Pregnancy is a period that places great physiological stress on both the mother and the fetus. When pregnancy is compounded by endocrine disorders such as hypothyroidism, the potential for maternal and fetal adverse outcomes can be immense. While a lot of attention has been focused on the adverse fetal outcomes consequent to hypothyroidism, attention is also being gradually directed towards the adverse maternal outcomes of this disorder. Role of antibody positivity in influencing outcomes in a euthyroid woman, also needs further clarification. Prompt diagnosis and treatment of hypothyroidism in pregnancy is very essential. Subclinical hypothyroidism also needs to be detected and treated to prevent adverse outcomes, especially maternal. Since women with hypothyroidism during pregnancy, especially of the autoimmune variety might have a flare up of the disorder post-partum, or might continue to require thyroxine replacement post-partum, adequate follow-up is mandatory. While targeted case finding is generally practised, recent evidence seems to indicate that universal screening might be a better option. In conclusion, routine screening, early confirmation of diagnosis and prompt treatment. Allied with regular post-partum follow up, is required to ensure favourable maternal and fetal outcomes.
Thyroid physiology is perceptibly modified during normal pregnancy. These alterations take place throughout gestation, help to prepare the maternal thyroid gland to cope with the metabolic demands of pregnancy, are reversible post-partum and the interpretation of these changes can pose a challenge to the treating physician.
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.
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.
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
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.
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.
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.
Due to pregnancy thyroid economy is affected with changes in iodine metabolism, TBG and development of maternal goiter. The incidence of hypothyroidism in pregnancy is quite common with autoimmune hypothyroidism being the most important cause. Overt as well as subclinical hypothyroidism has a varied impact on maternal and neonatal outcome. After multiple studies also, routine screening in pregnancy for hypothyroidism can still not be recommended. Management mainly comprises of dosage adjustments as soon as pregnancy is diagnosed based on results of thyroid function tests. The aim should be to keep FT4 at the upper end of normal range.
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.
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.
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
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.
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.
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.
Due to pregnancy thyroid economy is affected with changes in iodine metabolism, TBG and development of maternal goiter. The incidence of hypothyroidism in pregnancy is quite common with autoimmune hypothyroidism being the most important cause. Overt as well as subclinical hypothyroidism has a varied impact on maternal and neonatal outcome. After multiple studies also, routine screening in pregnancy for hypothyroidism can still not be recommended. Management mainly comprises of dosage adjustments as soon as pregnancy is diagnosed based on results of thyroid function tests. The aim should be to keep FT4 at the upper end of normal range.
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.
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.
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 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.
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.
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 provides an overview of thyroid function and disorders during pregnancy. It discusses how the thyroid gland and thyroid function tests change normally during pregnancy. It also covers hyperthyroidism and hypothyroidism in pregnancy, including their effects on the fetus and neonate. Key points include that both hyperthyroidism and hypothyroidism can lead to adverse pregnancy outcomes if not properly treated, and maternal thyroid antibodies can affect the fetal thyroid gland. Precise diagnosis and treatment of thyroid disorders is important for maternal and fetal health.
This document defines and discusses transverse lie, which occurs when the long axis of the fetus lies perpendicular to the maternal spine. Key points include:
- Transverse lie has an incidence of about 1 in 300 births and is more common in multiparous women and preterm fetuses.
- Diagnosis involves abdominal and vaginal exams to identify the fetal parts in unusual positions.
- Spontaneous delivery is very rare and management typically involves external cephalic version to change the lie, followed by induction if successful. Cesarean delivery is required if version fails or the fetus is in distress.
This document discusses breech presentation, including its definition, types, diagnosis, and management. Some key points:
- Breech presentation is when the buttocks or lower limbs present first. It occurs in 3.5% of term deliveries and up to 25% of preterm deliveries.
- Types include complete breech, frank breech, and footling breech. Diagnosis is made through inspection, palpation, auscultation, and ultrasound.
- Management options are external cephalic version, vaginal delivery for some cases, or caesarean section which is recommended for complicated breeches or large babies. Vaginal delivery carries risks of complications for
The document summarizes the management of hypertensive disorders in pregnancy. It defines hypertension and the different types of hypertensive disorders that can occur during pregnancy including gestational hypertension, preeclampsia, eclampsia, chronic hypertension, and preeclampsia superimposed on chronic hypertension. It discusses the risk factors, pathogenesis, clinical manifestations, diagnostic criteria, and management approaches for non-severe and severe preeclampsia, including antihypertensive treatment and seizure prophylaxis.
This document discusses HIV/AIDS, including transmission, signs and symptoms, stages of infection, treatment and prevention of mother-to-child transmission. It notes that HIV can be transmitted sexually, through infected body fluids or from mother to child. The stages of infection are acute infection, clinical latency and AIDS. Signs may include flu-like symptoms during acute infection and infections over time as immunity declines. Prevention of mother-to-child transmission is important, as without intervention up to 45% of babies may be infected, but can be reduced to less than 5% with antiretroviral treatment and safe delivery practices.
Seizures during pregnancy can cause: Slowing of the fetal heart rate. Decreased oxygen to the fetus. Fetal injury, premature separation of the placenta from the uterus (placental abruption) or miscarriage due to trauma, such as a fall, during a seizure
hyperthyroidism, thyrotoxicosis, grave disease, thyroid storm, pregnancy, high risk pregnancy, pregnancy complications, management of thyrotoxicosis and thyroid storm in pregnancy
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.
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
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
This document discusses the management of asthma during pregnancy. It notes that asthma is common in pregnancy, with respiratory changes occurring due to anatomical and hormonal factors. Pregnancy can affect asthma severity, with courses varying between women. Well controlled asthma is important for limiting risks to the pregnancy. Treatment follows a stepwise approach, initially using inhaled corticosteroids. Close monitoring is needed to prevent exacerbations while minimizing medication risks for the fetus. Inhaled beta-agonists are generally considered safe options for relief of symptoms during pregnancy.
This document discusses premature rupture of membranes (PROM), which is the spontaneous rupture of membranes before the onset of labor. It defines PROM as occurring beyond 28 weeks of gestation but before labor, and preterm PROM (PPROM) as occurring between 28-37 weeks.
The document outlines the risk factors, symptoms, diagnosis, and management of PROM depending on gestational age. Evaluation involves history, physical exam including speculum exam, and tests like nitrazine, ferning, fetal fibronectin, and ultrasound. Management often involves expectant monitoring, antibiotics, corticosteroids, and tocolytics to prolong the pregnancy if it is prior to 34 weeks. The goals are
Cervical incompetence, also called cervical insufficiency, is a condition where the cervix begins to dilate and efface before pregnancy has reached term, often resulting in miscarriage. Risk factors include a history of preterm birth, multiple abortions, cervical procedures, or congenital uterine abnormalities. Diagnosis involves a history of second trimester losses and physical exam findings of cervical shortening or dilatation. Treatment options during pregnancy include bed rest, progesterone supplementation, cerclage procedures to reinforce the cervix, and sometimes pessary devices. The goal is to prevent premature dilation and maintain the pregnancy until full term.
Preterm labor is defined as the onset of labor before 37 weeks of gestation. It can be spontaneous or medically indicated and accounts for a majority of neonatal deaths and disabilities. Risk factors include multiple pregnancies, infections, cervical insufficiency, and genetic factors. Management involves tocolytic drugs to delay labor, corticosteroids to improve neonatal outcomes, and careful fetal monitoring during labor. Prematurity and its complications remain a major challenge in obstetrics.
THYROID DISORDER IN PREGNANCY -Kamal.pptxAkshitRana26
The document discusses thyroid dysfunction in pregnancy, including physiological changes in the thyroid gland during pregnancy, screening and management of hypothyroidism and hyperthyroidism, and the effects of thyroid disorders and iodine deficiency on maternal and fetal health. Key points covered include the increased demand for thyroid hormones during pregnancy, screening guidelines for thyroid disorders, and treatment approaches for hypothyroidism including levothyroxine dosage optimization.
This document discusses thyroid disorders in newborns. It covers thyroid physiology in the fetus and newborn, causes of congenital hypothyroidism including thyroid dysgenesis and dyshormonogenesis, clinical features of hypothyroidism, and methods for screening and diagnosis of congenital hypothyroidism in newborns. It also addresses transient hypothyroidism, sick euthyroid syndrome, and the importance of newborn screening to detect congenital hypothyroidism.
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.
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 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.
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.
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 provides an overview of thyroid function and disorders during pregnancy. It discusses how the thyroid gland and thyroid function tests change normally during pregnancy. It also covers hyperthyroidism and hypothyroidism in pregnancy, including their effects on the fetus and neonate. Key points include that both hyperthyroidism and hypothyroidism can lead to adverse pregnancy outcomes if not properly treated, and maternal thyroid antibodies can affect the fetal thyroid gland. Precise diagnosis and treatment of thyroid disorders is important for maternal and fetal health.
This document defines and discusses transverse lie, which occurs when the long axis of the fetus lies perpendicular to the maternal spine. Key points include:
- Transverse lie has an incidence of about 1 in 300 births and is more common in multiparous women and preterm fetuses.
- Diagnosis involves abdominal and vaginal exams to identify the fetal parts in unusual positions.
- Spontaneous delivery is very rare and management typically involves external cephalic version to change the lie, followed by induction if successful. Cesarean delivery is required if version fails or the fetus is in distress.
This document discusses breech presentation, including its definition, types, diagnosis, and management. Some key points:
- Breech presentation is when the buttocks or lower limbs present first. It occurs in 3.5% of term deliveries and up to 25% of preterm deliveries.
- Types include complete breech, frank breech, and footling breech. Diagnosis is made through inspection, palpation, auscultation, and ultrasound.
- Management options are external cephalic version, vaginal delivery for some cases, or caesarean section which is recommended for complicated breeches or large babies. Vaginal delivery carries risks of complications for
The document summarizes the management of hypertensive disorders in pregnancy. It defines hypertension and the different types of hypertensive disorders that can occur during pregnancy including gestational hypertension, preeclampsia, eclampsia, chronic hypertension, and preeclampsia superimposed on chronic hypertension. It discusses the risk factors, pathogenesis, clinical manifestations, diagnostic criteria, and management approaches for non-severe and severe preeclampsia, including antihypertensive treatment and seizure prophylaxis.
This document discusses HIV/AIDS, including transmission, signs and symptoms, stages of infection, treatment and prevention of mother-to-child transmission. It notes that HIV can be transmitted sexually, through infected body fluids or from mother to child. The stages of infection are acute infection, clinical latency and AIDS. Signs may include flu-like symptoms during acute infection and infections over time as immunity declines. Prevention of mother-to-child transmission is important, as without intervention up to 45% of babies may be infected, but can be reduced to less than 5% with antiretroviral treatment and safe delivery practices.
Seizures during pregnancy can cause: Slowing of the fetal heart rate. Decreased oxygen to the fetus. Fetal injury, premature separation of the placenta from the uterus (placental abruption) or miscarriage due to trauma, such as a fall, during a seizure
hyperthyroidism, thyrotoxicosis, grave disease, thyroid storm, pregnancy, high risk pregnancy, pregnancy complications, management of thyrotoxicosis and thyroid storm in pregnancy
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.
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
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
This document discusses the management of asthma during pregnancy. It notes that asthma is common in pregnancy, with respiratory changes occurring due to anatomical and hormonal factors. Pregnancy can affect asthma severity, with courses varying between women. Well controlled asthma is important for limiting risks to the pregnancy. Treatment follows a stepwise approach, initially using inhaled corticosteroids. Close monitoring is needed to prevent exacerbations while minimizing medication risks for the fetus. Inhaled beta-agonists are generally considered safe options for relief of symptoms during pregnancy.
This document discusses premature rupture of membranes (PROM), which is the spontaneous rupture of membranes before the onset of labor. It defines PROM as occurring beyond 28 weeks of gestation but before labor, and preterm PROM (PPROM) as occurring between 28-37 weeks.
The document outlines the risk factors, symptoms, diagnosis, and management of PROM depending on gestational age. Evaluation involves history, physical exam including speculum exam, and tests like nitrazine, ferning, fetal fibronectin, and ultrasound. Management often involves expectant monitoring, antibiotics, corticosteroids, and tocolytics to prolong the pregnancy if it is prior to 34 weeks. The goals are
Cervical incompetence, also called cervical insufficiency, is a condition where the cervix begins to dilate and efface before pregnancy has reached term, often resulting in miscarriage. Risk factors include a history of preterm birth, multiple abortions, cervical procedures, or congenital uterine abnormalities. Diagnosis involves a history of second trimester losses and physical exam findings of cervical shortening or dilatation. Treatment options during pregnancy include bed rest, progesterone supplementation, cerclage procedures to reinforce the cervix, and sometimes pessary devices. The goal is to prevent premature dilation and maintain the pregnancy until full term.
Preterm labor is defined as the onset of labor before 37 weeks of gestation. It can be spontaneous or medically indicated and accounts for a majority of neonatal deaths and disabilities. Risk factors include multiple pregnancies, infections, cervical insufficiency, and genetic factors. Management involves tocolytic drugs to delay labor, corticosteroids to improve neonatal outcomes, and careful fetal monitoring during labor. Prematurity and its complications remain a major challenge in obstetrics.
THYROID DISORDER IN PREGNANCY -Kamal.pptxAkshitRana26
The document discusses thyroid dysfunction in pregnancy, including physiological changes in the thyroid gland during pregnancy, screening and management of hypothyroidism and hyperthyroidism, and the effects of thyroid disorders and iodine deficiency on maternal and fetal health. Key points covered include the increased demand for thyroid hormones during pregnancy, screening guidelines for thyroid disorders, and treatment approaches for hypothyroidism including levothyroxine dosage optimization.
This document discusses thyroid disorders in newborns. It covers thyroid physiology in the fetus and newborn, causes of congenital hypothyroidism including thyroid dysgenesis and dyshormonogenesis, clinical features of hypothyroidism, and methods for screening and diagnosis of congenital hypothyroidism in newborns. It also addresses transient hypothyroidism, sick euthyroid syndrome, and the importance of newborn screening to detect congenital hypothyroidism.
overview of anatomy and physiology of the thyroid gland,fetal period and pregnancy physiological changes ....then overview of congenital hypothyroidism plus management
Discusses how maternal thyroid physiology changes in pregnancy, the issues of thyroid disease in pregnancy, how to interpret thyroid test results in the pregnant woman and how to manage common thyroid diseases in pregnancy
This document discusses congenital hypothyroidism. It begins by outlining the synthesis of thyroid hormones and defects that can cause congenital hypothyroidism. It then describes the development and functional maturity of the thyroid gland as well as physiological changes in thyroid hormones after birth, noting differences in premature versus term infants. The major causes of congenital hypothyroidism are then summarized, including thyroid dysgenesis, dyshormonogenesis, and transient causes. Clinical manifestations and screening guidelines via newborn screening are also covered at a high level.
A complete presentation on hypothroidism endocrine disorder based on latest editon of harrison and reference books. this presentation will help to learn about this second most common endocrine disorder.
The thyroid gland is located in the neck and secretes thyroid hormones T3 and T4. It consists of two lobes connected by an isthmus. The thyroid follicles contain colloid and principle follicular cells that secrete thyroid hormones. Congenital hypothyroidism is caused by inadequate thyroid hormone production in newborns and can lead to cretinism if untreated. Early treatment with levothyroxine replacement therapy prevents intellectual disability and growth issues.
This document discusses tips about hypothyroidism in reproduction and pregnancy from recent guidelines by ACOG and ATA. It notes that thyroid disorders are common in young women and pregnancy, and that maternal and fetal thyroid function are closely related. Untreated hypothyroidism can lead to adverse pregnancy outcomes. Thyroid autoantibodies are associated with increased rates of early pregnancy loss. The document discusses thyroid physiology and how the thyroid gland and hormone levels change during pregnancy to meet increased demands. It also discusses iodine status, nutrition, and recommendations for iodine intake during pregnancy and lactation. The relationship between thyroid autoantibodies and pregnancy complications in euthyroid women is also summarized.
This document discusses congenital hypothyroidism, including:
1. It is a preventable cause of mental retardation that occurs in 1 in 3000-4000 live births worldwide and 1 in 2500-2800 in India.
2. The most common cause is thyroid dysgenesis, which accounts for 75-80% of cases.
3. Newborn screening programs allow for early detection and treatment to prevent morbidity, particularly neurodevelopmental disabilities.
1) Hypothyroidism in pregnancy can be caused by iodine deficiency, Hashimoto's thyroiditis, or other rare causes. It affects both mother and fetus.
2) For pregnant women, routine thyroid screening is controversial but may be recommended for those with risk factors. Hypothyroidism symptoms are similar to normal pregnancy symptoms.
3) Untreated hypothyroidism in pregnancy poses risks to both mother and fetus, including complications of pregnancy, cognitive impairments, and cretinism in the fetus. Treatment is with levothyroxine supplementation.
Lecture 6. Endocrine diseases and pregnancy (1).pdftotohaamzaa
The document discusses several key points regarding endocrine diseases and pregnancy:
1) The thyroid gland has important functions in maintaining pregnancy, including increased T4 requirements by the mother and fetus' dependence on maternal hormones in early pregnancy.
2) Physiological changes include suppression of TSH and increases in thyroid hormones and binding proteins, maintaining normal free levels.
3) Iodine deficiency is a major cause of thyroid issues worldwide, and intake of 250 μg/day is recommended for pregnant women.
4) Hypothyroidism occurs in 1% of pregnancies and requires thyroxine treatment. Thyrotoxicosis also requires medication management to prevent complications.
This document provides information on congenital hypothyroidism, including its causes, presentation, diagnosis, and treatment. There are several types of congenital hypothyroidism, with the most common being thyroid dysgenesis, which accounts for 70% of cases and results from abnormal thyroid gland development. Other permanent causes include thyroid dyshormonogenesis and TSH resistance. Transient causes in the newborn include exposure to antithyroid drugs in utero or iodine excess/deficiency. Early diagnosis and treatment of congenital hypothyroidism is important to prevent intellectual disability, as there is an inverse relationship between the age of treatment initiation and later IQ. Treatment involves lifelong thyroid hormone replacement therapy.
A power point presentation on thyroid hormones and thyroid inhibitors on subject of pharmacology suitable for reading by undergraduate medical students.
The thyroid gland is located in the anterior neck and consists of two lobes connected by an isthmus. It receives blood supply from the superior and inferior thyroid arteries and drains into the internal jugular and brachiocephalic veins. The thyroid synthesizes the hormones T3 and T4 through a process involving trapping of iodine, production of thyroglobulin, iodination of thyroglobulin, and release of T3 and T4. Thyroid hormone synthesis is regulated by TSH from the pituitary gland. Thyroid hormones increase metabolism and have important roles in growth, brain development, heart function, and thermogenesis. Pregnancy increases the demand for thyroid hormones to support the mother
THYROID HORMONE.pptx by Subham Panja,Asst. Professor, Department of B.Sc MLT,...Subham Panja
The document summarizes the thyroid gland and its hormones. It discusses that the thyroid gland produces three hormones: thyroxine (T4), triiodothyronine (T3), and calcitonin. T4 makes up 90% of hormone production while T3 is 9-10%. The hormones are synthesized from iodine and tyrosine, stored in thyroglobulin vesicles, and released into blood circulation via binding proteins. The hormones act to increase basal metabolic rate and stimulate growth, accelerating protein synthesis and mitochondrial activity in most tissues.
The document summarizes the structure and function of the thyroid gland. It discusses that the thyroid gland is located in the front of the neck and is butterfly shaped with two lobes connected by an isthmus. It produces important hormones like thyroxine and triiodothyronine which regulate metabolism. The thyroid takes up iodine and uses it to produce the hormones through a series of steps in a negative feedback loop involving the hypothalamus and pituitary gland. The hormones have wide-ranging effects on growth, development, and metabolic processes in nearly all tissues of the body. Diseases like hypothyroidism and Graves' disease can disrupt the thyroid's normal functioning.
The thyroid gland has two primary functions: secreting thyroid hormones which maintain metabolism, and secreting calcitonin which regulates calcium levels. Congenital hypothyroidism is caused by thyroid hormone deficiency present at birth and can cause mental retardation if not treated. It is usually diagnosed through newborn screening and treated with thyroid hormone replacement medication. Early treatment leads to a better prognosis, while delayed treatment is associated with lower IQ scores.
This document discusses thyroid physiology during pregnancy. It notes that pregnancy causes profound alterations in thyroid function due to hormonal changes and the fetus's dependence on maternal iodine and thyroid hormones. Specifically, estrogen levels increase TBG during pregnancy, resulting in lower free thyroid hormone levels and increased TSH stimulation. Iodine requirements also increase in pregnancy due to renal clearance and diversion to the fetus, making iodine deficiency a particular risk. Proper prenatal care requires understanding how thyroid function changes during pregnancy and common thyroid disorders that can affect women and fetal development.
The document discusses the embryology, anatomy, physiology and diseases of the thyroid and parathyroid glands. It describes how the thyroid develops from the pharynx and how the parathyroid glands develop from pouches in the pharynx. It discusses the location and function of the thyroid and parathyroid glands, and how thyroid hormones are synthesized and regulated. It also summarizes the causes, symptoms, diagnosis and treatment of hypothyroidism.
The thyroid gland secretes the hormones thyroxine (T4) and triiodothyronine (T3), which regulate metabolism and growth. T4 makes up the majority of thyroid hormones produced, but T3 is the more biologically active form. Their secretion is controlled by TSH from the pituitary gland. Thyroid hormones increase basal metabolic rate, stimulate lipid, carbohydrate and protein metabolism, and affect growth and development, especially of the nervous system. They also increase heart rate and contractility, causing a hyperdynamic circulation.
Similar to Hypothyroidism in pregnancy by DR ALKA MUKHERJEE DR APURVA MUKHERJEE NAGPUR M.S. (20)
Management of anaemia in pregnancy BY DR ALKA MUKHERJEE DR APURVA MUKHERJEE N...alka mukherjee
Prenatal vitamins typically contain iron. Taking a prenatal vitamin that contains iron can help prevent and treat iron deficiency anemia during pregnancy. In some cases, your health care provider might recommend a separate iron supplement. During pregnancy, you need 27 milligrams of iron a day.
Good nutrition also can prevent iron deficiency anemia during pregnancy. Dietary sources of iron include lean red meat, poultry and fish. Other options include iron-fortified breakfast cereals, prune juice, dried beans and peas.
The iron from animal products, such as meat, is most easily absorbed. To enhance the absorption of iron from plant sources and supplements, pair them with a food or drink high in vitamin C — such as orange juice, tomato juice or strawberries. If you take iron supplements with orange juice, avoid the calcium-fortified variety. Although calcium is an essential nutrient during pregnancy, calcium can decrease iron absorption.
How is iron deficiency anemia during pregnancy treated?
If you are taking a prenatal vitamin that contains iron and you are anemic, your health care provider might recommend testing to determine other possible causes. In some cases, you might need to see a doctor who specializes in treating blood disorders (hematologist). If the cause is iron deficiency, additional supplemental iron might be suggested. If you have a history of gastric bypass or small bowel surgery or are unable to tolerate oral iron, you might need intravenous iron administration. Oral iron is recommended as the first line treatment, with repeated checking of Hb at 2 to 3 weeks after starting treatment to assess compliance, correct administration and response to treatmentOnce Hb reaches the normal range, it is recommended that iron replacement should continue for three months and until at least six weeks postpartumIntravenous (IV) iron is recommended for women who could not tolerate or respond to oral iron, and for those with moderately severe to severe anemia (Hb ≤ 90 g/LHb be measured within 24 to 48 hours after delivery in women with blood loss more than 500 mL, those with uncorrected anemia detected during pregnancy or those with symptoms suggestive of anemia postnatallyOral iron is recommended for women with Hb <100 g/L postpartum, who are hemodynamically stable, asymptomatic or mild symptomatic
Anemia signs and symptoms include:
• Fatigue
• Weakness
• Pale or yellowish skin
• Irregular heartbeats
• Shortness of breath
• Dizziness or lightheadedness
• Chest pain
• Cold hands and feet
• Headache
Keep in mind, however, that symptoms of anemia are often similar to general pregnancy symptoms. Regardless of whether or not you have symptoms, you'll have blood tests to screen for anemia during pregnancy. If you're concerned about your level of fatigue or any other symptoms, talk to your health care provider.
Secondary amenorrhoea by dr alka mukherjee dr apurva mukherjeealka mukherjee
The first step in the evaluation of any patient with secondary amenorrhea is a urine pregnancy test. Every contraceptive method has a failure rate, and anyone who is menstruating is potentially fertile, regardless of age. [5][6]
If the pregnancy test is negative, consider the clinical picture: hirsutism, acne, and a long history of infrequent and irregular menses suggest polycystic ovarian syndrome. By the Rotterdam criteria, a patient may be diagnosed with PCOS if she has two of the following: clinical or chemical hyperandrogenism, oligo- or amenorrhea, or polycystic ovaries on ultrasound. So if a patient has evidence of hirsutism and oligo- or amenorrhea, she can be diagnosed with PCOS without further laboratory testing or imaging.
If history and physical exam are not consistent with PCOS, a TSH should be ordered. Both hyper- and hypothyroidism can lead to menstrual dysfunction.
If TSH is normal, check a serum prolactin. Elevated serum prolactin suggests prolactinoma.
Early pregnancy loss by dr alka mukherjee dr apurva mukherjee nagpur ms indiaalka mukherjee
Early pregnancy loss, or loss of an intrauterine pregnancy within the first trimester, is encountered commonly in clinical practice. Obstetricians and gynecologists should understand the use of various diagnostic tools to differentiate between viable and nonviable pregnancies and offer the full range of therapeutic options to patients, including expectant, medical, and surgical management.
Early pregnancy loss is defined as a nonviable, intrauterine pregnancy with either an empty gestational sac or a gestational sac containing an embryo or fetus without fetal heart activity within the first 12 6/7 weeks of gestation 1. In the first trimester, the terms miscarriage, spontaneous abortion, and early pregnancy loss are used interchangeably, and there is no consensus on terminology in the literature.
Pprom by dr alka mukherjee dr apurva mukherjee nagpur indiaalka mukherjee
Preterm premature rupture of the membranes (PPROM) is a pregnancy complication. In this condition, the sac (amniotic membrane) surrounding your baby breaks (ruptures) before week 37 of pregnancy. Once the sac breaks, you have an increased risk for infection. You also have a higher chance of having your baby born early.
In most cases of PPROM, the cause is not known.
These things may increase risk:
• Having a preterm birth in a previous pregnancy
• Having an infection in your reproductive system
• Vaginal bleeding during pregnancy
• Smoking during pregnancy
Symptoms can occur a bit differently in each pregnancy. They can include:
• A sudden gush of fluid from your vagina
• Leaking of fluid from your vagina
• A feeling of wetness in your vagina or underwear
Call your healthcare provider right away if you have these symptoms.
The symptoms of this health problem may be similar to symptoms of other conditions. See your healthcare provider for a diagnosis.
Diagnosis
• pH (acid-base) balance testing. The pH balance of amniotic fluid is different from vaginal fluid and urine. Your healthcare provider will put the fluid on a test strip to check the balance.
• Looking at a sample under a microscope. When amniotic fluid is dry, it has a fern-like pattern.
• ultrasound exam. This is done to check the amount of amniotic fluid around baby.
Public education on breast cancer hindi by dr alka mukherjee nagpur ms i...alka mukherjee
Abnormal lump — Breast cancer can be discovered when a lump or other change in the breast or armpit is found by a woman herself or by her healthcare provider. In addition to a lump, other abnormal changes may include dimpling of the skin, a change in the size or shape of one breast, retraction (pulling in) of the nipple when it previously pointed outward, or a discoloration of the skin of the breast not related to infection or skin conditions such as psoriasis or eczema.Mammogram — A mammogram is a very low-dose X-ray of the breast. The breast tissue is compressed for the X-ray, which decreases the thickness of the tissue and holds the breast in position, so the radiologist can find abnormalities more accurately. Each breast is compressed between two panels and X-rayed from two directions (top-down and side-to-side) to make sure all the tissue is examined. Mammograms are currently the best screening modality to detect breast cancer. Some mammograms capture images digitally, offering better clarity, the ability to adjust the image, and a decreased likelihood that the woman will need to return on a different day for repeat pictures.
Cancer cervix awareness in hindi by dr alka mukherjee nagpur ms indiaalka mukherjee
Cervical cancer occurs when the cells in the cervix grow abnormally or out of control. The cervix is part of the female reproductive system. The exact cause of cervical cancer is unknown. Certain strains of the human papillomavirus (HPV), a sexually transmitted disease, cause the majority of cervical cancer.
A new vaccine is available to prevent infection against the two types of HPV that are responsible for the majority of cervical cancer cases and the two types of HPV that are responsible for the majority of genital wart cases. A pap smear test is a preventive measure that can detect precancerous or cancerous cells. Precancerous cells are 100% curable.
Telehealth medico legal aspects by dr alka mukherjee nagpur ms indiaalka mukherjee
The term telehealth includes a broad range of technologies and services to provide patient care and improve the healthcare delivery system as a whole. Telehealth is different from telemedicine because it refers to a broader scope of remote healthcare services than telemedicine. While telemedicine refers specifically to remote clinical services, telehealth can refer to remote non-clinical services, such as provider training, administrative meetings, and continuing medical education, in addition to clinical services. According to the World Health Organization, telehealth includes, “Surveillance, health promotion and public health functions.”
Telemedicine involves the use of electronic communications and software to provide clinical services to patients without an in-person visit. Telemedicine technology is frequently used for follow-up visits, management of chronic conditions, medication management, specialist consultation and a host of other clinical services that can be provided remotely via secure video and audio connections.
Evolution and current practices in emergency contraceptives BY DR ALKA MUKHER...alka mukherjee
This document provides information on emergency contraceptives, including their evolution and current practices. It discusses various emergency contraceptive methods such as the Yuzpe regimen, levonorgestrel pills, mifepristone, copper IUDs, and the recently approved ulipristal acetate. It summarizes the mechanisms of action, effectiveness, appropriate timing, side effects, limitations and safety considerations of the different emergency contraceptive options. The document concludes that emergency contraception can effectively reduce unintended pregnancies and abortions if provided correctly and in a timely manner after unprotected intercourse.
Screening for gestational diabetes an update by dr alka mukherjee nagpur ms i...alka mukherjee
Gestational Diabetes Mellitus (GDM) is defined as any glucose intolerance with the onset or first recognition during pregnancy. This definition helps for diagnosis of unrecognized pre-existing Diabetes also. Hyperglycemia in pregnancy is associated with adverse maternal and prenatal outcome. It is important to screen, diagnose and treat Hyperglycemia in pregnancy to prevent an adverse outcome. There is no international consensus regarding timing of screening method and the optimal cut-off points for diagnosis and intervention of GDM. DIPSI recommends non-fasting Oral Glucose Tolerance Test (OGTT) with 75g of glucose with a cut-off of ≥ 140 mg/dl after 2-hours, whereas WHO (1999) recommends a fasting OGTT after 75g glucose with a cut-off plasma glucose of ≥ 140 mg/dl after 2-hour. The recommendations by ADA/IADPSG for screening women at risk of diabetes is as follows, for first and subsequent trimester at 24-28 weeks a criteria of diagnosis of GDM is made by 75 g OGTT and fasting 5.1mmol/l, 1 hour 10.0mmol/l, 2 hour 8.5mmol/l by universal glucose tolerance testing. Critics of these criteria state that it causes over diagnosis of GDM and unnecessary interventions, the controversy however continues. The ACOG still prefer a 2 step procedure, GCT with 50g glucose non-fasting if value > 7.8mmol/l followed by 3-hour OGTT for confirmation of diagnosis. In conclusion based on Hyperglycemia and Adverse Pregnancy Outcome (HAPO) study as mild degree of dysglycemia are associated with adverse outcome and high prevalence of Type II DM to have international consensus It recommends IADPSG criteria, though controversy exists. The IADPSG criteria is the only outcome based criteria, it has the ability to diagnose and treat GDM earlier, thereby reducing the fetal and maternal complications associated with GDM. This one step method has an advantage of simplicity in execution, more patient friendly, accurate in diagnosis and close to international consensus. Keeping in the mind the diversity and variability of Indian population, judging international criteria may not be conclusive, thus further comparative studies are required on different diagnostic criteria in relation to adverse pregnancy outcomes
Hague convention for inter country adoption by dr alka mukherjee nagpur ms indiaalka mukherjee
The Hague Convention on the Protection of Children and Co-operation in Respect of Intercountry Adoption (Convention) is an international agreement to safeguard intercountry adoptions. Concluded on May 29, 1993 in The Hague, the Netherlands, the Convention establishes international standards of practices for intercountry adoptions. The United States signed the Convention in 1994, and the Convention entered into force for the United States on April 1, 2008The Convention applies to all adoptions by U.S. citizens habitually resident in the United States of children habitually resident in any country outside of the United States that is a party to the Convention (Convention countries). Adopting a child from a Convention country is similar in many ways to adopting a child from a country not party to the Convention. However, there are some key differences. In particular, those seeking to adopt may receive greater protections if they adopt from a Convention country.
The Convention requires that countries who are party to it establish a Central Authority to be the authoritative source of information and point of contact in that country. The Department of State is the U.S. Central Authorityfor the Convention.
The Convention aims to prevent the abduction, sale of, or trafficking in children, and it works to ensure that intercountry adoptions are in the best interests of children.
The Convention recognizes intercountry adoption as a means of offering the advantage of a permanent home to a child when a suitable family has not been found in the child's country of origin. It enables intercountry adoption to take place when, among other steps:
1. The child has been deemed eligible for adoption by the child's country of origin; and
2. Due consideration has been given to finding an adoption placement for the child in its country of origin.
The role of judiciary & the legal procedure in an adoption case by dr alka mu...alka mukherjee
Central Adoption Resource Authority (CARA) is the nodal agency to monitor and regulate in-country and intra-country adoption and is a part of Ministry of Women and child care.
Following are the certain essential conditions in order to be eligible to adopt a child:
• The procedure for adoption is different in case of Indian citizen, NRI or a foreign citizen and a child can be adopted by any of the three.
• Irrespective of their gender or marital status, any person is eligible to adopt.
• Provided that a couple is adopting a child, they should have completed two years of stable marriage and both should agree for the adoption.
• 25 years should be the minimum age difference between the child and the adoptive parents.
WHEN CAN A CHILD BE ELIGIBLE TO BE ADOPTED?
• Any orphan, surrendered or abandoned child is legally declared free for adoption by the child welfare committee as per the guidelines of the Central Government of India.
• A child without a legal parent or a guardian or the parents are not capable of taking care of the child anymore is said to be an orphan.
• When a child is deserted or unaccompanied by parents or a guardian and the child welfare committee has declared the child to be abandoned, a child is considered to be abandoned.
• Renounce on account of physical, social and emotional factors that are beyond the control of parents or the guardian is called a surrendered child as declared by the child welfare committee.
• In case of adoption, a child requires to be “legally free”. A child is considered to be legally free if even after trying their level best the police fails to find the true parent or guardian of the child.
WHAT ARE THE NORMAL CONDITIONS TO BE FULFILLED BY PARENTS?
• The adoptive parents need to be mentally, physically and emotionally stable.
• The adoptive parents should be financially stable.
• The adoptive parents should not be suffering from any life- threatening diseases.
• Apart from cases of special needs children, couples with three or more kids are not allowed for adoption.
• A single female is allowed to adopt a child of any gender but a single male is not allowed to adopt a girl child.
• The maximum age limit of a single parents should be 55 years.
Laws , rules & regulations governing adoptions in india by dr alka mukherjee ...alka mukherjee
ADOPTION IN INDIA
The custom and practice of adoption in India dates back to the ancient times. Although the act of adoption remains the same, the objective with which this act is carried out has differed. It usually ranged from the humanitarian motive of caring and bringing up a neglected or destitute child, to a natural desire for a kid as an object of affection, a caretaker in old age, and an heir after death.[iii]
But since adoption comes under the ambit of personal laws, there has not been a scope in the Indian scenario to incorporate a uniform law among the different communities which consist of this melting pot. Hence, this law is governed by various personal laws of different religions.
Adoption is not permitted in the personal laws of Muslims, Christians, Parsis and Jews in India. Hence they usually opt for guardianship of a child through the Guardians and Wards Act, 1890.
Indian citizens who are Hindus, Jains, Sikhs, or Buddhists are allowed to formally adopt a child. The adoption is under the Hindu Adoption and Maintenance Act of 1956 that was enacted in India as a part of the Hindu Code Bills. It brought about a few reforms that liberalized the institution of adoption.
Tuberculosis in prenancy by dr alka mukherjee dr apurva mukherjee nagpur ms i...alka mukherjee
Prevention of Tuberculosis
The BCG vaccine has been incorporated into the National immunization policy of many countries, especially the high burden countries, thereby conferring active immunity from childhood. Nonimmune women travelling to tuberculosis endemic countries should also be vaccinated. It must, however, be noted that the vaccine is contraindicated in pregnancy [72].
The prevention, however, goes beyond this as it is essentially a disease of poverty. Improved living condition is, therefore, encouraged with good ventilation, while overcrowding should be avoided. Improvement in nutritional status is another important aspect of the prevention.
Pregnant women living with HIV are at higher risk for TB, which can adversely influence maternal and perinatal outcomes [73]. As much as 1.1 million people were diagnosed with the co-infection in 2009 alone [2]. Primary prevention of HIV/AIDS is, therefore, another major step in the prevention of tuberculosis in pregnancy. Screening of all pregnant women living with HIV for active tuberculosis is recommended even in the absence of overt clinical signs of the disease.
Isoniazid preventive therapy (IPT) is another innovation of the World Health Organisation that is aimed at reducing the infection in HIV positive pregnant women based on evidence and experience and it has been concluded that pregnancy should not be a contraindication to receiving IPT. However, patient's individualisation and rational clinical judgement is required for decisions such as the best time to provide IPT to pregnant women
Torch infections during pregnancy by dr alka mukherjee nagpur ms indiaalka mukherjee
TORCH Syndrome refers to infection of a developing fetus or newborn by any of a group of infectious agents. "TORCH" is an acronym meaning (T)oxoplasmosis, (O)ther Agents, (R)ubella (also known as German Measles), (C)ytomegalovirus, and (H)erpes Simplex. Infection with any of these agents (i.e., Toxoplasma gondii, rubella virus, cytomegalovirus, herpes simplex viruses) may cause a constellation of similar symptoms in affected newborns. These may include fever; difficulties feeding; small areas of bleeding under the skin, causing the appearance of small reddish or purplish spots; enlargement of the liver and spleen (hepatosplenomegaly); yellowish discoloration of the skin, whites of the eyes, and mucous membranes (jaundice); hearing impairment; abnormalities of the eyes; and/or other symptoms and findings. Each infectious agent may also result in additional abnormalities that may be variable, depending upon a number of factors (e.g., stage of fetal development
How to develope your personality by dr alka mukherjee nagpur ms indiaalka mukherjee
Personality is what makes a person a unique person, and it is recognizable soon after birth. A child's personality has several components: temperament, environment, and character. Temperament is the set of genetically determined traits that determine the child's approach to the world and how the child learns about the world. There are no genes that specify personality traits, but some genes do control the development of the nervous system, which in turn controls behavior.
A second component of personality comes from adaptive patterns related to a child's specific environment. Most psychologists agree that these two factors—temperament and environment—influence the development of a person's personality the most. Temperament, with its dependence on genetic factors, is sometimes referred to as "nature," while the environmental factors are called "nurture."
While there is still controversy as to which factor ranks higher in affecting personality development, all experts agree that high-quality parenting plays a critical role in the development of a child's personality. When parents understand how their child responds to certain situations, they can anticipate issues that might be problematic for their child. They can prepare the child for the situation or in some cases they may avoid a potentially difficult situation altogether. Parents who know how to adapt their parenting approach to the particular temperament of their child can best provide guidance and ensure the successful development of their child's personality.
Finally, the third component of personality is character—the set of emotional, cognitive, and behavioral patterns learned from experience that determines how a person thinks, feels, and behaves. A person's character continues to evolve throughout life, although much depends on inborn traits and early experiences. Character is also dependent on a person's moral development .
Personality by dr alka mukherjee nagpur ms indiaalka mukherjee
The word personality itself stems from the Latin word persona, which refers to a theatrical mask worn by performers in order to either project different roles or disguise their identities.
At its most basic, personality is the characteristic patterns of thoughts, feelings, and behaviors that make a person unique. It is believed that personality arises from within the individual and remains fairly consistent throughout life.
While there are many different definitions of personality, most focus on the pattern of behaviors and characteristics that can help predict and explain a person's behavior.
Explanations for personality can focus on a variety of influences, ranging from genetic explanations for personality traits to the role of the environment and experience in shaping an individual's personality.
Qualitative blood loss in obstetric hemorrhage by dr alka mukherjee indiaalka mukherjee
• Quantitative methods of measuring obstetric blood loss have been shown to be more accurate than visual estimation in determining obstetric blood loss.
• Studies that have compared visual estimation to quantitative measurement have found that visual estimation is more likely to underestimate the actual blood loss when volumes are high and overestimate when volumes are low.
• Although quantitative measurement is more accurate than visual estimation for identifying obstetric blood loss, the effectiveness of quantitative blood loss measurement on clinical outcomes has not been demonstrated.
• Implementation of quantitative assessment of blood loss includes the following two items: 1) use of direct measurement of obstetric blood loss (quantitative blood loss) and 2) protocols for collecting and reporting a cumulative record of blood loss postdelivery.
Dysmenorrhea and related disorders by dr alka mukherjee dr apurva mukherjee n...alka mukherjee
Dysmenorrhea is a common symptom secondary to various gynecological disorders, but it is also represented in most women as a primary form of disease. Pain associated with dysmenorrhea is caused by hypersecretion of prostaglandins and an increased uterine contractility. The primary dysmenorrhea is quite frequent in young women and remains with a good prognosis, even though it is associated with low quality of life. The secondary forms of dysmenorrhea are associated with endometriosis and adenomyosis and may represent the key symptom. The diagnosis is suspected on the basis of the clinical history and the physical examination and can be confirmed by ultrasound, which is very useful to exclude some secondary causes of dysmenorrhea, such as endometriosis and adenomyosis. The treatment options include non-steroidal anti-inflammatory drugs alone or combined with oral contraceptives or progestins.
Dyspareunia & vulvodynia by dr alka mukherjee dr apurva mukherjee nagpur m.s....alka mukherjee
This document discusses dyspareunia (recurring pain during sexual intercourse) and vulvodynia (chronic genital pain). It describes the causes, symptoms, diagnosis, and treatment options. Dyspareunia and vulvodynia can have physical and psychological causes, and treatment may involve medications, physical therapy, cognitive behavioral therapy, and sometimes surgery. A multidisciplinary approach is often needed to properly diagnose and address the underlying causes of genital pain.
Chronic pelvic pain by dr alka mukherjee dr apurva mukherjee nagpur m.s. indiaalka mukherjee
Chronic pelvic pain in women is defined as persistent, noncyclic pain perceived to be in structures related to the pelvis and lasting more than six months. Often no specific etiology can be identified, and it can be conceptualized as a chronic regional pain syndrome or functional somatic pain syndrome. It is typically associated with other functional somatic pain syndromes (e.g., irritable bowel syndrome, nonspecific chronic fatigue syndrome) and mental health disorders (e.g., posttraumatic stress disorder, depression). Diagnosis is based on findings from the history and physical examination. Pelvic ultrasonography is indicated to rule out anatomic abnormalities. Referral for diagnostic evaluation of endometriosis by laparoscopy is usually indicated in severe cases. Curative treatment is elusive, and evidence-based therapies are limited. Patient engagement in a biopsychosocial approach is recommended, with treatment of any identifiable disease process such as endometriosis, interstitial cystitis/painful bladder syndrome, and comorbid depression. Potentially beneficial medications include depot medroxyprogesterone, gabapentin, nonsteroidal anti-inflammatory drugs, and gonadotropin-releasing hormone agonists with add-back hormone therapy. Pelvic floor physical therapy may be helpful. Behavioral therapy is an integral part of treatment. In select cases, neuromodulation of sacral nerves may be appropriate. Hysterectomy may be considered as a last resort if pain seems to be of uterine origin, although significant improvement occurs in only about one-half of cases. Chronic pelvic pain should be managed with a collaborative, patient-centered approach.
Osteoporosis - Definition , Evaluation and Management .pdfJim Jacob Roy
Osteoporosis is an increasing cause of morbidity among the elderly.
In this document , a brief outline of osteoporosis is given , including the risk factors of osteoporosis fractures , the indications for testing bone mineral density and the management of osteoporosis
Mercurius is named after the roman god mercurius, the god of trade and science. The planet mercurius is named after the same god. Mercurius is sometimes called hydrargyrum, means ‘watery silver’. Its shine and colour are very similar to silver, but mercury is a fluid at room temperatures. The name quick silver is a translation of hydrargyrum, where the word quick describes its tendency to scatter away in all directions.
The droplets have a tendency to conglomerate to one big mass, but on being shaken they fall apart into countless little droplets again. It is used to ignite explosives, like mercury fulminate, the explosive character is one of its general themes.
10 Benefits an EPCR Software should Bring to EMS Organizations Traumasoft LLC
The benefits of an ePCR solution should extend to the whole EMS organization, not just certain groups of people or certain departments. It should provide more than just a form for entering and a database for storing information. It should also include a workflow of how information is communicated, used and stored across the entire organization.
Cell Therapy Expansion and Challenges in Autoimmune DiseaseHealth Advances
There is increasing confidence that cell therapies will soon play a role in the treatment of autoimmune disorders, but the extent of this impact remains to be seen. Early readouts on autologous CAR-Ts in lupus are encouraging, but manufacturing and cost limitations are likely to restrict access to highly refractory patients. Allogeneic CAR-Ts have the potential to broaden access to earlier lines of treatment due to their inherent cost benefits, however they will need to demonstrate comparable or improved efficacy to established modalities.
In addition to infrastructure and capacity constraints, CAR-Ts face a very different risk-benefit dynamic in autoimmune compared to oncology, highlighting the need for tolerable therapies with low adverse event risk. CAR-NK and Treg-based therapies are also being developed in certain autoimmune disorders and may demonstrate favorable safety profiles. Several novel non-cell therapies such as bispecific antibodies, nanobodies, and RNAi drugs, may also offer future alternative competitive solutions with variable value propositions.
Widespread adoption of cell therapies will not only require strong efficacy and safety data, but also adapted pricing and access strategies. At oncology-based price points, CAR-Ts are unlikely to achieve broad market access in autoimmune disorders, with eligible patient populations that are potentially orders of magnitude greater than the number of currently addressable cancer patients. Developers have made strides towards reducing cell therapy COGS while improving manufacturing efficiency, but payors will inevitably restrict access until more sustainable pricing is achieved.
Despite these headwinds, industry leaders and investors remain confident that cell therapies are poised to address significant unmet need in patients suffering from autoimmune disorders. However, the extent of this impact on the treatment landscape remains to be seen, as the industry rapidly approaches an inflection point.
Travel vaccination in Manchester offers comprehensive immunization services for individuals planning international trips. Expert healthcare providers administer vaccines tailored to your destination, ensuring you stay protected against various diseases. Conveniently located clinics and flexible appointment options make it easy to get the necessary shots before your journey. Stay healthy and travel with confidence by getting vaccinated in Manchester. Visit us: www.nxhealthcare.co.uk
Promoting Wellbeing - Applied Social Psychology - Psychology SuperNotesPsychoTech Services
A proprietary approach developed by bringing together the best of learning theories from Psychology, design principles from the world of visualization, and pedagogical methods from over a decade of training experience, that enables you to: Learn better, faster!
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Histololgy of Female Reproductive System.pptxAyeshaZaid1
Dive into an in-depth exploration of the histological structure of female reproductive system with this comprehensive lecture. Presented by Dr. Ayesha Irfan, Assistant Professor of Anatomy, this presentation covers the Gross anatomy and functional histology of the female reproductive organs. Ideal for students, educators, and anyone interested in medical science, this lecture provides clear explanations, detailed diagrams, and valuable insights into female reproductive system. Enhance your knowledge and understanding of this essential aspect of human biology.
2. ANATOMY
2
A Small Butterfly Shaped ENDOCRINE Gland At The Base Of
The Neck, Against C5, C6, C7 & T1.
Consist Of Right & Left Lobe Joined By Isthmus, A 3rd
Pyramidal Lobe Might Project Upwards From Isthmus
Capsules – 2 – True & False
Larger In Females Than Males
Development – Ectoderm Of The Floor Of Primitive Oral
Cavity
3. HISTOLOGY OF THE THYROID GLAND
Thyroid gland contains
numerous follicles,
composed of follicle
cells and colloid.
Maintenance of normal metabolic
activity-continuous production of
thyroid hormone at right
concentration
Coordinated interaction between
Hypothalamus, Pituitary & Thyroid.
CLASSIC EXAMPLE-ENDOCRINE
FEEDBACK MECHANISM
4. FUNCTIONS OF THYROID GLAND
Major function-
absorption of
iodine
Synthesis &
secretion of two
important
hormones,T3&T4
-Metabolic
Homeostasis Of
The Body
Parafollicular cells
of thyroid gland-
CALCITONIN
-CALCIUM
HOMEOSTASIS OF
BODY
T4 –major thyrois
hormone,thyroid
gland produces
100%
Half life of T4 -7
days
4
5. THYROID HORMONES
Two hormones are
secreted by Thyroid
gland
1.
Tetraiodothyronine
(T4) usually called
Thyroxine
2. Triiodothyronine
(T3)
Thyroid secretes 80
mcg of T4,
but only 5 mcg of
T3/day.
Derived from an
amino acid
(tyrosine)
Thyroid hormones
are made from
Tyrosine and Iodine
6. MATERNAL THYROID PHYSIOLOGY
• During pregnancy, maternal thyroid function is modulated by three
factors.
• An increase in HCG concentration that stimulate the thyroid glands,
• Significant increases in urinary iodide excretion resulting in a fall in
plasma iodine concentration
• An increase in thyroxine – binding globulin (TBG) DURING The first
trimester , resulting in increased binding of thyroxine
• Total T3 & T4 are increased, but Free T4 & Free T3 remain normal & patient remains
euthyroid.
• Increased T4 & T3 in early pregnancy help to maintain the hyper metabolic state
• Sometimes, estimation of TSH during pregnancy is erroneous due to interference by
HCG .
• Therefore during pregnancy, it is always advisable to get FT3 & FT4 done rather than
Total T4 & T3.
8. HCG & THYROID PHYSIOLOGY IN PREGNANCY
8
Human chorionic gonadotropin (HCG), secreted by the placenta, also
impacts thyroid function because it simulates thyroid‐stimulating hormone
(TSH) activity in vivo, thereby suppressing its secretion.
The structure of HCG is similar to TSH. HCG mimics & acts like TSH.
Throughout pregnancy, TSH values are lower than in the pre‐pregnant state,
and may even be below the classical lower limit of 0.4 miu/L.
Since the levels of HCG decrease as the pregnancy increases, the levels of
TSH follow the reverse trend.
Serum hCG has intrinsic thyrotropic activity, which increases after fertilization
and peaks at 10 to 12 weeks.
Hence, in the first trimester , free T3 and T4 levels increase slightly and TSH
levels decrease in the first trimester with a readjustment in the second and
third trimesters, when hCG levels decrease.
As a consequence, cut-offs to determine hypothyroidism in pregnancy are
different in the first trimester and the rest of the pregnancy.
9. EFFECT OF HCG
• Pregnancy results in number
of important physiological &
hormonal changes that alter
thyroid function due to
influence of two main
hormones.
• 1. HCG
• 2. Estrogen
• Baby remains dependent on
mother for ingestion of
adequate amount of iodine
which is essential for
synthesis of thyroid
hormones
10. The most notable change is the increase in thyroxine-binding globulin
(TBG).
This begins early in the first trimester, plateaus during midgestation,
and persists until shortly after delivery.
This is due to stimulation of TBG synthesis by elevated maternal
estrogen levels, and more importantly, due to a reduced hepatic
clearance of TBG because of estrogen-induced sialylation.
This increased TBG concentration leads to an expansion of the extra-
thyroidal pool and results in elevated total T3 and T4 levels due to an
increase in maternal thyroid hormone synthesis.
Maternal thyroid hormone synthesis is also increased due to an
accelerated renal clearance of iodide resulting from the increased
maternal glomerular filtration rate.
TBG & MATERNAL THYROID PHYSIOLOGY
11. PLACENTAL DEIODINASES & MATERNAL THYROID
PHYSIOLOGY
Enhanced metabolism of T4 in the second and third
trimesters, due to a rise in placental type II and type III
deiodinases, which convert T4 to T3 and T4 to reverse T3
and T2 respectively, act as further impetus to T4 synthesis.
Plasma iodide levels decrease due to both increased
thyroxine metabolism and increased renal iodide
clearance.
All these changes lead to an increase in the size of the
thyroid gland in 15% of pregnant women, which returns to
normal in the post-partum period.
12. PHYSIOLOGY OF THE FETAL THYROID
• Fetal thyroid gland develops as an out pouching in midline of the anterior
pharyngeal floor, migrates caudally, to reach its final position by 7 weeks of
gestation.
• Fetal thyroid is capable of trapping iodine by 12 weeks and can synthesize
thyroxine by 14 weeks of gestation.
• However, significant hormone secretion is not seen till 18–20 weeks of
gestation. Thereafter, fetal TSH, T4, and TBG gradually rise to adult levels by
36 weeks gestation.
• But T3 and free T3 levels do not rise to adult levels , as placental type III
deiodinase converts most fetal T4 to reverse T3; the fetal brain which has
elevated levels of type II deiodinase, is an exception.
• TSH transfer across placenta is not significant, but T3 and T4 transport can
be considerable. This is of special relevance in congenital hypothyroidism,
where studies have shown that umbilical cord T4 levels in neonates with
congenital hypothyroidism can be up to 50% of the normal.
• This transferred T4 can play a crucial role in near normal fetal cognitive
development in congenital hypothyroidism. Transplacental transfer of TRH,
iodine, anti-thyroid drugs and thyroid stimulatory immunoglobulin (TSI)
also occurs
13. THYROID PHYSIOLOGY IN PREGNANCY
Pregnancy is Iodide-Deficient state
BMR by 15-20%
Iodine clearance due to increased GFR (upto 50%) &
reduced tubular re-absorption
Hence requirement of Thyroxin & Iodine In Pregnancy.
Iodine Requirement:
Non-pregnant Females 150 microg/day
Pregnancy &
Breastfeeding
200-250 microg/day
14. THYROID PHYSIOLOGY IN PREGNANCY
Estrogen stimulates TBG production from liver.
Normally T3 & T4 occur in two forms:
Bound with TBG
Free(Active)
On account of increased TBG, Bound form increases.
15. PREGNANCY IS A STRESS TEST FOR THE THYROID,
Pregnancy impacts the
functioning of the thyroid
gland profoundly and is
associated with
a 10%–40% increase in the
size of the gland
(iodine‐replete areas show
greater increase),
a 50% increase in the
production of thyroxine
(T4) and triiodothyronine
(T3), and
a 50% increase in the daily
requirement of iodine.
These physiological changes -
pregnant, iodine‐deficient, euthyroid
woman in the first trimester
hypothyroid during the later stages
of pregnancy and postpartum
thyroiditis in women with underlying
Hashimoto's disease who were
euthyroid prior to conception.
Ten percent to 20% of all
pregnant women in the
first trimester of
pregnancy are thyroid
peroxidase (TPO) or
thyroglobulin (Tg)
antibody positive and
euthyroid.
Sixteen percent of the
women who are euthyroid
and positive for TPO or Tg
antibody in the first
trimester will develop a
TSH that exceeds 4.0
mIU/L by the third
trimester, and
16. EPIDEMIOLOGY OF THYROID DISEASE
• 1.8% of world total population.
• Second only to DM as most
common endocrine disorder.
• Incidence increases with age.
• More common in females.
• 2-3% of older women.
• 42 million people in India suffer
from thyroid disease
•5 common thyroid diseases in
India.
•Hypothyroidism(Highest)
•Hyperthyroidism
•Goitre and Iodine Deficiency
disorders
•Hashimotos’s thyroiditis
•Thyroid Cancer
1. [Last accessed on 2011 April 2]. Available from:http://www.ias.ac.in/currsci/oct252000/n%20kochupillai.PDF .
2. Desai PM. Disorders of the Thyroid Gland in India. Indian J Pediatr. 1997;64:11–20. [PubMed]
3. Usha Menon V, Sundaram KR, Unnikrishnan AG, Jayakumar RV, Nair V, Kumar H. High prevalence of undetected thyroid disorders in an iodine
sufficient adult south Indian population. J Indian Med Assoc. 2009;107:72–7. [PubMed]
Over 40 Million Indians suffer from
Thyroid disorders of which
Hypothyroidism is a major concern.
17. Hypothyroidism is difficult to be diagnosed during pregnancy as the signs can
belong to pregnancy itself.
Changes in thyroid function have a major negative impact on both mother and
fetus.
Thyroid pathology worsens
during pregnancy.
Hypothyroidism can be pre-
existent or may begin
during pregnancy period.
Most of the patients who
presented hypothyroidism
during pregnancy have a
history of thyroid disease
for which they have
undergone treatment
(medical, surgical or
radioisotopes).
Complications that arise
depend on the severity of
hypothyroidism, on how
appropriately and early the
treatment will be initiated,
on other obstetrical and
extragenital pathologies
associated with the present
pregnancy.
Clinical symptoms –
polymorphic & nonspecific,
and are related mainly to
the time of occurrence and
to the severity of thyroid
hormone deficiency.
The appropriate, early
administered treatment and
maintenance of a normal
level of thyroid hormones
minimize the risk of
maternal and fetal
complications and make it
possible that the pregnancy
may be carried to term
without severe
complications.
18. HORMONAL CHANGES AND METABOLIC NEEDS
DURING PREGNANCY
• Result in profound alterations of biochemical and clinical
parameters which characterize the thyroid gland, changes that
express themselves through a state of thyroid hyperstimulation
and a relative hypothyroxinemy or a subclinic hypothyroidism.
• When pregnancy overlaps maternal endocrine imbalance,
undesirable consequences for both mother and fetus may appear.
• Associated with an increased risk of abortion, habitual abortion,
premature delivery, intrauterine fetal death, fetal retardation and
fetal congenital anomalies, congenital hypothyroidism, postpartum
bleeding, anemia, post-partum depression and cardiac
dysfunction, which leads to increased maternal morbidity,
perinatal morbidity and mortality
19. 19
Hypothyroidism common in pregnancy.
Two types –
.Overt hypothyroidism – defined as increased serum TSH [> 10 miu/ l]
associated with decreased concentration of thyroxine as a result of
negative feedback
.Subclinical hypothyroidism –increase in serum TSH [ 4-10 m iu/ l] with
normal concentration of thyroxine & triidothyronine.
Incidence – overt-0.2 – 2.5
- Subclinical- 5- 20 %
- Thyroid antibodies > 60 % females in reproductive age grp
20. WHAT HYPOTHYROIDISM?
• Under-activity of the thyroid
• Decreased secretion of thyroid hormones
• Deficiency of T3 and T4
Clinical manifestations due to deficiency of
thyroid hormones
Clinical manifestation depends on
Age of the patient
The cause of the disorder
Primary Hypothyroidism-
Caused by damage to the thyroid gland
Secondary Hypothyroidism-
Caused by damage to the pituitary gland &
therefore low production of Thyroid Stimulating
Hormone (TSH)
Tertiary Hypothyroidism-
Caused by the failure of the hypothalamus to release
Thyrotropin-releasing hormone (TRH)
21. PREVALENCE OF MATERNAL HYPOTHYROIDISM
• Maternal Hypothyroidism is much
more common than generally
acknowledged.
• The recent data shows alarmingly
high prevalence of the maternal
hypothyroidism both in India as well
as in USA.
23. ROLE OF THYROID
HORMONES:
• Essential for normal growth of tissues
• Stimulates basal metabolic rate.
• Increases intestinal glucose reabsorption & ATP production
• Development of the skeletal system & musculature.
• Essential for normal brain development & regulates
synaptogenesis, neuronal integration, myelination
• Deficiency lead to short stature & mental deficits
24. • Fatigue
• Increased sensitivity to
cold
• Constipation
• Dry skin
• Weight gain
• Puffy face
• Hoarseness
• Muscle weaknes
• Elevated blood cholesterol
level
• Muscle aches, tenderness
and stiffness
• Pain, stiffness or swelling in
your joints
• Heavier than normal or
irregular menstrual periods
• Thinning hair
• Slowed heart rate
• Depression
• Impaired memory
• Enlarged thyroid gland
(goiter)
HYPOTHYROIDISM: SIGNS AND SYMPTOMS
25. HYPOTHYROIDISM IN PREGNANCY
• Elevated serum TSH concentration
2.5% of pregnancies
• In iodine sufficent environment
- Hashimoto’s thyroiditis
- Prior radioactive iodine treatment
- Surgical ablation of Graves’
disesase
- Less common causes :
Overtreatment of hyperthyroidism
with thionamides , transient
hypothyroidism owing to
postpartum thyroditis ,
medications that alter the
absorption or metabolism of
levothyroxine , and pituitary
hypothalamic disease
25
• One of the most common endocrine
disorders in pregnancy1
• Most common cause: endemic iodine
deficiency2
• Women with hypothyroidism carry
an increased risk of infertility,
miscarriage, and obstetric
complications1
• Foetal complications: premature
birth, low-birth weight (LBW), fetal
distress in labor, fetal death,
perinatal death, and congenital
hypothyroidism1
• Even an untreated subclinical
hypothyroidism during pregnancy
can lead to cognitive impairment in
the offspring.3
28. COMPLICATIONS OF MATERNAL HYPOTHYROIDISM IF NOT
TREATED
Labor – diskinetic, longer due to the existence of the hypomyotonia and the simultaneous cardio-
breathing problems; hypokinesis
Anomalies of fetus cardiac rhytm (FCR) – fetal suffering: alterations of the basic cardiac rhythm
(tachycardia, bradicardia), of FCR variability (diminution until their loss or periodical variations of
FCR in relation with the uterus contractions, a type of belated slow-ups)
APGAR mark – frequently lower at pregnant women who continued to be hypothyroidic until the
due term
Vitiated pelvis (limit pelvis) which can be the reason of various cephalic-pelvis disproportions
Presentations that are close to distocia – pelvic presentation
Post-partum haemorrhages occur through uterus hypotony and through coagulation disorders
(problem of the plaque adhesiveness)
Post-partum depression, post-partum thyroiditis, hypogalactia
29. THE CAUSES OF THE HYPOTONY AND HYPO-
CONTRACTIONS IN HYPOTHYROIDISM
The causes of hypotony are
the endogen intoxications,
the change of muscular tissue,
the myxedema impregnation,
the hypovitaminosis (B1 vitamin),
affecting the transmission of the nervous
influx, affecting the endocrine
metabolism,
water-electrolitic change which leads to
the change of the functional biometrical
schemes and to the change of the
interaction between actin and myosin:
a)the K and the intracellular Mg decrease due
to the metabolic acidosis and therefore the
contraction is more difficult, Ca decreases and
the equilibrium of P, bicarbonate and H ions is
disturbed;
B) the metabolic acidosis also modifies the
extracellular distribution of Na, Ca, Mg and K
and has a negative influence on the
contractions through the decrease of the
membrane potential, which leads to
insufficient contraction.
Hypotonia, having a tonus less than
10 mmHg,
Hypokinesis - Hypokinesis
(contractions which are rarer than
two within 10 minutes with the
contraction value of less then
25mmHg)
Labour is slow or long, with
possibilities of interruption,
real uterus inertia, which can be
primitive (ante-partum determined)
or secondary (intra-partum
determined).
The insufficient labour - 35.2% at
the pregnant women, who
remained with hypothyroidism at
the end of pregnancy.
30. LOW APGAR score
APGAR score depends of the uterus-placenta circulation and the proper
oxygenation of the fetal-placenta complex during pregnancy and it is
frequently lower at pregnant women who continued to have
hypothyroidism until the due term.
In hypothyroidism, the cardiac debit is not adequate and the uterus-
placenta circulation becomes insufficient, which induces a moderate and
chronic fetal hypoxia, fetal bradycardia, fetal hypotrophy, diminution of
fetal moves and an insufficient tolerance of the delivery by the fetus.
The intrauterine chronic hypoxia of the newborn can be met in the
literature at variable percentages between 14%-22% at pregnant women
with hypothyroidism.
A series of studies, with recent reconfirmed results, showed that the
treatment with T4 can improve the obstetrical prognosis but it does not
modify the neurological development of the newborn on the long term,
the cognitive performances being changed;
the maternal hypothyroixinemia on early term pregnancies can have
irreversible negative effects on the newborn's state and placenta. Some
antioxidants (retinol, tocopherol etc.), are usually used in the treatment of
the fetal-placenta insufficiency.
31. VITIATED PELVIS (LIMIT PELVIS)
Intricate mechanisms (direct and
indirect effects of the thyroid
hormones) since the very beginning
of the pre-gestation period, which
can affect the pelvic bones (lower
bone density, even osteoporosis), of
the spine (multiple deformations),
problems of the articulations
through the specific infiltration,
various artropaties, inflammatory or
non-inflammatory, poliartritis,
artrosis.
Excessive deposits of mucous
polysaccharides and glucose in the
tissues, affecting protein synthesis,
diminution of the insulin level, as a
growth factor, can lead to various
muscles and skeleton symptoms.
A clear mechanism is not
established, but a decrease in the
proliferation of the cartilage cells
and bone tissue and
chondrocalcinosis
32. POST-PARTUM HEMORRHAGES IN HYPOTHYROIDISM
Are produced both through the uterus hypotony and coagulation problems,
with plaque adhesiveness problem.
Various studies (Leung, Buckshee, Davis) from the literature indicate a
percentage between 7% and 19%.
POST-PARTUM THYROIDITIS
The etiology of the post-partum thyroiditis has not been well-understood yet
but a problem in the self immunity can be probably caused by a constant
increase of the level of anti-microzomes antibody in the first trimester of the
pregnancy. Post-partum thyroiditis affects 2-7% of the pregnant women. The
hypothyroid phase follows a hyperthyroid phase and it manifests after 5-7
months in post-partum.
33. FUTURE SEQUALAE
The hypothyroid can
remain permanent (12-
61%) and euthyroiditis
appears in 5% of the
cases.
According to recent
studies, the incidence
has very wide limits,
between 1.1-2.1%,
within the first year
after delivery;
The presence of the thyroid
antibodies during the first
trimester of the pregnancy
determines an increase by
35% of the incidence and
the risk of developing a
post-partum thyroid is of
50%; if they are still
present in the third
trimester, the risk increases
by 80%; the relapse, with a
similar evolution and
intensity, usually appears
after future pregnancies.
34. POSTPARTUM DEPRESSION & PUERPERIAL PSYCHOSIS
IN HYPOTHYROIDISM
The level of hormone production by the placenta has a major role in the development of
psychological disequilibrium in puerperium.
The depression of pituitary function and the reduction of adrenaline and thyroid hormones
production may be included among the potential pathogenic factors;
low levels of progesterone or free tryptophan from the plasma,
the free usage of agents having vasoactive potential during intrapartum and postpartum and the
chronic lack of beta-endorphine along with the increase of the dopaminergic activity may be
responsible for these changes.
During post-partum, the adrenocorticotropic-hormone and the arginine-vasopressin are being
released, and carried through the portal circulation system until reaching the hypophysis where they
induce the production of ACTH, which reacts upon the corticoadrenal and releases cortisol.
35. COMPLICATIONS IN PREGNANCY, DELIVERY AND ON THE NEWBORN.
The increase of the preeclampsia incidence, of the premature delivery, of
the post-partum depressions and haemorrhages could be explained
through a maturation process of the placenta and they appear especially
if there is a severe hypothyroidism, but they have been also signalled in
the cases of subclinical hypothyroidism.
Complications in the pregnancies associated with hypothyroidism are
complex and serious, with an important increase of the maternal
morbidity, and perinatal morbidity and mortality. ❑
37. INCREASED PREGNANCY LOSS RATE IN THYROID ANTIBODY
NEGATIVE WOMEN WITH TSH LEVELES BETWEEN 2.5 AND
5.0 THE FIRST TRIMESTER OF PREGNANCY
Evaluated 4123 Thyroid
TPO Ab negative pregnant women
with TSH =/< 5mlU/LA
TSH < 2.5mlU/L TSH 2.5-5.0mlU/L
Not given any treatment for TSH correction
38. RECOMMENDATIONS & TAKE HOME
• RECOMMENDATION 1 - Trimester-specific reference ranges
for TSH, as defined in populations with optimal iodine
intake, should be applied. Level B-USPSTF
• RECOMMENDATION 2 - If trimester-specific reference ranges
for TSH are not available in the laboratory, the following
reference ranges are recommended:
• first trimester, 0.1–2.5 mIU/L;
• second trimester, 0.2–3.0 mIU/L;
• third trimester, 0.3–3.0 mIU/L.
Level I-USPSTF
39. • RECOMMENDATION 3 - The optimal method to assess serum
FT4 during pregnancy is measurement of T4 in the dialysate or
ultrafiltrate of serum samples employing on-line
extraction/liquid chromatography/tandem mass
spectrometry (LC/MS/MS). Level A-USPSTF
• RECOMMENDATION 4 - If FT4 measurement by LC/MS/MS is
not available, clinicians should use whichever measure or
estimate of FT4 is available in their laboratory, being aware of
the limitations of each method. Serum TSH is a more accurate
indication of thyroid status in pregnancy than any of these
alternative methods. Level A-USPSTF
• RECOMMENDATION 5 - In view of the wide variation in the
results of FT4 assays, method-specific and trimester-specific
reference ranges of serum FT4 are required. Level B-USPSTF
40. • RECOMMENDATION 6 - OH should be treated in pregnancy.
This includes women with a TSH concentration above the
trimester-specific reference interval with a decreased FT4, and
all women with a TSH concentration above 10.0 mIU/L
irrespective of the level of FT4. Level A-USPSTF
• RECOMMENDATION 7 - Isolated hypothyroxinemia should not
be treated in pregnancy. Level C-USPSTF
41. : How is isolated hypothyroxinemia defined in
pregnancy?
• Isolated hypothyroxinemia is defined as a normal maternal TSH concentration in
conjunction with FT4 concentrations in the lower 5th or 10th percentile of the
reference range.
What adverse outcomes are associated with isolated hypothyroxinemia in
pregnancy?
It is debated whether isolated hypothyroxinemia causes any adverse effects on the
developing fetus. Pop and colleagues reported a decrease in psychomotor test
scores among offspring born to women with FT4 indices in the lowest 10th
percentile. These mothers often had normal serum TSH values.
Li et al. observed a similar reduction in the IQ of the offspring whose mothers
experienced either hypothyroidism or isolated hypothyroxinemia during the
first trimester.
Henrichs and colleagues recently published data from the Generation R study,
conducted in the Netherlands - prospective, nonrandomized investigation
evaluated communication development in children born to women with
isolated hypothyroxinemia. A 1.5- to 2-fold increased risk of adverse findings (at
3 years of age) was associated with maternal FT4 in the lower 5th and 10th
percentiles.
42. RECOMMENDATION 8 - SCH has been associated with adverse maternal
and fetal outcomes. However, due to the lack of randomized
controlled trials there is insufficient evidence to recommend for or
against universal LT4 treatment in TAb− pregnant women with
SCH. Level I-USPSTF
RECOMMENDATION 9 - Women who are positive for TPOAb and have
SCH should be treated with LT4. Level B-USPSTF
RECOMMENDATION 10 - The recommended treatment of maternal
hypothyroidism is with administration of oral LT4. It is strongly
recommended not to use other thyroid preparations such as T3 or
desiccated thyroid. Level A-USPSTF
RECOMMENDATION 11 - The goal of LT4 treatment is to normalize
maternal serum TSH values within the trimester-specific pregnancy
reference range (first trimester, 0.1–2.5 mIU/L; second trimester, 0.2–
3.0 mIU/L; third trimester, 0.3–3.0 mIU/L). Level A-USPSTF
43. • RECOMMENDATION 12 - Women with SCH in pregnancy who are not initially
treated should be monitored for progression to OH with a serum TSH and
FT4 approximately every 4 weeks until 16–20 weeks gestation and at least once
between 26 and 32 weeks gestation. This approach has not been prospectively
studied. Level I-USPSTF
• RECOMMENDATION 13 - Treated hypothyroid patients (receiving LT4) who are
newly pregnant should independently increase their dose of LT4 by ∼25%–30%
upon a missed menstrual cycle or positive home pregnancy test and notify
their caregiver promptly. One means of accomplishing this adjustment is to
increase LT4 from once daily dosing to a total of nine doses per week (29%
increase). Level B-USPSTF
• RECOMMENDATION 14 - There exists great inter- individual variability
regarding the increased amount of T4 (or LT4) necessary to maintain a normal
TSH throughout pregnancy, with some women requiring only 10%–20%
increased dosing, while others may require as much as an 80% increase. The
etiology of maternal hypothyroidism, as well as the preconception level of
TSH, may provide insight into the magnitude of necessary LT4 increase.
Clinicians should seek this information upon assessment of the patient after
pregnancy is confirmed. Level A-USPSTF
44. RECOMMENDATION 15 - Treated hypothyroid patients (receiving LT4) who
are planning pregnancy should have their dose adjusted by their
provider in order to optimize serum TSH values to <2.5 mIU/L
preconception. Lower preconception TSH values (within the
nonpregnant reference range) reduce the risk of TSH elevation during
the first trimester. Level B-USPSTF
RECOMMENDATION 16 - In pregnant patients with treated
hypothyroidism, maternal serum TSH should be monitored
approximately every 4 weeks during the first half of pregnancy
because further LT4 dose adjustments are often required. Level B-
USPSTF
RECOMMENDATION 17 - In pregnant patients with treated
hypothyroidism, maternal TSH should be checked at least once
between 26 and 32 weeks gestation. Level I-USPSTF
RECOMMENDATION 18 - Following delivery, LT4 should be reduced to the
patient's preconception dose. Additional TSH testing should be
performed at approximately 6 weeks postpartum. Level B-USPSTF
45. RECOMMENDATION 19 - In the care of women with adequately
treated Hashimoto's thyroiditis, no other maternal or fetal thyroid
testing is recommended beyond measurement of maternal thyroid
function (such as serial fetal ultrasounds, antenatal testing, and/or
umbilical blood sampling) unless for other pregnancy
circumstances. Level A-USPSTF
RECOMMENDATION 20 - Euthyroid women (not receiving LT4) who
are TAb+ require monitoring for hypothyroidism during pregnancy.
Serum TSH should be evaluated every 4 weeks during the first half
of pregnancy and at least once between 26 and 32 weeks
gestation. Level B-USPSTF
RECOMMENDATION 21 - A single RCT has demonstrated a reduction
in postpartum thyroiditis from selenium therapy. No subsequent
trials have confirmed or refuted these findings. At present,
selenium supplementation is not recommended for TPOAb+
women during pregnancy. Level C-USPSTF
46. CONGENITAL HYPOTHYROIDISM
• Abnormality in the development of thyroid gland (dysgenesis or agenesis)
and defect in the biosynthesis of thyroid hormones
• Prevalence rate 1 in 4000 newborn infants in regions of sufficient daily
iodine intake
• 2:1 incidence in females compared with males
• Causes: Endemic iodine deficiency, genetic mutation, and hemangiomas
• Routine thyroid function screening in neonates is recommended since no
apparent clinical manifestation
• Untreated congenital hypothyroidism results in development of cretinism
• Do not delay diagnosis of congenital hypothyroidism until physical
manifestations are seen
– Mental retardation
– Deafness
– Short stature
– Characteristic facial deformities
47. CONGENITAL HYPOTHYROIDISM:
CLINICAL FEATURES
Roberts CGP et al. Lancet. 2004;363: 793-803.
Infants Children and Adolescents
Hypothermia Growth failure
Poor feeding Markedly delayed bone maturation
Bradycardia
Delayed eruption of permanent
teeth
Jaundice Muscle pseudohypertrophy
Enlarged posterior fontanel Delayed or precocious puberty
Umbilical hernia Pituitary enlargement
Galactorrhoea
48. MANAGEMENT OF CONGENITAL HYPOTHYROIDISM
• Goal: To normalize T4 within 2 weeks and TSH within 1 month
• Assess permanence of congenital hypothyroidism
– If initial thyroid scan shows ectopic/absent gland, congenital
hypothyroidism is permanent
– If initial TSH is <50 mIU/L and there is no increase in TSH after
newborn period, off- therapy period is recommended at 3 years
of age
– If TSH increases during the off-therapy period, consider the
condition as permanent congenital hypothyroidism
• Medications: LT4: 10-15 g/kg by mouth once-daily
• Monitoring: Recheck T4 and TSH
– At 2-4 weeks after initiation of LT4 treatment
– Every 1-2 months in the first 6 months
– Every 3-4 months between 6 months and 3 years of age
– Every 6-12 months from 3 years of age to end of growth
Rose SR and Brown RS. Pediatrics. 2006;117(6):2290-2303.
Congenital hypothyroidism occurs due to the agenesis or dysgenesis of thyroid gland and defect in the biosynthesis of the thyroid hormones. The prevalence rate of congenital hypothyroidism is 1 in 4000 of new born infants in regions of sufficient daily intake of iodine. Incidence in female infants is twice more that of males.
The major cause for congenital hypothyroidism is endemic iodine deficiency. Other causes in neonates include genetic mutation and hemangiomas.(/p794/col2/para2)
Most of the affected infants do not show obvious clinical manifestations, hence the practice of routine screening for thyroid function is recommended for all the newborn infants.(/p797/col1/para4)
Congenital hypothyroidism when left untreated results in a syndrome known as Cretinism. Do not delay diagnosis of congenital hypothyroidism until physical manifestations are seen which is characterized by mental retardation, deafness, short stature, and facial deformities.(/p794/col1/para1)
Reference
Roberts CGP, Ladenson PW. Hypothyroidism. Lancet. 2004;363:793-803.
In infants, congenital hypothyroidism is present with hypothermia, poor feeding, bradycardia, jaundice, enlarged posterior fontanel, and umbilical hernia.
In children and adolescents with congenital hypothyroidism, the clinical manifestations include growth failure with delayed bone maturation, delay in the eruption of permanent teeth, pseudo hypertrophy of muscles, enlargement of pituitary gland, galactorrhoea, and delayed or precocious puberty.(/p797/col1/para4)
Reference
Roberts CGP, Ladenson PW. Hypothyroidism. Lancet. 2004;363:793-803.
The goal of therapy in the management of congenital hypothyroidism is to normalize TSH values, and maintain T4 and free T4 hormone levels in the upper half of the reference range.
Permanence of congenital hypothyroidism can be assessed by the presence of ectopic or absence of thyroid gland in the thyroid scan. If the initial TSH values are less than 50 mIU/L, with no rise in TSH values after newborn period, off therapy is tried at 3 years. If TSH increases during the off-therapy period, the condition may be considered as permanent congenital hypothyroidism.
During the phase of initial work-up, detailed history and physical examination of the child is recorded. This is followed by referring the patient to pediatric endocrinologist. The serum TSH and FT4 values are reassessed, followed by thyroid ultrasonography and/or thyroid scan to confirm the diagnosis of congenital hypothyroidism.
Congenital hypothyroidism can be managed by administering oral, once daily, LT4 at a dose of 10 to 15 mcg/day. T4 and TSH levels are monitored 2 to 4 weeks after initiation of the treatment. During the first 6 months, monitoring hormone levels every 1 to 2 months, and between 6 months and 3 years of age, monitoring hormone levels every 3 to 4 months is recommended. From 3 years of age to end of growth period, monitoring every 6 to 12 months is recommended.(/p2297/col1/table1)
Reference
Rose SR, Brown RS. Update of newborn screening and therapy for congenital hypothyroidism. Pediatrics. 2006;117(6):2290-2303.