function changes during pregnancy due to increases in thyroid binding globulin, human chorionic gonadotropin, and other factors. This can cause hyperthyroidism or hypothyroidism.
2. Hyperthyroidism occurs in 0.2% of pregnancies, often due to Graves' disease. It increases risk of complications. Hypothyroidism occurs in 2-3% and also increases risks if not treated.
3. Postpartum thyroiditis involves transient hyperthyroidism and/or hypothyroidism after delivery. Long term hypothyroidism can occur. Thyroid cancer diagnosis and treatment requires consideration of pregnancy.
A normal pregnancy results in a number of important reversible physiological and hormonal changes that alter thyroid structure and more importantly function.
Understanding these change are important to interpreting, identifying and managing of thyroid disease in pregnancy.
The document discusses the effects of pregnancy on thyroid physiology and function. It notes that thyroid stimulating hormone (TSH) levels are initially suppressed in the first trimester due to increased human chorionic gonadotropin (hCG) but become a reliable indicator again later in pregnancy. It provides references ranges for TSH, free T4, and total T4 in pregnancy and discusses screening and treatment of hypothyroidism. Maternal hypothyroidism can impact both maternal and fetal health outcomes.
1. Thyroid disorders are common in pregnancy, affecting 1-2% of pregnant women. Optimal management is important for pregnancy outcomes.
2. Hypothyroidism and hyperthyroidism can cause complications for both mother and fetus if not treated properly. Levothyroxine is the treatment of choice for hypothyroidism. Antithyroid drugs are used to treat hyperthyroidism.
3. Factors like hCG and estrogen increase thyroid function in pregnancy, requiring adjustments to diagnosis and treatment of thyroid disorders compared to non-pregnant individuals. Monitoring of thyroid levels is important during and after pregnancy.
The document discusses thyroid physiology and function during pregnancy. It notes that the hypothalamus-pituitary-thyroid axis is regulated by negative feedback, with TRH and TSH levels inversely related to T3 and T4 levels. During pregnancy, thyroid function is impacted due to increases in TBG, TT4, and TT3 to support fetal development. The document outlines screening recommendations for hypothyroidism in pregnancy, treatment with levothyroxine to maintain normal TSH levels, and potential complications of untreated maternal hypothyroidism such as preterm birth, low birth weight, and impaired neurodevelopment.
Over the past several years it has been proved that maternal thyroid disorder influence the outcome of mother and fetus, during and also after pregnancy. The most frequent thyroid disorder in pregnancy is maternal hypothyroidism. It is associated with fetal loss, placental abruptions, pre-eclampsia, preterm delivery and reduced intellectual function in the offspring.1 In pregnancy, overt hypothyroidism is seen in 0.2% cases2 and sub clinical hypothyroidism in 2.3% cases3. Fetal loss, fetal growth restriction, pre-eclampsia and preterm delivery are the usual complications of overt hyperthyroidism (low TSH and high T3, T4) seen in 2 of 1000 pregnancies whereas mild or sub clinical hyperthyroidism (suppressed TSH alone) is seen in
1.7% of pregnancies and not associated with adverse outcomes4. Autoimmune positive euthyroid pregnancy shows doubling of incidence of miscarriage and preterm delivery. Worldwide more than 20 million people develop neurological sequel due to intra uterine, iodine deprivation5. Other problems of thyroid disorders in pregnancy are post partum thyroiditis, thyroid nodules and cancer, hyper emesis gravidarum etc. Debates and disputes persist regarding several protocol and management plan in this specific spectrum of diseases.
THYROID DISEASES IN PREGNANCY BY DR SHASHWAT JANIDR SHASHWAT JANI
This document discusses thyroid disorders in pregnancy. It provides information on thyroid physiology changes during pregnancy, screening and management of thyroid dysfunction. Key points include: thyroid hormones play a key role in fetal development; pregnancy causes changes in thyroid binding globulin, placental conversion of T4 to reverse T3, and increased renal clearance of thyroid hormones; screening is recommended for high risk women and with a TSH cutoff of 2.5 mIU/L in the first trimester. Management involves treatment of hypothyroidism and hyperthyroidism to prevent complications of each condition for both mother and fetus.
1. Thyroid function changes during pregnancy due to increases in thyroid binding globulin, human chorionic gonadotropin, and other factors. This can cause hyperthyroidism or hypothyroidism.
2. Hyperthyroidism occurs in 0.2% of pregnancies, often due to Graves' disease. It increases risk of complications. Hypothyroidism occurs in 2-3% and also increases risks if not treated.
3. Postpartum thyroiditis involves transient hyperthyroidism and/or hypothyroidism after delivery. Long term hypothyroidism can occur. Thyroid cancer diagnosis and treatment requires consideration of pregnancy.
The document summarizes thyroid disorders in pregnancy. Some key points:
- Thyroid disorders are among the most common endocrine conditions affecting 1-2% of pregnancies. Proper management is important for pregnancy outcomes.
- Hypothyroidism can cause complications for both mother and fetus like preeclampsia, preterm birth, and developmental delays. Treatment is levothyroxine.
- Hyperthyroidism in pregnancy is usually Graves' disease and may improve during pregnancy due to immunosuppressive effects but often worsens postpartum. Treatment focuses on maintaining normal thyroid levels.
- Postpartum thyroiditis is an autoimmune condition causing transient thyroid dysfunction after delivery
This document discusses thyroid disease in pregnancy. It begins by outlining the anatomy and physiology of the thyroid gland and how thyroid function changes during pregnancy. It then discusses specific thyroid disorders that can occur during pregnancy, including hyperthyroidism (overactive thyroid), hypothyroidism (underactive thyroid), and subclinical hypothyroidism. For each condition, it describes the potential maternal and fetal effects, diagnostic criteria, and treatment recommendations. The document provides detailed information on evaluating and managing thyroid disease to optimize outcomes for both the mother and baby.
This document discusses thyroid disorders in pregnancy. It notes that hypothyroidism affects 0.05% of pregnant women while hyperthyroidism, mainly Graves' disease, affects 0.05-0.2%. Postpartum thyroiditis occurs in 5-10% of women. The thyroid gland normally enlarges in pregnancy due to increased vascularity. HCG and estrogen levels rise, decreasing TSH and free T4 levels. Treatment aims to maintain euthyroidism. Hyperthyroidism is treated mainly with antithyroid drugs like PTU or carbimazole. Hypothyroidism is treated with levothyroxine. Postpartum thyroiditis can cause transient hyperthyroidism or hyp
This document discusses several autoimmune and endocrine conditions that can affect pregnancy, including their presentation, diagnosis, and management. It covers thyroid disease, rheumatoid arthritis, immune thrombocytopenic purpura, myasthenia gravis, and systemic lupus erythematosus. For each condition, it describes associated risks for the mother and fetus, as well as recommendations for treatment and monitoring during pregnancy and delivery. The goal is to maintain maternal and fetal health while minimizing medication exposure for the baby.
Maternal thyroid physiology is modulated during pregnancy by increases in hCG, urinary iodide excretion, and thyroxine-binding globulin. Thyroid disorders complicating pregnancy include hyperthyroidism, hypothyroidism, and postpartum thyroiditis. Hyperthyroidism is treated during pregnancy with antithyroid medications to maintain normal thyroid hormone levels. Hypothyroidism requires increasing levothyroxine doses during pregnancy. Postpartum thyroiditis involves transient hyperthyroid and hypothyroid phases due to thyroid autoimmunity after delivery.
This document discusses thyroid diseases in pregnancy. It notes that normal pregnancy causes physiological changes that alter thyroid function. It then discusses hypothyroidism and hyperthyroidism in pregnancy. Hypothyroidism complicates 1-3/1000 pregnancies and can cause maternal risks like infertility and fetal risks like low IQ. It is managed by replacing levothyroxine. Hyperthyroidism affects 2/1000 pregnancies and can cause maternal risks like heart failure. It is managed medically with antithyroid drugs or surgically with thyroidectomy. Nursing management involves monitoring for recurrence of symptoms postpartum. Preconception counseling is also important.
This document discusses pregnancy induced hypertension (PIH), also known as preeclampsia. PIH is a multisystem disorder characterized by high blood pressure and protein in the urine that develops during pregnancy. It can lead to serious complications for both the mother and baby if untreated. The document covers the definition, classification, signs and symptoms, risk factors, pathogenesis, diagnosis, and management of mild and severe cases of PIH.
1) Recent research has found that fetal fibronectin testing and ultrasound assessment of cervical length can help predict preterm birth in symptomatic women, though fetal fibronectin may have limited accuracy within 7 days.
2) Nifedipine and atosiban appear to be effective tocolytic options with fewer side effects than alternatives like ritodrine and indomethacin. Tocolysis is generally not continued past 48 hours except in special cases.
3) Antenatal corticosteroids between 24-34 weeks can help reduce fetal morbidity from preterm birth. Routine antibiotics without ruptured membranes do not prolong pregnancy or improve neonatal outcomes. Bed rest does not lower preterm
Hypertensive disorders are a leading cause of maternal and neonatal morbidity and mortality worldwide. Preeclampsia is characterized by new onset hypertension and proteinuria after 20 weeks of gestation and can progress to eclampsia with seizures. It is diagnosed when blood pressure is ≥140/90 mmHg on two occasions at least 4 hours apart accompanied by ≥300mg protein in 24 hour urine or a urine protein creatinine ratio of >0.3. Treatment involves blood pressure control with medications like labetalol, nifedipine and magnesium sulfate to prevent seizures. Delivery is usually required to resolve preeclampsia though timing depends on gestational age and maternal/fetal stability. Close monitoring of mother and
Thyroid diseases with pregnancy RCOG vs ACOGBasem Hamed
Universal screening for thyroid disease in pregnancy is not recommended. Levels of TSH and free T4 should be measured to diagnose thyroid disease in pregnancy. The first-line screening test used to assess thyroid status in patients is TSH level. Pregnant women with overt hypothyroidism should be treated with adequate thyroid hormone replacement to minimize the risk of adverse outcomes. The level of TSH should be monitored in pregnant women being treated for hypothyroidism. The level of free T4 should be monitored in pregnant women being treated for hyperthyroidism.
Heart disease occurs in approximately 1% of pregnancies and can be caused by rheumatic heart disease, congenital heart defects, or other conditions like ischemic heart disease. Diagnosis involves taking a medical history and performing a physical exam, chest X-ray, electrocardiogram, and echocardiogram. Pregnancy places additional strain on the heart and can exacerbate existing heart conditions or lead to heart failure. Management involves rest, diet, infection prevention, hospitalization if decompensation occurs, and possibly medical treatments like diuretics, beta blockers, or surgical treatments such as cardiac surgery or therapeutic abortion in severe cases. During labor, vaginal delivery is preferred if possible but induction is not recommended if acute heart
1) Intrahepatic cholestasis of pregnancy (ICP) is a liver disorder that causes pruritus (itching) without a rash and occurs in the second half of pregnancy.
2) Diagnosis involves elevated fasting bile acids and liver enzymes as well as ruling out other causes. Ursodeoxycholic acid is the first line treatment to improve symptoms and liver function.
3) ICP can lead to fetal complications like stillbirth so careful monitoring and early delivery may be considered for severe cases. Management involves treatment with UDCA and rifampicin as well as lifestyle changes to reduce symptoms.
1) Recurrent pregnancy loss is defined as three or more consecutive pregnancy losses before 20 weeks of gestation. A thorough investigation should be conducted to identify potentially treatable causes.
2) Common etiological factors include uterine anomalies, immunological issues such as antiphospholipid syndrome, endocrine disorders such as thyroid disease or diabetes, genetic factors, and thrombophilic disorders.
3) Evaluation involves a detailed history, physical exam, ultrasound, hormonal and immunological testing. Uterine anomalies require hysteroscopy or laparoscopy. Treatment depends on the underlying cause but may include surgery, medication, lifestyle changes, or cerclage. The goal is to identify modifiable risk factors.
This document discusses prolactinomas, which are pituitary tumors that cause excessive prolactin secretion. It describes the clinical presentation, diagnosis, and management approaches for prolactinomas. Microprolactinomas are small tumors less than 10mm, while macroprolactinomas are larger tumors. The first line treatment is dopamine agonist medication to reduce prolactin levels. Surgical removal may be considered for resistant cases or tumors pressing on nearby structures. Prolactinomas are generally managed medically but require monitoring due to risks of vision changes or hypogonadism from high prolactin levels.
This document summarizes thyroid disease in pregnancy. It discusses how thyroid function changes normally during pregnancy, with relative iodine deficiency and increased levels of thyroid binding globulin and T4 in early gestation. It notes that hyperthyroidism in pregnancy is usually caused by Graves' disease. Left untreated, it can lead to risks for both mother and fetus, including heart failure, thyroid storm, growth restriction and preterm labor. Management involves achieving an euthyroid state through medications like thionamides or propranolol, with close monitoring of thyroid function tests during pregnancy and treatment of any thyroid storm that may occur during labor and delivery.
Management of postterm pregnancy involves balancing risks to the fetus and mother. Postterm is defined as past 42 weeks gestation. Accurately dating the pregnancy is important to avoid false diagnosis. Risks to the fetus include stillbirth, meconium aspiration, and macrosomia. Risks to the mother include dystocia and infection. Studies show inducing labor at 41 weeks reduces stillbirths without increasing C-sections. Methods of antenatal testing after 41 weeks are debated, though monitoring is recommended. While an unfavorable cervix was viewed as a risk factor for C-section, recent evidence suggests underlying issues may be more important. Further research is needed to determine the optimal time for induction to minimize risks
This document discusses morbidly adherant placenta, also known as placenta accreta spectrum (PAS), which is becoming more common due to rising cesarean section rates. PAS occurs when the placenta invades deeply into the uterine wall and does not separate normally during delivery, potentially causing life-threatening hemorrhage. Early diagnosis through ultrasound screening and counseling of patients at high risk, such as those with prior uterine scarring, allows for improved maternal outcomes through preparedness and planned hysterectomy if needed. The key is anticipating PAS, making an accurate prenatal diagnosis, and being prepared to perform an emergency hysterectomy to control bleeding and save the mother's life if manual placental removal fails.
This document discusses epilepsy and pregnancy. Some key points:
- Epilepsy affects 0.5% of women of childbearing age and is the most common neurological disorder complicating pregnancy.
- Seizure frequency may increase, decrease or remain unchanged during pregnancy, depending on the individual. The risk of seizures is highest around delivery.
- Antiepileptic medications used to treat epilepsy can cause birth defects, especially sodium valproate which has been linked to neural tube defects. The risk increases with multiple medications and higher valproate doses.
- Women with epilepsy need folic acid, careful monitoring of seizure frequency and medication levels during pregnancy, and fetal screening for birth defects. Managing epilepsy treatment aims to control
This document discusses thyroid disorders in pregnancy. It notes that thyroid disorders are common in pregnancy, affecting 1-2% of pregnancies with overt disease and 3-5% with subclinical disease. Thyroid screening and treatment in pregnancy can help improve outcomes for both mother and baby, though guidelines vary on who and when to screen. The document reviews thyroid changes in pregnancy, screening recommendations, treatment of hypothyroidism and hyperthyroidism, and complications like postpartum thyroid dysfunction.
This document discusses thyrotoxicosis (hyperthyroidism) during pregnancy. It notes the physiological changes in thyroid function during pregnancy, including increases in thyroid binding globulin and decreases in plasma iodide levels. It describes the signs and symptoms of maternal hyperthyroidism as well as its most common cause, Graves' disease. Guidelines are provided for clinical management, including use of thionamide medications like propylthiouracil to control thyroid levels while monitoring the fetus. Treatment may also include beta blockers, iodine, or subtotal thyroidectomy in rare cases. Radioactive iodine therapy is contraindicated in pregnancy due to risks to the fetal thyroid.
The document summarizes thyroid disorders in pregnancy. Some key points:
- Thyroid disorders are among the most common endocrine conditions affecting 1-2% of pregnancies. Proper management is important for pregnancy outcomes.
- Hypothyroidism can cause complications for both mother and fetus like preeclampsia, preterm birth, and developmental delays. Treatment is levothyroxine.
- Hyperthyroidism in pregnancy is usually Graves' disease and may improve during pregnancy due to immunosuppressive effects but often worsens postpartum. Treatment focuses on maintaining normal thyroid levels.
- Postpartum thyroiditis is an autoimmune condition causing transient thyroid dysfunction after delivery
This document discusses thyroid disease in pregnancy. It begins by outlining the anatomy and physiology of the thyroid gland and how thyroid function changes during pregnancy. It then discusses specific thyroid disorders that can occur during pregnancy, including hyperthyroidism (overactive thyroid), hypothyroidism (underactive thyroid), and subclinical hypothyroidism. For each condition, it describes the potential maternal and fetal effects, diagnostic criteria, and treatment recommendations. The document provides detailed information on evaluating and managing thyroid disease to optimize outcomes for both the mother and baby.
This document discusses thyroid disorders in pregnancy. It notes that hypothyroidism affects 0.05% of pregnant women while hyperthyroidism, mainly Graves' disease, affects 0.05-0.2%. Postpartum thyroiditis occurs in 5-10% of women. The thyroid gland normally enlarges in pregnancy due to increased vascularity. HCG and estrogen levels rise, decreasing TSH and free T4 levels. Treatment aims to maintain euthyroidism. Hyperthyroidism is treated mainly with antithyroid drugs like PTU or carbimazole. Hypothyroidism is treated with levothyroxine. Postpartum thyroiditis can cause transient hyperthyroidism or hyp
This document discusses several autoimmune and endocrine conditions that can affect pregnancy, including their presentation, diagnosis, and management. It covers thyroid disease, rheumatoid arthritis, immune thrombocytopenic purpura, myasthenia gravis, and systemic lupus erythematosus. For each condition, it describes associated risks for the mother and fetus, as well as recommendations for treatment and monitoring during pregnancy and delivery. The goal is to maintain maternal and fetal health while minimizing medication exposure for the baby.
Maternal thyroid physiology is modulated during pregnancy by increases in hCG, urinary iodide excretion, and thyroxine-binding globulin. Thyroid disorders complicating pregnancy include hyperthyroidism, hypothyroidism, and postpartum thyroiditis. Hyperthyroidism is treated during pregnancy with antithyroid medications to maintain normal thyroid hormone levels. Hypothyroidism requires increasing levothyroxine doses during pregnancy. Postpartum thyroiditis involves transient hyperthyroid and hypothyroid phases due to thyroid autoimmunity after delivery.
This document discusses thyroid diseases in pregnancy. It notes that normal pregnancy causes physiological changes that alter thyroid function. It then discusses hypothyroidism and hyperthyroidism in pregnancy. Hypothyroidism complicates 1-3/1000 pregnancies and can cause maternal risks like infertility and fetal risks like low IQ. It is managed by replacing levothyroxine. Hyperthyroidism affects 2/1000 pregnancies and can cause maternal risks like heart failure. It is managed medically with antithyroid drugs or surgically with thyroidectomy. Nursing management involves monitoring for recurrence of symptoms postpartum. Preconception counseling is also important.
This document discusses pregnancy induced hypertension (PIH), also known as preeclampsia. PIH is a multisystem disorder characterized by high blood pressure and protein in the urine that develops during pregnancy. It can lead to serious complications for both the mother and baby if untreated. The document covers the definition, classification, signs and symptoms, risk factors, pathogenesis, diagnosis, and management of mild and severe cases of PIH.
1) Recent research has found that fetal fibronectin testing and ultrasound assessment of cervical length can help predict preterm birth in symptomatic women, though fetal fibronectin may have limited accuracy within 7 days.
2) Nifedipine and atosiban appear to be effective tocolytic options with fewer side effects than alternatives like ritodrine and indomethacin. Tocolysis is generally not continued past 48 hours except in special cases.
3) Antenatal corticosteroids between 24-34 weeks can help reduce fetal morbidity from preterm birth. Routine antibiotics without ruptured membranes do not prolong pregnancy or improve neonatal outcomes. Bed rest does not lower preterm
Hypertensive disorders are a leading cause of maternal and neonatal morbidity and mortality worldwide. Preeclampsia is characterized by new onset hypertension and proteinuria after 20 weeks of gestation and can progress to eclampsia with seizures. It is diagnosed when blood pressure is ≥140/90 mmHg on two occasions at least 4 hours apart accompanied by ≥300mg protein in 24 hour urine or a urine protein creatinine ratio of >0.3. Treatment involves blood pressure control with medications like labetalol, nifedipine and magnesium sulfate to prevent seizures. Delivery is usually required to resolve preeclampsia though timing depends on gestational age and maternal/fetal stability. Close monitoring of mother and
Thyroid diseases with pregnancy RCOG vs ACOGBasem Hamed
Universal screening for thyroid disease in pregnancy is not recommended. Levels of TSH and free T4 should be measured to diagnose thyroid disease in pregnancy. The first-line screening test used to assess thyroid status in patients is TSH level. Pregnant women with overt hypothyroidism should be treated with adequate thyroid hormone replacement to minimize the risk of adverse outcomes. The level of TSH should be monitored in pregnant women being treated for hypothyroidism. The level of free T4 should be monitored in pregnant women being treated for hyperthyroidism.
Heart disease occurs in approximately 1% of pregnancies and can be caused by rheumatic heart disease, congenital heart defects, or other conditions like ischemic heart disease. Diagnosis involves taking a medical history and performing a physical exam, chest X-ray, electrocardiogram, and echocardiogram. Pregnancy places additional strain on the heart and can exacerbate existing heart conditions or lead to heart failure. Management involves rest, diet, infection prevention, hospitalization if decompensation occurs, and possibly medical treatments like diuretics, beta blockers, or surgical treatments such as cardiac surgery or therapeutic abortion in severe cases. During labor, vaginal delivery is preferred if possible but induction is not recommended if acute heart
1) Intrahepatic cholestasis of pregnancy (ICP) is a liver disorder that causes pruritus (itching) without a rash and occurs in the second half of pregnancy.
2) Diagnosis involves elevated fasting bile acids and liver enzymes as well as ruling out other causes. Ursodeoxycholic acid is the first line treatment to improve symptoms and liver function.
3) ICP can lead to fetal complications like stillbirth so careful monitoring and early delivery may be considered for severe cases. Management involves treatment with UDCA and rifampicin as well as lifestyle changes to reduce symptoms.
1) Recurrent pregnancy loss is defined as three or more consecutive pregnancy losses before 20 weeks of gestation. A thorough investigation should be conducted to identify potentially treatable causes.
2) Common etiological factors include uterine anomalies, immunological issues such as antiphospholipid syndrome, endocrine disorders such as thyroid disease or diabetes, genetic factors, and thrombophilic disorders.
3) Evaluation involves a detailed history, physical exam, ultrasound, hormonal and immunological testing. Uterine anomalies require hysteroscopy or laparoscopy. Treatment depends on the underlying cause but may include surgery, medication, lifestyle changes, or cerclage. The goal is to identify modifiable risk factors.
This document discusses prolactinomas, which are pituitary tumors that cause excessive prolactin secretion. It describes the clinical presentation, diagnosis, and management approaches for prolactinomas. Microprolactinomas are small tumors less than 10mm, while macroprolactinomas are larger tumors. The first line treatment is dopamine agonist medication to reduce prolactin levels. Surgical removal may be considered for resistant cases or tumors pressing on nearby structures. Prolactinomas are generally managed medically but require monitoring due to risks of vision changes or hypogonadism from high prolactin levels.
This document summarizes thyroid disease in pregnancy. It discusses how thyroid function changes normally during pregnancy, with relative iodine deficiency and increased levels of thyroid binding globulin and T4 in early gestation. It notes that hyperthyroidism in pregnancy is usually caused by Graves' disease. Left untreated, it can lead to risks for both mother and fetus, including heart failure, thyroid storm, growth restriction and preterm labor. Management involves achieving an euthyroid state through medications like thionamides or propranolol, with close monitoring of thyroid function tests during pregnancy and treatment of any thyroid storm that may occur during labor and delivery.
Management of postterm pregnancy involves balancing risks to the fetus and mother. Postterm is defined as past 42 weeks gestation. Accurately dating the pregnancy is important to avoid false diagnosis. Risks to the fetus include stillbirth, meconium aspiration, and macrosomia. Risks to the mother include dystocia and infection. Studies show inducing labor at 41 weeks reduces stillbirths without increasing C-sections. Methods of antenatal testing after 41 weeks are debated, though monitoring is recommended. While an unfavorable cervix was viewed as a risk factor for C-section, recent evidence suggests underlying issues may be more important. Further research is needed to determine the optimal time for induction to minimize risks
This document discusses morbidly adherant placenta, also known as placenta accreta spectrum (PAS), which is becoming more common due to rising cesarean section rates. PAS occurs when the placenta invades deeply into the uterine wall and does not separate normally during delivery, potentially causing life-threatening hemorrhage. Early diagnosis through ultrasound screening and counseling of patients at high risk, such as those with prior uterine scarring, allows for improved maternal outcomes through preparedness and planned hysterectomy if needed. The key is anticipating PAS, making an accurate prenatal diagnosis, and being prepared to perform an emergency hysterectomy to control bleeding and save the mother's life if manual placental removal fails.
This document discusses epilepsy and pregnancy. Some key points:
- Epilepsy affects 0.5% of women of childbearing age and is the most common neurological disorder complicating pregnancy.
- Seizure frequency may increase, decrease or remain unchanged during pregnancy, depending on the individual. The risk of seizures is highest around delivery.
- Antiepileptic medications used to treat epilepsy can cause birth defects, especially sodium valproate which has been linked to neural tube defects. The risk increases with multiple medications and higher valproate doses.
- Women with epilepsy need folic acid, careful monitoring of seizure frequency and medication levels during pregnancy, and fetal screening for birth defects. Managing epilepsy treatment aims to control
This document discusses thyroid disorders in pregnancy. It notes that thyroid disorders are common in pregnancy, affecting 1-2% of pregnancies with overt disease and 3-5% with subclinical disease. Thyroid screening and treatment in pregnancy can help improve outcomes for both mother and baby, though guidelines vary on who and when to screen. The document reviews thyroid changes in pregnancy, screening recommendations, treatment of hypothyroidism and hyperthyroidism, and complications like postpartum thyroid dysfunction.
This document discusses thyrotoxicosis (hyperthyroidism) during pregnancy. It notes the physiological changes in thyroid function during pregnancy, including increases in thyroid binding globulin and decreases in plasma iodide levels. It describes the signs and symptoms of maternal hyperthyroidism as well as its most common cause, Graves' disease. Guidelines are provided for clinical management, including use of thionamide medications like propylthiouracil to control thyroid levels while monitoring the fetus. Treatment may also include beta blockers, iodine, or subtotal thyroidectomy in rare cases. Radioactive iodine therapy is contraindicated in pregnancy due to risks to the fetal thyroid.
The document summarizes physiological changes in thyroid function during pregnancy and management of hyperthyroidism. Key points:
1) Thyroid binding globulin, TT4, and TT3 levels increase during pregnancy to compensate for decreased FT4 and FT3. TSH decreases in the first trimester and increases in the second and third trimesters.
2) Hyperthyroidism in pregnancy is usually caused by Graves' disease and can cause complications if unmanaged. Treatment involves antithyroid medications like PTU and carbimazole.
3) Treatment aims to control hyperthyroidism rapidly and maintain euthyroidism with the lowest effective drug dose to avoid fetal hypothyroidism or goiter
Thyroid disorders are common in pregnancy and can affect both mother and fetus if not properly managed. Hypothyroidism, the most common disorder, affects 2-3% of pregnancies and can cause complications like preterm birth and low birth weight if the mother is not treated with levothyroxine. The treatment aims to maintain normal TSH and free T4 levels through frequent monitoring and dose adjustments. Universal screening is not recommended but high-risk women should be tested. Neonatal screening helps detect congenital hypothyroidism early to prevent intellectual disability. Proper treatment and monitoring by endocrinologists and obstetricians can help ensure positive outcomes.
Hyperthyroidism and hypothyroidism can complicate pregnancy and cause issues for both the mother and fetus. Hyperthyroidism occurs in 2 per 1000 pregnancies and can lead to miscarriage, preterm delivery, preeclampsia, and cardiac failure in the mother as well as intrauterine growth restriction and premature birth in the fetus. It is caused by thyroid stimulating antibodies crossing the placenta and producing neonatal hyperthyroidism. Hypothyroidism can cause complications like preeclampsia and anemia if untreated. Treatment involves monitoring thyroid levels and adjusting medication doses as thyroid needs increase in pregnancy.
This document discusses thyroid function and hypothyroidism during pregnancy. It begins with an overview of thyroid physiology and the changes that occur during pregnancy, including increases in thyroid binding globulin and decreases in free thyroid hormones. It then discusses fetal thyroid development and the risks of maternal hypothyroidism. The document outlines the causes, signs, and laboratory tests for hypothyroidism and how the condition can impact pregnancy outcomes if uncontrolled. It recommends treatment with levothyroxine to maintain thyroid stimulating hormone levels in the appropriate range for pregnancy trimesters. The goal of treatment is to minimize risks of adverse effects for both the mother and fetus.
This document discusses hyperthyroidism (excess thyroid hormone). There are two main types - those caused by excess hormone production and those caused by release of stored hormone. Primary causes include Graves' disease while secondary causes include Plummer's disease and toxic nodules. Signs and symptoms, investigations, and treatment options like antithyroid drugs, surgery, and radioiodine are described for different patient groups. Management involves controlling hyperthyroidism and returning the patient to a euthyroid state.
The document provides information on Addisonian crisis, also known as an acute adrenal crisis. It begins with objectives of being able to promptly identify and treat an Addisonian crisis to save a patient's life, as the presentation can mimic other conditions. The document then contrasts acute adrenal crisis with Addison's disease, which develops more gradually over months to years. It provides an overview of epidemiology, anatomy, physiology of the adrenal glands and cortisol. It describes the signs and symptoms of Primary/Addison's adrenal insufficiency and discusses various causes including autoimmune disease and exogenous steroid use. Acute adrenal crisis can be fatal if not identified and treated immediately with cortisol replacement.
This document summarizes guidelines and studies on screening and management of subclinical hypothyroidism during pregnancy. Key points include:
- Guidelines from thyroid societies recommend trimester-specific reference ranges for TSH and treatment of SCH with levothyroxine.
- Studies show mixed results on associations between SCH and adverse pregnancy/child outcomes, and limited benefits of levothyroxine treatment.
- Targeted high-risk screening misses a significant percentage of women with thyroid dysfunction compared to universal screening.
- While evidence is still limited, most experts recommend universal screening to detect and treat overt hypothyroidism given potential benefits.
This document discusses the management of various endocrine diseases in pregnancy, including hypothyroidism, hyperthyroidism, prolactinoma, and Addison's disease. It provides guidance on treatment, monitoring, risks of under-treatment, and complications for each condition. Case examples are presented and management strategies are outlined, emphasizing the importance of optimizing treatment to reduce risks while minimizing harm to the mother and fetus. Close monitoring is recommended for conditions like Graves' disease and prolactinoma.
This document summarizes the case of a patient presenting with symptoms of myxedema crisis including loss of consciousness for 5 days. On examination, the patient was found to have hypothyroid features including an unrousable mental state, dry skin, bradycardia, and hypothermia. Laboratory tests confirmed very high TSH levels and low FT3 and FT4, consistent with severe untreated hypothyroidism. The patient was treated with intravenous thyroxine, hydrocortisone, saline and antibiotics. Myxedema crisis carries high mortality if not treated but can be managed with thyroid hormone replacement and treating any underlying infections or precipitating causes.
This presentation was present by my friend during emergency posting seminar with Dr.Mohd. Kamal Mohd. Arshad. I upload this ppt here for all of us and my own reference too. Good luck in your life.
This document discusses thyrotoxicosis, which results from excess thyroid hormone production regardless of cause. It is one of the more common endocrine disorders seen by family physicians. The causes of thyrotoxicosis include Graves' disease, toxic multinodular goiter, solitary toxic nodule, and thyroiditis. Graves' disease is an autoimmune condition characterized by a diffuse goiter, ophthalmopathy, and dermopathy. Toxic multinodular goiter develops from autonomy in a pre-existing nodular goiter. A solitary toxic nodule refers to autonomy developing in an otherwise normal thyroid. Thyroiditis can cause a transient thyrotoxic phase followed by hypothyroidism. Treatment depends on
This document discusses the contemporary management of subclinical hypothyroidism during pre-conception and pregnancy. It begins by outlining the physiological changes in thyroid function that occur during pregnancy, including increases in thyroid-binding globulin and human chorionic gonadotropin that impact thyroid hormone levels. It then defines hypothyroidism and subclinical hypothyroidism. While the risks of untreated overt hypothyroidism on maternal and fetal health are well-established, the risks and benefits of treating subclinical hypothyroidism are still debated. Treatment of subclinical hypothyroidism in pregnancy aims to normalize maternal thyroid function and reduce risks, though randomized controlled trials are still needed.
This document discusses diabetic ketoacidosis (DKA), providing information on its pathophysiology, classification, precipitating factors, signs and symptoms, laboratory investigations, management, and goals of treatment. It classifies DKA as mild, moderate or severe based on plasma glucose, arterial pH, serum bicarbonate, urine ketones, and anion gap. The key aspects of management include fluid resuscitation to restore intravascular volume, insulin therapy to reduce glucose and ketone levels, and potassium supplementation to correct deficiencies. Bicarbonate supplementation is only recommended if the pH is less than 6.9.
This document discusses hyperosmolar hyperglycemic state (HHS), also known as hyperosmolar hyperglycemic nonketotic syndrome (HHNK). It defines HHS as a life-threatening emergency characterized by severe hyperglycemia, hyperosmolality, and dehydration without significant ketoacidosis. The document outlines diagnostic features, etiology, symptoms, physical exam findings, complications, differential diagnosis, investigations, and management of HHS.
The document discusses thyroid disease in pregnancy. It describes the physiological changes in thyroid function during pregnancy, including increases in thyroid binding globulin and thyroid hormone levels. It covers the signs, symptoms, risks and treatment of both hyperthyroidism and hypothyroidism in pregnancy. For hyperthyroidism, the most common cause is Graves' disease. Risks include early pregnancy loss, fetal growth issues, and neonatal hyperthyroidism. Treatment involves antithyroid medications. For hypothyroidism, the most common causes are Hashimoto's thyroiditis and iodine deficiency. Risks include infertility, miscarriage, and impaired neurodevelopment. Treatment is levothyroxine supplementation.
A 58-year-old woman presents with symptoms of hyperthyroidism including anxiety, tremors, sweating, palpitations and insomnia. On exam she has a modest, non-tender goiter. Thyroid function tests show a suppressed TSH and elevated free T4, consistent with primary hyperthyroidism. A thyroid uptake scan shows diffuse homogeneous uptake, consistent with Graves' disease. She is started on methimizole to treat her hyperthyroidism due to Graves' disease.
Thyroid storm, or thyrotoxic crisis, is a life-threatening complication of hyperthyroidism characterized by multisystem involvement. It occurs when a precipitating event causes a sudden increase in thyroid hormone levels in a patient with hyperthyroidism. Common precipitants include discontinuing antithyroid medication or thyroid surgery. Thyroid storm requires prompt treatment with beta-blockers, antithyroid drugs, iodine, glucocorticoids, and supportive care to reduce mortality, which is estimated at 8-25% without treatment. Symptoms include fever, tachycardia, heart failure, neurological changes, and gastrointestinal issues. Diagnosis is clinical based on symptoms and elevated thyroid hormone levels
This document summarizes information about hyperthyroidism and hypothyroidism, including their common causes, symptoms, signs, investigations, and treatment approaches. The most common causes are Graves' disease, multinodular goiter, and solitary thyroid adenomas. Common symptoms include weight loss, heat intolerance, palpitations, and tremors. Diagnostic testing involves measuring T3, T4, and TSH levels. Treatment depends on the underlying cause, and may include antithyroid drugs, radioactive iodine, surgery, or beta-blockers to control symptoms.
Khadeeja Nasser, a 35-year-old woman, presented with fatigue, weight gain, cold intolerance, dry skin, constipation, and irregular periods over the past six months. Examination found fatigue, puffy face, slow pulse, dry skin, and sluggish reflexes. Labs found elevated TSH and low T4, with positive thyroid peroxidase antibodies. This suggests Hashimoto's thyroiditis causing hypothyroidism. Hypothyroidism presents with the symptoms described and is diagnosed by elevated TSH and low T4. It is managed with levothyroxine replacement.
Thyroid storm is basically a life threatening acute exacerbation of the clinical features of thyrotoxicosis.
Thyroid storm also known as thyroid crisis is an acute, life threatening hypermetabolic state induced by excessive activity of thyroid hormones in individuals with thyrotoxicosis.
Exact pathogenesis not understood.
No clear cut clinical feature separation from thyrotoxicosis.
precipitants of thyroid storm include the following
Infection, especially pneumonia
Cerebrovascular accident
Acute coronary syndrome, Congestive heart failure
Pulmonary embolus
Diabetic ketoacidosis
Parturition / toxemia
Major trauma
Surgery
Iodine 131 Rx or iodine contrast agents
Rapid withdrawl of antithyroid medications
Although the exact pathogenesis of thyroid storm is not fully understood, the following theories have been proposed:
Patients with thyroid storm reportedly have relatively higher levels of free THs than patients with uncomplicated thyrotoxicosis, although total TH levels may not be increased.
Adrenergic receptor activation is another hypothesis. Sympathetic nerves innervate the thyroid gland, and catecholamines stimulate TH synthesis. In turn, increased THs increase the density of beta-adrenergic receptors, thereby enhancing the effect of catecholamines.
The dramatic response of thyroid storm to beta-blockers and the precipitation of thyroid storm after accidental ingestion of adrenergic drugs such as pseudoephedrine support this theory. This theory also explains normal or low plasma levels and urinary excretion rates of catecholamines.
However, it does not explain why beta-blockers fail to decrease TH levels in thyrotoxicosis.
Another theory suggests a rapid rise of hormone levels as the pathogenic source. A drop in binding protein levels, which may occur postoperatively, might cause a sudden rise in free hormone levels. In addition, hormone levels may rise rapidly when the gland is manipulated during surgery, during vigorous palpation during examination, or from damaged follicles following RAI therapy.
Other proposed theories include alterations in tissue tolerance to THs, the presence of a unique catecholaminelike substance in thyrotoxicosis, and a direct sympathomimetic effect of TH as a result of its structural similarity to catecholamines.
General symptoms
Fever
Profuse sweating
Poor feeding and weight loss
Respiratory distress
Fatigue (more common in older adolescents)
GI symptoms
Nausea and vomiting
Diarrhea
Abdominal pain
Jaundice
Neurologic symptoms
Anxiety (more common in older adolescents)
Altered behavior
Seizures, coma
THYROID DISORDERS IN PREGNANCY LAST.pptxrohiljain11
This document discusses thyroid disorders in pregnancy. It notes that thyroid function changes significantly during pregnancy, with increases in thyroid-binding globulin and human chorionic gonadotropin stimulating the thyroid. Both hypothyroidism and hyperthyroidism can cause complications if not properly managed. The document outlines diagnostic criteria and treatment guidelines for hypothyroidism and hyperthyroidism in each trimester, including dose adjustments and monitoring of levothyroxine treatment or use of antithyroid medications. Postpartum thyroiditis and fetal monitoring are also discussed.
This document summarizes thyroid storm, an extreme manifestation of hyperthyroidism. It describes the etiology as usually involving a precipitating factor in addition to hyperthyroidism. Signs and symptoms are severe and can involve multiple organ systems. Management requires promptly blocking thyroid hormone synthesis and secretion, blocking peripheral thyroid hormone action, and providing supportive care measures to stabilize the patient's homeostasis and address underlying causes.
Hyperthyroidism and thyrotoxicosis occur when the thyroid gland overproduces thyroid hormones. Thyroid storm is a life-threatening exacerbation of thyrotoxicosis caused by factors like infection, surgery, or medication changes. It involves fever, sweating, tachycardia, anxiety, and heart failure. Treatment focuses on cooling the patient, blocking further hormone production with antithyroid drugs and iodine, and supporting heart and brain function with beta-blockers and glucocorticoids. Thyroidectomy may be required for severe cases not responding to medical management.
The thyroid gland is located in the lower neck and produces thyroid hormones that regulate metabolism. Hyperthyroidism occurs when the thyroid gland is overactive and produces excessive thyroid hormones. Graves' disease is the most common cause of hyperthyroidism and results in symptoms like nervousness, rapid heartbeat, weight loss, and bulging eyes. Treatment options for hyperthyroidism include radioactive iodine therapy which destroys the thyroid gland, anti-thyroid medications that reduce hormone production, or surgery to remove part of the thyroid gland.
This document provides an overview of thyroid disorders and diagnostic tests. It discusses various thyroid function tests including TSH, free T4, T3, and thyroid antibodies. It describes how to interpret abnormal thyroid function test results and outlines approaches to common thyroid disorders like Graves' disease, subacute thyroiditis, and hypothyroidism. Treatment options for hyperthyroidism such as antithyroid medications, radioiodine therapy, and surgery are also summarized. The document is intended as a brief review of key endocrinology concepts that will be covered in more detail in video lectures.
Archer USMLE step 3 Endocrinology lecture notes. These lecture notes are samples and are intended for use with Archer video lectures. For video lectures, please log in at http://www.ccsworkshop.com/Pay_Per_View.html
1. The thyroid gland secretes two main hormones: thyroxine (T4) and triiodothyronine (T3) in a ratio of 15:1.
2. T4 and T3 are bound to serum proteins and transported through the bloodstream, with the free unbound levels regulating thyroid function.
3. Peripherally, T4 is converted to the more potent T3, which enters cells and binds nuclear receptors to increase protein synthesis and cellular metabolism.
Thyroid storm is a life-threatening exacerbation of hyperthyroidism that can be fatal if not treated promptly and aggressively. It is usually precipitated by stress in individuals with poorly controlled hyperthyroidism. Signs and symptoms involve multiple organ systems and include fever, tachycardia, heart failure, gastrointestinal issues, and altered mental status. Treatment requires addressing the underlying hyperthyroidism with antithyroid drugs, iodine, beta-blockers, and glucocorticoids to suppress hormone production and effects. Managing precipitating factors, supportive care, and monitoring for complications are also important.
Graves' disease is an autoimmune disorder causing hyperthyroidism in 60-80% of cases. Genetic and environmental factors contribute to susceptibility. Smoking increases the risk of ophthalmopathy. Hyperthyroidism is caused by thyroid stimulating immunoglobulins that activate the TSH receptor and cause overproduction of thyroid hormones. Treatment involves antithyroid drugs, radioiodine ablation, or surgery. Ophthalmopathy may cause eye swelling, bulging, and vision issues. Thyroiditis refers to inflammation of the thyroid and can be acute, subacute, or chronic depending on duration and symptoms. Subacute thyroiditis causes thyroid pain and temporary changes in thyroid function. Pregnancy causes changes in
Diagnosis and treatment of hypothyroidism.pptxvivianOkoli1
Hypothyroidism is a common endocrine disorder where the thyroid gland does not produce enough hormones. It can be caused by iodine deficiency, autoimmune disease, or drugs/radiation affecting the thyroid. Symptoms are often subtle and vary in children, women, and elderly people. Laboratory tests show low thyroid hormones and high TSH. Treatment is with levothyroxine replacement to restore hormone levels, with dose adjustments over time based on symptoms and follow-up tests. In severe cases, myxoedema coma requires emergency treatment in hospital.
Thyroid storm, also known as thyrotoxic crisis, is a life-threatening complication of hyperthyroidism characterized by sudden multisystem involvement. It can occur in any diagnosed or undiagnosed case of hyperthyroidism. Thyroid storm is diagnosed clinically based on symptoms involving the central nervous, cardiovascular, gastrointestinal and hepatic systems. Treatment involves controlling adrenergic tone with beta-blockers, reducing thyroid hormone synthesis with thionamides, and blocking peripheral thyroid hormone conversion. Aggressive treatment is required for patients scoring above 45 on the Burch-Wartofsky Point Scale or meeting the criteria for definite or suspected thyroid storm per the Japanese Thyroid Association guidelines.
This document discusses endocrine diseases and their implications for anesthesia. It covers both hyperthyroidism and hypothyroidism in detail. For hyperthyroidism, it describes the signs and symptoms, causes, effects on the cardiovascular system, and treatment approaches including antithyroid medications, beta blockers, iodine, and surgery. It provides guidance on preoperative preparation and intraoperative management. For hypothyroidism, it discusses signs and symptoms, effects on the cardiovascular system, diagnosis, and treatment with levothyroxine. It notes risks for anesthesia and importance of rendering patients euthyroid prior to elective surgery.
This document provides information on thyroid emergencies including thyroid storm and myxedema coma. It reviews the pathophysiology of thyroid diseases and hormones. Thyroid storm is a life-threatening exacerbation of thyrotoxicosis that can be precipitated by stressors. It requires rapid cooling, beta blockade, antithyroid medications, steroids and treating the underlying cause. Myxedema coma is a rare complication of untreated hypothyroidism with high mortality. It presents with altered mental status and hypothermia requiring thyroid hormone replacement.
Does Over-Masturbation Contribute to Chronic Prostatitis.pptxwalterHu5
In some case, your chronic prostatitis may be related to over-masturbation. Generally, natural medicine Diuretic and Anti-inflammatory Pill can help mee get a cure.
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8 Surprising Reasons To Meditate 40 Minutes A Day That Can Change Your Life.pptxHolistified Wellness
We’re talking about Vedic Meditation, a form of meditation that has been around for at least 5,000 years. Back then, the people who lived in the Indus Valley, now known as India and Pakistan, practised meditation as a fundamental part of daily life. This knowledge that has given us yoga and Ayurveda, was known as Veda, hence the name Vedic. And though there are some written records, the practice has been passed down verbally from generation to generation.
Basavarajeeyam is a Sreshta Sangraha grantha (Compiled book ), written by Neelkanta kotturu Basavaraja Virachita. It contains 25 Prakaranas, First 24 Chapters related to Rogas& 25th to Rasadravyas.
2. Thyroid disease is the second most common
endocrine disease affecting women of
reproductive age
3. a generic term referring to a clinical and biochemical
state resulting in over-production of and exposure to
thyroid hormone
Overt hyperthyroidism complicates approximately 2 in
1,000 pregnancies.
4. Pregnant women with hyperthyroidism are at
increased risk for:
spontaneous pregnancy loss
congestive heart failure
thyroid storm
preterm birth
Preeclampsia
fetal growth restriction, and
increased perinatal morbidity and mortality
5. the most common cause of thyrotoxicosis in
pregnancy
An autoimmune condition characterized by
production of thyroid-stimulating immunoglobulin
(TSI) and thyroid-stimulating hormone binding
inhibitory immunoglobulin (TBII)
facilitate the thyroid-stimulating hormone
(TSH) receptor in the mediation of thyroid
stimulation and inhibition
6. Hyperthyroidism- thyrotoxicosis resulting from an
abnormally functioning thyroid gland.
Thyroid storm- acute, severe exacerbation of
hyperthyroidism
7. associated with hyperemesis gravidarum
can be due to high levels of human chorionic
gonadotropin (hCG) resulting from molar pregnancy
high hCG levels TSH receptor stimulation and
temporary hypothyroidism
rarely symptomatic
treatment with antithyroxine drugs- not beneficial
expectant management
not associated with poor pregnancy outcomes
8. Thyroxine (T4), the major secretory product of the
thyroid gland, is converted in peripheral tissues to
triiodothyronine (T3)
T3- biologically active form
T4- secretion is under the direct control of pituitary
TSH
T4 and T3 are transported in the peripheral circulation
bound to thyroxine-binding globulin (TBG),
transthyretin (formerly called "prealbumin") and
albumin.
Less than 0.05% of plasma T4, and less than 0.5% of
plasma T3, are unbound and able to interact with
target tissues
9. 20 weeks' gestation
reduced hepatic clearance
estrogen-induced change in the structure of TBG that
prolongs serum half-life
plasma TBG increases 2.5 folds 25% to 45%
increase in serum total T4 (TT4) from a pregravid level
of 5 to 12 mg to 9 to 16 mg
** Total T3 (TT3) increases by about 30% in the first
trimester and by 50% to 65% later
10. Pregnancy increase in available protein transient
change in free T4 (FT4) and free thyroxine index (FTI)
in the first trimester (possibly related to an increase in
hCG)
Increased concentrations of TSH stimulate
restoration of the free serum T4 level, such that FT4
and FTI levels are generally maintained within the
normal non-pregnant range
11. Increase in volume
Echo structure remains unchanged (Plasma iodide
levels decrease in pregnancy due to fetal use of iodide
and increased maternal renal clearance)
15% to 18% increase in size of the thyroid gland
enlargement usually resolves after delivery
not associated with abnormal thyroid function tests
12. Mild hyperthyroidism:
Fatigue
increased appetite
Vomiting
Palpitations
Tachycardia
heat intolerance,
Increased urinary
frequency
Insomnia
Emotional instability
The suspicion increases if
patient has
Tremor
Nervousness
frequent stools
excessive sweating
brisk reflexes
muscle weakness
goiter
Hypertension
weight loss.
Grave's ophthalmopathy (stare,
lid lag and retraction,
exophthalmos)
dermopathy (localized or
pretibial myxedema)
13. Untreated hyperthyroidism poses considerable
maternal and fetal risks, including preterm delivery,
severe preeclampsia, heart failure, and thyroid storm
14.
15. - a hypermetabolic complication of hyperthyroidism:
hyperpyrexia (temperature >41ºC)
cardiovascular compromise (tachycardia out of
proportion to the fever, dysrhythmia, cardiac failure)
gastrointestinal upset (diarrhea)
central nervous system changes (restlessness,
nervousness, changed mental status, confusion, and
seizures).
16. Thyroid storm is a clinical diagnosis, and treatment
should be initiated before confirmatory test results
are available.
17. Other signs of thyrotoxicosis in any patient with
postpartum congestive heart failure:
tachycardia
severe hypertension
central nervous system (CNS) features, such as coma
after cesarean section or seizures suggestive of
eclampsia
Delay in diagnosis increase the risk of maternal
mortality
18. Thyroid storm is usually seen in patients with poorly
controlled hyperthyroidism complicated by additional
physiologic stressors, such as infection, surgery,
thromboembolism, preeclampsia, and parturition
19. CBC (Leukocytosis)
Thyroid function test results
are consistent with
hyperthyroidism (elevated
FT4/FT3 and depressed TSH)
but they may not always
correlate with the severity of
the thyroid storm
Baseline electrolyte
(occasionally hypercalcemia)
Glucose
Renal
Liver function testing
(elevated hepatic enzymes)
Coagulation studies
CT or MRI of the brain
(unconscious patients,
signs of focal CNS signs)
blood, uterine and wound
cultures (as appropriate)
chest x-ray
12-lead electrocardiogram
(ECG) and continuous
cardiac monitoring
Pulse oximetry
blood gas analysis
20. Thyroid storm is a clinical diagnosis based on
severe signs of thyrotoxicosis:
significant hyperpyrexia (>103ºF or >41ºC)
neuropsychiatric symptoms
Tachycardia with a pulse rate exceeding 140 beats/min
congestive heart failure
Gastrointestinal symptoms (nausea and vomiting)
accompanied by liver compromise
21. Obstetric intensive care unit (ICU)/ ICU that has
continuous fetal monitoring and can handle an
emergent delivery
Therapy is designed to:
Reduce the synthesis and release of thyroid hormone
Remove thyroid hormone from the circulation and
increase the concentration of TBG
Block the peripheral conversion of T4 to T3
Block the peripheral actions of thyroid hormone
Treat the complications of thyroid storm and provide
support
Identify and treat potential precipitating conditions
22. Supportive adjunctive care for the patient in thyroid storm
are:
IV fluids and electrolytes
Cardiac monitoring
Consideration of pulmonary artery catheterization
(central hemodynamic monitoring to guide beta-blocker
therapy during hyperdynamic cardiac failure)
Cooling measures: blanket, sponge bath, acetaminophen,
avoid salicylates (risk of increased T4). Acetaminophen
is the drug of choice
Oxygen therapy (consider arterial line to follow serial
blood gases)
Nasogastric tube
23. Reduce synthesis of thyroid hormones:
Thionamides : propylthiouracil (PTU)
Methimazole)
inhibit iodination of tyrosine -- leading to reduce
synthesis of thyroid hormones and block peripheral
conversion of T4 to T3
can reduce the T3 concentration by 75%
24. Iodide (Lugol's iodine, SSKI (Strong Solution of
Potassium Iodide), sodium iodide, orografin, or lithium
carbonate)
inhibit proteolysis of thyroglobulin block the
release of stored hormone
**Because one of the side effects is an initial increase in
production of thyroid hormone, it is therefore very
important to start PTU before you give iodides
25. Glucocorticoids
block release of stored hormone (as do iodides), and
peripheral conversion of T4 to T3 (as do thionamides)
They may also bolster adrenal function, and prevent
adrenal insufficiency
26. PTU orally or via nasogastric tube, 300-800 mg loading dose
followed by 150-300 mg every 6 hours
One hour after instituting PTU give: Sodium iodide, 500 mg every
8-12 hours or oral Lugol's solution, 30-60 drops daily in divided
doses.
Iodides may be discontinued after initial improvement
Give adrenal glucocorticoids (Hydrocortisone, 100 mg IV every 8
hour, or Prednisone, 60 mg PO every day, or
Dexamethasone, 8 mg PO every day)
Glucocorticoids may be discontinued after initial improvement
27. Beta-blocker agents --
Propranolol can be used to control autonomic symptoms
(especially tachycardia)
Some effect on inhibition of peripheral conversion of T4 to T3,
but will not alter thyroid hormone release nor prevent thyroid
storm.
Use with caution: it has a tendency to increase pulmonary
diastolic pressure, and cardiac failure is a frequent
presentation of thyroid storm
Reserved for heart rates of 120 beats per minute or higher
Propranolol, labetalol, and esmolol
28. Propranolol,1-2 mg/min IV or dose sufficient to slow heart rate
to 90 bpm; or 20-80 mg PO or via nasogastric tube every 4-6
hourly
Esmolol, a short-acting beta-acting antagonist given IV with a
loading dose of 250 to 500 µg/kg of body weight followed by a
continuous infusion at 50 to 100 µg/kg/min
Echocardiogram and/or pulmonary artery catheter to help guide
management, especially in cardiac failure
If patient has severe bronchospasm -- give 1-5 mg reserpine
every 4-6 hours or 1 mg/kg orally of guanethidine every 12
hours.
29. Heart failure due to cardiomyopathy from excessive
thyroxine in women with uncontrolled
hyperthyroidism is more common in pregnant women
Same treatment as that of thyroid storm
Medical emergency
Give phenobarbital to control restlessness
Phenobarbital: 30 to 60 mg orally every 6-8 hours as
needed
Plasmapheresis or peritoneal dialysis
to remove circulating thyroid hormone
reserved for patients who do not respond to conventional therapy
Subtotal thyroidectomy (during second-trimester pregnancy)
or radioactive iodine (postpartum)
for unsuccessful conventional therapy
30. Most asymptomatic women should have a TSH and free
T4 performed approximately 6 weeks postpartum
PTU and methimazole are excreted in breast milk
PTU is largely protein bound and does not seem to pose
a significant risk to the breastfed infant
Methimazole has been found in breastfed infants of
treated women in amounts sufficient to cause thyroid
dysfunction
at low doses (10-20 mg/d) it does not seem to pose a major risk to
the nursing infant
31. PTU
first-line treatment for Grave's disease in pregnancy due
to lower risks of teratogenicity than methimazole.
It crosses the human placenta and associated with fetal
hypothyroidism
Cordocentesis is sometimes recommended to test fetal
thyroid function
does not readily crosses membranes
milk concentrations are quite low
32. Methimazole (Thiamazole, Mercazole, Tapazole):
Second-line treatment of Grave's disease
crosses the human placenta and can induce fetal goiter
and even cretinism in a dose-dependent fashion
commonly associated with fetal anomalies such as
aplasia cutis, esophageal atresia, and choanal atresia
Long-term follow-up studies of exposed children:
no deleterious effects on their thyroid function or physical
and intellectual development with doses up to 20 mg/d
excreted in breast milk
33. The American College of Obstetricians and
Gynecologists (ACOG) recommends treatment for
women with a systolic blood pressure higher than
170 mmHg and/or diastolic blood pressure above
109 mmHg
There is no consensus whether lesser degrees of
hypertension require treatment during pregnancy
because antihypertensive therapy improves only
the maternal, not the fetal, outcome in women with
mild to moderate chronic hypertension
34. Radioactive iodine (iodine-131; I-131):
contraindicated in pregnant women
cost-effective, safe, and reliable treatment for
hyperthyroidism in non-pregnant women
ACOG recommendation: women should avoid pregnancy
for 4-6 months following treatment
Detrimental effects on the thyroid of the developing
fetus as a result of I-131 treatment for thyrotoxicosis of
the mother in the first trimester of pregnancy are
reported.
Breast-feeding should be avoided for at least 120 days
after treatment
35. Thyroid storm
a life-threatening condition, requiring early recognition and
aggressive therapy in an intensive care unit setting.
During gestation, women with hyperthyroidism should have
their thyroid function checked every 3-4 weeks.
Grave's disease represents the most common cause of
maternal hyperthyroidism during pregnancy
Only 0.2% of gestations are complicated by thyroid storm and
more than 90% of cases are caused by Grave's disease
Increased production of thyroid hormone occurs when
autoantibodies (thyroid-stimulating antibody [TSAb] --
formerly known as LATS [long-acting thyroid stimulator])
against TSH receptors -- acts as TSH agonists.
36.
37.
38. Thyroid Storm: Critical Care In Obstetrics
WHEC Practice Bulletin and Clinical Management
Guidelines for healthcare providers. Educational grant
provided by Women's Health and Education Center
(WHEC).
Published: 2 June 2010
Editor's Notes
Grave's disease, the most common cause of thyrotoxicosis in pregnancy, is an autoimmune condition characterized by production of thyroid-stimulating immunoglobulin (TSI) and thyroid-stimulating hormone binding inhibitory immunoglobulin (TBII)
These two antibodies facilitate the thyroid-stimulating hormone (TSH) receptor in the mediation of thyroid stimulation and inhibition, respectively.
Hyperthyroidism is thyrotoxicosis resulting from an abnormally functioning thyroid gland.
Thyroid storm is an acute, severe exacerbation of hyperthyroidism.
There is a unique form of hyperthyroidism associated with pregnancy called gestational transient thyrotoxicosis. It is typically associated with hyperemesis gravidarum, and can be due to high levels ofhuman chorionic gonadotropin (hCG) resulting from molar pregnancy. These high hCG levels lead to TSH receptor stimulation and temporary hypothyroidism. Women with gestational transient thyrotoxicosis are rarely symptomatic and treatment with antithyroxine drugs has not been shown to be beneficial (4). With expectant management of hyperemesis gravidarum, serum free T4 levels usually normalize in parallel with the decline in hCG concentrations as pregnancy progresses beyond the first trimester. Notably, TSH levels may remain partially depressed for several weeks after free T4 levels have returned to normal range. Gestational transient thyrotoxicosis has not been associated with poor pregnancy outcomes.
Impact of Pregnancy on Thyroid:
Thyroxine (T4), the major secretory product of the thyroid gland, is converted in peripheral tissues to triiodothyronine (T3), the biologically active form of this hormone. T4 secretion is under the direct control of pituitary TSH. The cell surface receptor for TSH is similar to the receptors for luteinizing hormone (LH) and human chorionic gonadotropin (hCG). T4 and T3 are transported in the peripheral circulation bound to thyroxine-binding globulin (TBG), transthyretin (formerly called "prealbumin") and albumin. Less than 0.05% of plasma T4, and less than 0.5% of plasma T3, are unbound and able to interact with target tissues (4). Routine T4 measurements reflect total serum concentration and may be altered by increases or decreases in concentrations of circulating proteins.
By 20 weeks' gestation, plasma TBG increases 2.5 folds because of reduced hepatic clearance and an estrogen-induced change in the str ucture of TBG that prolongs serum half-life (5). This TBG alteration causes significant changes in some of the test results in pregnancy. There is a 25% to 45% increase in serum total T4 (TT4) from a pregravid level of 5 to 12 mg to 9 to 16 mg. Total T3 (TT3) increases by about 30% in the first trimester and by 50% to 65% later
The increase in available protein binding induced by pregnancy causes a transient change in free T4 (FT4) and free thyroxine index (FTI) in the first trimester (possibly related to an increase in hCG). Increased concentrations of TSH stimulate restoration of the free serum T4 level, such that FT4 and FTI levels are generally maintained within the normal non-pregnant range
. Ultrasound evaluation of the thyroid gland during pregnancy shows an increase in volume, whereas its echo structure remains unchanged (Plasma iodide levels decrease in pregnancy due to fetal use of iodide and increased maternal renal clearance. The result in many pregnant women is a 15% to 18% increase in size of the thyroid gland. The enlargement usually resolves after delivery and is not associated with abnormal thyroid function tests.
Mild hyperthyroidism mimics symptoms of normal pregnancy, and can be present as fatigue, increased appetite, vomiting, palpitations, tachycardia, heat intolerance, increased urinary frequency, insomnia, and emotional instability. The suspicion increases if patient has tremor, nervousness, frequent stools, excessive sweating, brisk reflexes, muscle weakness, goiter, hypertension, or weight loss. Grave's ophthalmopathy (stare, lid lag and retraction, exophthalmos) and dermopathy (localized or pretibial myxedema) are diagnostic.
The disease usually gets worse in the first trimester but typically moderates later in pregnancy. Untreated hyperthyroidism poses considerable maternal and fetal risks, including preterm delivery, severe preeclampsia, heart failure, and thyroid storm (8). Although nausea is common in early pregnancy, the occurrence of hyperemesis gravidarum together with weight loss can signify overt hyperthyroidism. Thyroid testing may be beneficial in these circumstances.
The characteristics of thyroid storm, which is a hypermetabolic complication of hyperthyroidism, and hyperpyrexia (temperature >41ºC), cardiovascular compromise (tachycardia out of proportion to the fever, dysrhythmia, cardiac failure), gastrointestinal upset (diarrhea), and central nervous system changes (restlessness, nervousness, changed mental status, confusion, and seizures). Thyroid storm is a clinical diagnosis, and treatment should be initiated before confirmatory test results are available
. In many patients there is absence of classic symptoms. Be alert for other signs of thyrotoxicosis in any patient with postpartum congestive heart failure, tachycardia, and severe hypertension (9). Occasionally, the diagnosis may be obfuscated by central nervous system (CNS) features, such as coma after cesarean section or seizures suggestive of eclampsia. The resulting delay in diagnosis can increase the risk of maternal mortality.
patients with focal CNS signs that do not respond to specific thyroid storm therapy are at risk of atrial fibrillation and CNS embolization so investigate for cerebral emboli and prescribe anticoagulants if necessary.
A echocardiogram is helpful for management in cases where cardiac decompensation is suspected.
Pulse oximetry should be used to monitor peripheral arterial oxygen saturation
blood gas analysis will help acid-base balance assessment.
Thyroid storm is a clinical diagnosis based on severe signs of thyrotoxicosis:
with significant hyperpyrexia (>103ºF or >41ºC) and neuropsychiatric symptoms that are essential for the clinical diagnosis. Tachycardia with a pulse rate exceeding 140 beats/min is not uncommon, and congestive heart failure is a frequent complication. Gastrointestinal symptoms such as nausea and vomiting, accompanied by liver compromise, have been reported.
Management of thyroid storm is best accomplished in an obstetric intensive care unit (ICU), or an ICU that has continuous fetal monitoring and can handle an emergent delivery. Therapy is designed to:
Reduce the synthesis and release of thyroid hormone;
Remove thyroid hormone from the circulation and increase the concentration of TBG;
Block the peripheral conversion of T4 to T3;
Block the peripheral actions of thyroid hormone;
Treat the complications of thyroid storm and provide support;
Identify and treat potential precipitating conditions.
Supportive adjunctive care for the patient in thyroid storm are:
IV fluids and electrolytes;
Cardiac monitoring;
Consideration of pulmonary artery catheterization (central hemodynamic monitoring to guide beta-blocker therapy during hyperdynamic cardiac failure);
Cooling measures: blanket, sponge bath, acetaminophen, avoid salicylates (risk of increased T4). Acetaminophen is the drug of choice;
Oxygen therapy (consider arterial line to follow serial blood gases);
Nasogastric tube if patient is unable to swallow (may be only avenue for propylthiouracil administration).
Medication to reduce synthesis of thyroid hormones are: thionamides (propylthiouracil (PTU) and methimazole); iodide and glucocorticoids. These drugs should be started as soon as diagnosis of thyroid storm is made. PTU and methimazole inhibit iodination of tyrosine -- leading to reduce synthesis of thyroid hormones and block peripheral conversion of T4 to T3 (11). These drugs alone can reduce the T3 concentration by 75%. Iodide can be in the form of Lugol's iodine, SSKI (Strong Solution of Potassium Iodide), sodium iodide, orografin, or lithium carbonate (for use in patients allergic to iodine). These drugs function by inhibiting proteolysis of thyroglobulin and thereby blocking the release of stored hormone. Because one of the side effects is an initial increase in production of thyroid hormone, it is therefore very important to start PTU before you give iodides. Glucocorticoids block release of stored hormone (as do iodides), and peripheral conversion of T4 to T3 (as do thionamides). They may also bolster adrenal function, and prevent adrenal insufficiency, although data in support of this particular benefit are few (12). Start PTU before giving iodides.
Propylthiouracil (PTU) followed at least 1 hour later by iodides to block T4 release (IV sodium iodide or oral Lugol's):
PTU orally or via nasogastric tube, 300-800 mg loading dose followed by 150-300 mg every 6 hours;
One hour after instituting PTU give: Sodium iodide, 500 mg every 8-12 hours or oral Lugol's solution, 30-60 drops daily in divided doses.
Iodides may be discontinued after initial improvement.
Give adrenal glucocorticoids to inhibit peripheral conversion of T4 to T3. Consider any of the following options as appropriate:
Hydrocortisone, 100 mg IV every 8 hour, or
Prednisone, 60 mg PO every day, or
Dexamethasone, 8 mg PO every day
Glucocorticoids may be discontinued after initial improvement.
Medications to control maternal tachycardia: beta-blocker agents -- propranolol can be used to control autonomic symptoms (especially tachycardia). Beta-adrenergic blockade may have some effect on inhibition of peripheral conversion of T4 to T3, but will not alter thyroid hormone release nor prevent thyroid storm. Use propranolol with caution because it has a tendency to increase pulmonary diastolic pressure, and cardiac failure is a frequent presentation of thyroid storm. Treatment with a beta-blocker to control tachycardia is usually reserved for heart rates of 120 beats per minute or higher. Propranolol, labetalol, and esmolol have all been used successfully in pregnancy (13).
Commonly following dosages are used:
Propranolol, 1-2 mg/min IV or dose sufficient to slow heart rate to 90 bpm; or 20-80 mg PO or via nasogastric tube every 4-6 hourly;
Esmolol, a short-acting beta-acting antagonist given IV with a loading dose of 250 to 500 µg/kg of body weight followed by a continuous infusion at 50 to 100 µg/kg/min may also be used.
Consider a echocardiogram and/or pulmonary artery catheter to help guide management, especially in cardiac failure;
If patient has severe bronchospasm -- give 1-5 mg reserpine every 4-6 hours or 1 mg/kg orally of guanethidine every 12 hours.
Propranolol, 1-2 mg/min IV or dose sufficient to slow heart rate to 90 bpm; or 20-80 mg PO or via nasogastric tube every 4-6 hourly
Esmolol, a short-acting beta-acting antagonist given IV with a loading dose of 250 to 500 µg/kg of body weight followed by a continuous infusion at 50 to 100 µg/kg/min may also be used
Consider a echocardiogram and/or pulmonary artery catheter to help guide management, especially in cardiac failure
If patient has severe bronchospasm -- give 1-5 mg reserpine every 4-6 hours or 1 mg/kg orally of guanethidine every 12 hours.
Reserpine?
Guanethidine?
Heart failure due to cardiomyopathy from excessive thyroxine in women with uncontrolled hyperthyroidism is more common in pregnant women (14). Treatment of thyroid storm or thyrotoxic heart failure is similar. They both should be treated as medical emergencies.
Phenobarbital: 30 to 60 mg orally every 6-8 hours as needed to control restlessness.
After initial clinical management, iodides and glucocorticoids can be discontinued. Reserve plasmapheresis or peritoneal dialysis to remove circulating thyroid hormone for patients who do not respond to conventional therapy. Prescribe anticoagulants if appropriate. If conventional therapy is unsuccessful: consider subtotal thyroidectomy (during second-trimester pregnancy) or radioactive iodine (postpartum).
Postpartum Care:
Women with Grave's disease should be followed up closely after delivery, because recurrence or aggravation of symptoms is not uncommon in the first few months of postpartum. Most asymptomatic women should have a TSH and free T4 performed approximately 6 weeks postpartum. Both PTU and methimazole are excreted in breast milk, but PTU is largely protein bound and does not seem to pose a significant risk to the breastfed infant. Methimazole has been found in breastfed infants of treated women in amounts sufficient to cause thyroid dysfunction. However, at low doses (10-20 mg/d) it does not seem to pose a major risk to the nursing infant. The American Academy of Pediatricians considers both compatible with breastfeeding
Teratogenic effects of Antithyroid Medications:
PTU, methimazole and whole category -- there is general consensus among clinicians that the lowest dose needed to keep T3 and T4 within the upper normal range for these women should be used (18). Because women previously ablated with either radioactive iodine or thyroidectomy may still be producing thyroid-stimulating antibodies (even though they are themselves euthyroid), the fetus remains at risk and should be monitored with serial ultrasonography for growth and early detection of goiter. No deleterious effects on neonatal thyroid function or on physical and intellectual development of breastfed infants have been described (19).
PTU: it is first-line treatment for Grave's disease in pregnancy due to lower risks of teratogenicity than methimazole. It crosses the human placenta and associated with fetal hypothyroidism
Cordocentesis is sometimes recommended to test fetal thyroid function. It does not readily crosses membranes and milk concentrations are quite low.
Methimazole (Thiamazole, Mercazole, Tapazole): it is the second-line treatment of Grave's disease. It crosses the human placenta and can induce fetal goiter and even cretinism in a dose-dependent fashion. It is also commonly associated with fetal anomalies such as aplasia cutis, esophageal atresia, and choanal atresia (20). Long-term follow-up studies of exposed children reveal no deleterious effects on their thyroid function or physical and intellectual development with doses up to 20 mg/d (19). It is excreted in breast milk.
Propranolol, labetalol and whole category: approximately 3% of women take an antihypertensive during pregnancy. The American College of Obstetricians and Gynecologists (ACOG) recommends treatment for women with a systolic blood pressure higher than 170 mmHg and/or diastolic blood pressure above 109 mmHg. There is no consensus whether lesser degrees of hypertension require treatment during pregnancy because antihypertensive therapy improves only the maternal, not the fetal, outcome in women with mild to moderate chronic hypertension (22).
Radioactive iodine (iodine-131; I-131): it is contraindicated in pregnant women. It is cost-effective, safe, and reliable treatment for hyperthyroidism in non-pregnant women (21). Although excreted from the body within 1 month, the ACOG recommendation is that women should avoid pregnancy for 4-6 months following treatment. No adequate reports or well-controlled studies in human fetuses are available. Detrimental effects on the thyroid of the developing fetus as a result of I-131 treatment for thyrotoxicosis of the mother in the first trimester of pregnancy are reported. Breast-feeding should be avoided for at least 120 days after treatment.