A Sluggish Thyroid Gland
PKGhatak,MD
The Thyroid gland produces a hormone called Thyroxine. Thyroxine is essential to all living cells and must be supplied constantly just like oxygen and sugar. It controls all chemical activities of the body acting like a metabolic thermostat. When the blood levels of thyroxine fall below the normal levels the condition is known as Hypothyroidism. It may be a temporary condition as seen in acute serious illness, prolonged malnutrition, and starvation; the thyroid function will return to normal with the reversal of the primary condition. When a disease affects the thyroid gland hypothyroidism will persist unless proper treatment is undertaken.
The thyroid gland has the shape of a monarch butterfly with wings half open. The gland is located in the neck below Adam’s apple and in front of the windpipe. It has a very rich blood supply. The thyroxine enters directly into the blood supply. The thyroid gland is under the control of the Anterior pituitary gland, which is located inside the skull below the brain, above the roof of the nose and in between the eyes. When the Anterior pituitary senses thyroid function is falling it sends out a chemical messenger – Thyroid Stimulating Hormone (TSH) to boost the thyroid gland activity. As production of the thyroxine increases the anterior pituitary scales back TSH release. This process of check and balance is known as the negative feedback loop.
The main hormone Thyroxine has four Iodine atoms bound to an amino acid Tyrosine (T4). In addition, the Triiodothyronine hormone (T3), containing three atoms of iodine is also produced by the thyroid gland in a smaller amount. Both T4 and T3 are carried in the blood bound to plasma proteins, and only a tiny amount (0.05%) remains free and is metabolically active. They are called Free T4 and Free T3 respectively. Though T3 in the blood is present in a smaller amount it plays a dominant role. It is 3 to 5 times more active than T4; it acts faster, disappears faster and is bound loosely to plasma proteins. In the tissues, most of the T4 is converted to T3 before it acts on the cells. In the thyroid gland, 80% of thyroid hormone is T4 and the rest 20% is T3. In blood T4 to T3 ratio is 40: 1.
We take in about 100 to 400 micrograms (mcg) of Iodine daily with food and drinks. The thyroid gland needs about 30 mcg of dietary iodine and the rest of the iodine is obtained by recycling the breakdown products of thyroxine. The thyroid gland takes up iodine from the blood by an active process because iodine concentration in the thyroid gland is higher than that of blood. The iodine is oxidized to iodide and then attached to the tyrosine residues of a glycoprotein. Cells of the thyroid follicle pick up iodinated glycoprotein and convert it into T4 and T3 within the follicular cells. And then release T4 and T3 in the blood when needed. Each and every one of these four steps of hormone production and subsequent release is controlled by TSH. At each stage, a specific enzyme is required for the completion of the process.
Decreased levels of circulating thyroid hormone will initiate the release of TSH from the anterior pituitary gland. TSH blood level is an accurate and sensitive test for the detection of hypofunction of the thyroid gland. TSH test has replaced most of the other tests used in earlier years. TSH is extremely useful in monitoring patients on thyroid replacement treatment and during pregnancy. A developing fetus starts making thyroxine at 18 weeks; in the second trimester mother’s blood supplies a good part of thyroxine to the growing child. If a mother is hypothyroid and remains untreated, the child will have a low IQ and even mental retardation.
Iodized salt, bread, milk and saltwater fish are the major source of iodine for the population in the USA. The population of countries deficient in dietary iodine and others who are unable to metabolize iodine because of high consumption of cassavas and turnips in their diet suffers from chronic iodine shortage. As a consequence, the thyroid gland enlarges. Many people present with an enlarged gland (goiter), and this condition is called Endemic Goiter. They may or may not show signs of hypothyroidism. But left untreated, most of them will have some complications in the long run. The treatment of endemic goiter is to supply Iodized salt or other forms of iodine in the diet.
Congenital deficiency of enzymes responsible for iodine transport or its incorporation into the glycoprotein and subsequent production of thyroxin may result in congenital hypothyroidism. These cases are rare. In still rare instances a child may be born without a thyroid gland. Often the disorder is not detected at birth because a mother has supplied thyroxine during pregnancy and by breastfeeding. A child presents with an enlarged thyroid gland at times the gland may have grown ten times the normal size. Such a Cretin child, as it is called, has a puffy face, enlarged tongue, and low forehead, increased hair, umbilical hernia and sluggish response to stimuli. Various neurological deficits, from deafness to paraplegia may be present. If treatment is delayed then mental retardation, deafness, muteness, stunted growth may be permanent.
The signs and symptoms of hypothyroidism are variable depending upon the severity and duration of the condition. Patients may complain of tiredness, fatigue, and weight gain, depression, falling asleep at inappropriate times and constipation. In some cases, muscle pain, pain in joints and effusion of knees are present. Cold sensitiveness, deafness, a decrease in taste and smell sensations may be present. A large tongue, non-pitting edema, puffy and watery eyes, menstrual disturbances in the female, thinning of hair and loss of the outer half of eyebrows, coarse skin, carpal tunnel syndrome may be present on examination. In some cases, fluid in the pericardial sac, pleural cavities, and ascites may be present. Patients may have slow mentation, confusion, and somnolence. The term Myxedema is used in the hypothyroid patient when weight gain, non-pitting edema, low serum sodium and fluid overload are present. Various psychiatric symptoms from disorientation, hallucination, paranoia, and psychosis in myxedema are commonly referred to as myxedema madness. In severe cases, a coma may result. When a patient presents with a myxedema coma the chance of survival is very poor.
In a given patient the precise cause of hypofunction of the thyroid gland may remain unknown. Viral infections either directly or by inducing an autoimmune response may damage the thyroid gland. Lymphocytic infiltration of the thyroid gland and subsequent hypofunction known by Hashimoto thyroiditis is well known. Infectious mononucleosis may damage the thyroid gland. Radiation to the neck, chest, and shoulder can damage the thyroid gland and result in decreased function. People with hepatitis C infection may develop autoimmune thyroiditis. Drugs used in the treatment of seizures like Dilantin, and Phenobarbital can lower T4 levels. Other drugs like Lithium and Amiodarone, Phenylbutazone, Sulfonamides Interferon alpha, and beta have significant adverse effects on thyroid function. Cancer, Sarcoidosis and thyroid surgery, and previous treatment with radioactive iodine may damage part or whole of the thyroid gland. TSH may be elevated in autoimmune diseases, acute psychiatric illnesses and in the elderly. Many drugs used in the treatment of various diseases may cause hypothyroidism or drugs may interfere with T4, T3, and TSH tests. One should be careful in interpreting those test results correctly.
In certain conditions of the Anterior Pituitary less than the normal amount of TSH is secreted, this results in decreased production of thyroxine. This condition is called Secondary Hypothyroidism.
The treatment of Hypothyroidism consists of: -
1. To supply thyroid hormone in the form of oral tablets.
2. Proper follow up with the adjustment of thyroid dose over the lifetime of a patient.
One tablet a day dose is inexpensive and effective. Iron and calcium tablets taken with thyroid medication interfere with the absorption of thyroid hormone. An antacid containing aluminum hydroxide, soy milk, proton-pump-inhibitor and many other agents also interfere with thyroid hormone absorption. It is recommended that thyroid tablets should be taken without other medications. The bioavailability of T4 varies from brand to brand. It is better to stay with one name brand or one manufacturer of a generic thyroid drug.
The results of hormone replacement therapy are excellent. Only in far advanced cases and in myxedema coma the results are not good.
The thyroid gland has the shape of a monarch butterfly with wings half open. The gland is located in the neck below Adam’s apple and in front of the windpipe. It has a very rich blood supply. The thyroxine enters directly into the blood supply. The thyroid gland is under the control of the Anterior pituitary gland, which is located inside the skull below the brain, above the roof of the nose and in between the eyes. When the Anterior pituitary senses thyroid function is falling it sends out a chemical messenger – Thyroid Stimulating Hormone (TSH) to boost the thyroid gland activity. As production of the thyroxine increases the anterior pituitary scales back TSH release. This process of check and balance is known as the negative feedback loop.
The main hormone Thyroxine has four Iodine atoms bound to an amino acid Tyrosine (T4). In addition, the Triiodothyronine hormone (T3), containing three atoms of iodine is also produced by the thyroid gland in a smaller amount. Both T4 and T3 are carried in the blood bound to plasma proteins, and only a tiny amount (0.05%) remains free and is metabolically active. They are called Free T4 and Free T3 respectively. Though T3 in the blood is present in a smaller amount it plays a dominant role. It is 3 to 5 times more active than T4; it acts faster, disappears faster and is bound loosely to plasma proteins. In the tissues, most of the T4 is converted to T3 before it acts on the cells. In the thyroid gland, 80% of thyroid hormone is T4 and the rest 20% is T3. In blood T4 to T3 ratio is 40: 1.
We take in about 100 to 400 micrograms (mcg) of Iodine daily with food and drinks. The thyroid gland needs about 30 mcg of dietary iodine and the rest of the iodine is obtained by recycling the breakdown products of thyroxine. The thyroid gland takes up iodine from the blood by an active process because iodine concentration in the thyroid gland is higher than that of blood. The iodine is oxidized to iodide and then attached to the tyrosine residues of a glycoprotein. Cells of the thyroid follicle pick up iodinated glycoprotein and convert it into T4 and T3 within the follicular cells. And then release T4 and T3 in the blood when needed. Each and every one of these four steps of hormone production and subsequent release is controlled by TSH. At each stage, a specific enzyme is required for the completion of the process.
Decreased levels of circulating thyroid hormone will initiate the release of TSH from the anterior pituitary gland. TSH blood level is an accurate and sensitive test for the detection of hypofunction of the thyroid gland. TSH test has replaced most of the other tests used in earlier years. TSH is extremely useful in monitoring patients on thyroid replacement treatment and during pregnancy. A developing fetus starts making thyroxine at 18 weeks; in the second trimester mother’s blood supplies a good part of thyroxine to the growing child. If a mother is hypothyroid and remains untreated, the child will have a low IQ and even mental retardation.
Iodized salt, bread, milk and saltwater fish are the major source of iodine for the population in the USA. The population of countries deficient in dietary iodine and others who are unable to metabolize iodine because of high consumption of cassavas and turnips in their diet suffers from chronic iodine shortage. As a consequence, the thyroid gland enlarges. Many people present with an enlarged gland (goiter), and this condition is called Endemic Goiter. They may or may not show signs of hypothyroidism. But left untreated, most of them will have some complications in the long run. The treatment of endemic goiter is to supply Iodized salt or other forms of iodine in the diet.
Congenital deficiency of enzymes responsible for iodine transport or its incorporation into the glycoprotein and subsequent production of thyroxin may result in congenital hypothyroidism. These cases are rare. In still rare instances a child may be born without a thyroid gland. Often the disorder is not detected at birth because a mother has supplied thyroxine during pregnancy and by breastfeeding. A child presents with an enlarged thyroid gland at times the gland may have grown ten times the normal size. Such a Cretin child, as it is called, has a puffy face, enlarged tongue, and low forehead, increased hair, umbilical hernia and sluggish response to stimuli. Various neurological deficits, from deafness to paraplegia may be present. If treatment is delayed then mental retardation, deafness, muteness, stunted growth may be permanent.
The signs and symptoms of hypothyroidism are variable depending upon the severity and duration of the condition. Patients may complain of tiredness, fatigue, and weight gain, depression, falling asleep at inappropriate times and constipation. In some cases, muscle pain, pain in joints and effusion of knees are present. Cold sensitiveness, deafness, a decrease in taste and smell sensations may be present. A large tongue, non-pitting edema, puffy and watery eyes, menstrual disturbances in the female, thinning of hair and loss of the outer half of eyebrows, coarse skin, carpal tunnel syndrome may be present on examination. In some cases, fluid in the pericardial sac, pleural cavities, and ascites may be present. Patients may have slow mentation, confusion, and somnolence. The term Myxedema is used in the hypothyroid patient when weight gain, non-pitting edema, low serum sodium and fluid overload are present. Various psychiatric symptoms from disorientation, hallucination, paranoia, and psychosis in myxedema are commonly referred to as myxedema madness. In severe cases, a coma may result. When a patient presents with a myxedema coma the chance of survival is very poor.
In a given patient the precise cause of hypofunction of the thyroid gland may remain unknown. Viral infections either directly or by inducing an autoimmune response may damage the thyroid gland. Lymphocytic infiltration of the thyroid gland and subsequent hypofunction known by Hashimoto thyroiditis is well known. Infectious mononucleosis may damage the thyroid gland. Radiation to the neck, chest, and shoulder can damage the thyroid gland and result in decreased function. People with hepatitis C infection may develop autoimmune thyroiditis. Drugs used in the treatment of seizures like Dilantin, and Phenobarbital can lower T4 levels. Other drugs like Lithium and Amiodarone, Phenylbutazone, Sulfonamides Interferon alpha, and beta have significant adverse effects on thyroid function. Cancer, Sarcoidosis and thyroid surgery, and previous treatment with radioactive iodine may damage part or whole of the thyroid gland. TSH may be elevated in autoimmune diseases, acute psychiatric illnesses and in the elderly. Many drugs used in the treatment of various diseases may cause hypothyroidism or drugs may interfere with T4, T3, and TSH tests. One should be careful in interpreting those test results correctly.
In certain conditions of the Anterior Pituitary less than the normal amount of TSH is secreted, this results in decreased production of thyroxine. This condition is called Secondary Hypothyroidism.
The treatment of Hypothyroidism consists of: -
1. To supply thyroid hormone in the form of oral tablets.
2. Proper follow up with the adjustment of thyroid dose over the lifetime of a patient.
One tablet a day dose is inexpensive and effective. Iron and calcium tablets taken with thyroid medication interfere with the absorption of thyroid hormone. An antacid containing aluminum hydroxide, soy milk, proton-pump-inhibitor and many other agents also interfere with thyroid hormone absorption. It is recommended that thyroid tablets should be taken without other medications. The bioavailability of T4 varies from brand to brand. It is better to stay with one name brand or one manufacturer of a generic thyroid drug.
The results of hormone replacement therapy are excellent. Only in far advanced cases and in myxedema coma the results are not good.
revised 2020
