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Kharkov National Medical University Department : pathophysiology Medicine: N2 KNMU Teacher :Natalya ** Abstract by** Abu baker maklef Group :17 Course:3 Faculty:M **Subject** ( Thyroid disorders ) (hypothyroidism and hyperthyroidism) Kharkov 2013 Contents 1-Introduction 2-Difference Between Hypothyroidism and Hyperthyroidism 3-Diagnosis Hypothyroidism and Hyperthyroidism 4-Hypothyroidism 4-1Definition 4-21Etiology 4-3Clinical manifestations 4-4Hypothyroidism Pathophysiology 4-5Symptoms 4-6Treatment 4-7Emergency Situation 5-Hyperthyroidism 5-1Definition 5-2Etiology 5-3Clinical manifestations 5-4Hypothyroidism Pathophysiology 5-4Symptoms 5-5Treatment 5-6Emergency Situations 6-Conclusion 7- References Introduction The thyroid is a small butterfly shaped gland that lies just under the skin below the Adam’s apple in the neck. It measures about 2 inches across. The thyroid gland secretes hormones that help regulate the body’s metabolism (how the body uses energy.) There are two main thyroid hormones: T3 (triiodothyronine) and T4 (thyroxine.) T3 is the more active form of hormone, and T4 is converted into T3 by the body as needed. Most of T3 and T4 are bound to proteins in the blood steam. They are inactive until they are separated from the protein. To make these hormones the thyroid gland uses proteins and iodine supplied by the diet. Normally the amount of thyroid hormones that is made and produced is controlled by the pituitary gland. This tiny gland is located at the base of the brain and controls several glands in the body in addition to the thyroid. The pituitary gland is itself controlled by hormones released by the hypothalamus (part of the base of the brain very near the pituitary gland.) The whole system is like a thermostat. For example, when the body senses there is not enough thyroid hormone the hypothalamus releases a hormone TRH (thyrotropin releasing hormone) that causes the pituitary to secrete TSH (thyroid stimulating hormone) that causes the thyroid gland to make and release thyroid hormone. When there is too much thyroid hormone the releasing hormones are turned off and the thyroid stops producing thyroid hormone. When the thyroid gland is overactive and produces too much thyroid hormone an individual develops hyperthyroidism. When the thyroid gland is under active and produces too little thyroid hormone an individual develops hypothyroidism. A section on each of these topics follows our general review of the thyroid gland. Individuals with developmental disabilities are more likely to develop thyroid gland disorders than people in the general population. Individuals with Down, Congenital Rubella, Klinefelter and Turner Syndromes are at particular risk. Annual screening of thyroid function should be a routine part of the health maintenance program for all individuals with developmental disabilities. Difference Between Hypothyroidism and Hyperthyroidism Hypothyroidism is a condition when there is a deficiency of thyroid hormone in the body. Hyperthyroidism is characterized by excessive amounts of thyroid hormone in the body. Both hypothyroidism and hyperthyroidism are extremely different cases. The signs and symptoms of hyperthyroidism include increased heart rate ‘“ tachycardia, increased activity of bowel movements, difficulty in sleeping, intolerance to heat, nervousness and palpitation, increased respiratory rate, increased moisture of the skin, increased metabolic rate, soft and fine hair, wandering mind, sweating, scanty menstrual periods, infertility, muscle weakness, nervousness and soft nails. In hypothyroidism, there are symptoms such as bradycardia- decreased heart rate, constipation, intolerance to cold, memory problems, coarse dry hair, slow speech movements, slow walking movements, dry skin, brittle nails, weight gain, fatigue, irritability, infertility, puffy face, loss of eyebrow hair, and heavy menstrual periods. The causes of hypothyroidism include medications like lithium carbonate, genetic, decreased level of iodine in the body, disturbances in the pituitary gland and hypothalamus, and infections mainly viral and bacterial. Hashimoto’s thyroiditis is an immune disorder in which the thyroid gland is attacked and damaged. Hyperthyroidism is caused by any growth present in the thyroid gland. Grave’s disease is an immunological disorder affecting the thyroid gland. The classical feature of it is exophthalmos ‘“ a protruding eye ball, which is absent in hypothyroidism. Hyperthyroidism can also lead to thyrotoxicosis. The treatment for hypothyroidism includes thyroid hormones. It is given life long to the patient. Thyroxine is the supplement given to the patient. Thyroxine is T4 hormone of the thyroid gland. The patient is advised to take this medication early in the morning. The treatment for hyperthyroidism is anti-thyroid drugs which include propylthiouracil. It will decrease the production of thyroid hormones. Before taking any medications for hypo or hyperthyroidism, the drug interactions should be considered. If there are high levels of thyroid stimulating antibodies in the blood of an infant, then the recommended treatment is exchange blood transfusion. This will decrease the antibody levels in the blood. The diagnosis for hypothyroidism and hyperthyroidism includes the estimation of levels T3 and T4, the thyroid hormones and TSH level. In hypothyroidism, there is decrease in the thyroid hormones level ‘“ T3 and T4 and increase in the levels of TSH. In hyperthyroidism, there are increased levels of thyroid hormones T3 and T4 and decrease in the levels of TSH. TSH is thyroid stimulating hormone. Diagnosis When screening for abnormalities of thyroid gland function most doctors will order blood tests that measure the level of TSH (thyroid stimulating hormone) and freeT4. Depending upon the results of these tests and upon the specific thyroid disorder, a number of other tests may be ordered. Some other tests include levels of T3, thyroxine-binding protein, antithyroid antibodies, and serum thyroglobulin. Occasionally tests that evaluate functional responses to stimulation of the thyroid or pituitary glands may be performed. The anatomy of the thyroid gland can be evaluated by a thyroid ultrasound or by a thyroid scan. The scan in done by injecting a minute amount of radioactive iodine into the individual, waiting 30 minutes and then measuring the radioactivity over the thyroid gland (which has the unique capacity of trapping iodine.) The scan produces a picture of the active part of the thyroid gland. A needle biopsy (taking a sample of tissue) or needle aspiration (taking a sample of fluid) from nodules in the thyroid gland can also be done by a physician. Hypothyroidism Definition Hypothyroidism Hypothyroidism is a condition in which the thyroid gland is under active and produces too little thyroid hormone. When the condition is very severe it is sometimes called myxedema because a substance collects in subcutaneous tissues (under the skin) that causes nonpitting edema. About 95% of the time hypothyroidism is the result of malfunction of the thyroid gland itself (primary hypothyroidism.) Causes of primary hypothyroidism can be either, congenital (something an individual is born with) or acquired (something an individual gets.) The most common causes of primary hypothyroidism are acquired and are the result of destruction of the gland by an autoimmune disease (such as Hashimoto’s thyroiditis) or by radioactive iodine therapy or surgery for hyperthyroidism. Other causes of primary hypothyroidism include goiter due to iodine deficiency and too much iodine in individuals with thyroid disease. Some drugs can also cause hypothyroidism including lithium carbonate, paraaminosalicylic acid, thiourea drugs, sulfonamides, phenylbutazone and others. Decades ago congenital hypothyroidism was a common cause of mental retardation and severe disability in affected children. Now thanks to newborn screening, most babies with this condition are diagnosed early, treated and the most devastating consequences of the disease are avoided. About 5% of the time hypothyroidism is the result of a problem outside of the thyroid gland itself (secondary hypothyroidism.) Tumors or other abnormalities of the hypothalamus or pituitary gland are examples of conditions that can cause secondary hypothyroidism. Rarely an individual’s tissues are resistant to thyroid hormone. Etiology Hypothyroidism is classified as primary when it is caused by failure of the stimulated thyroid gland to release adequate amounts of thyroxine and triiodothyronine, secondary when it is caused by inadequate pituitary secretion of thyrotropin (thyroid-stimulating hormone), and tertiary when it is due to insufficient production of thyrotropin-releasing hormone by the hypothalamus. Primary hypothyroidism is much more common than the other 2 forms. In the United States, primary hypothyroidism is most often the result of chronic autoimmune thyroiditis or of surgical or radioiodine ablation of an overactive thyroid gland (Kaplan 1999; Tews et al 2005; Devdhar et al 2007). Other causes include iodine deficiency, iodine excess, congenital conditions, and drugs or environmental chemicals that impair hormone biosynthesis, such as lithium, amiodarone, sulfonamides, sulfonylureas, carbamazepine, oxcarbazepine, phenytoin, valproate, interleukins, sunitinib and other tyrosine kinase inhibitors, propylthiouracil, methimazole , polychlorinated biphenyls, bisphenol-A, and polybrominated diphenyl Clinical manifestations The systemic manifestations of hypothyroidism include fatigue, lethargy, constipation, cold intolerance, menorrhagia, reduced appetite, weight gain, dry skin, dryness and thinning of the hair, and deepening of the voice. Patients with severe hypothyroidism have pale, cool skin that feels doughy, sparse hair, a large tongue, and periorbital puffiness. The heart is usually enlarged, and adynamic ileus can occur. Congenital hypothyroidism is associated with an increased risk of systemic malformations, especially cardiac and urogenital anomalies Altered mental status. Congenital hypothyroidism is associated with persistent, subtle, neurocognitive deficits, even though mental retardation is now rare because of newborn screening and early treatment Seizures. Seizures are most common in myxedema coma but can occur with less severe disease. In a series of 56 patients with adult myxedema, 10 patients (18%) presented with seizures or syncope (Jellinek 1962). The seizures are typically generalized, but complex partial seizures have also been reported. Strokes. No clear association is seen between hypothyroidism and strokes, but hypothyroidism is associated with diastolic hypertension and increased total and LDL cholesterol levels. It is also associated with elevated plasma homocysteine levels, and it may affect endothelial function and coagulation profiles. Thus, hypothyroidism affects stroke risk factors in ways that could lead to an increased risk of stroke, but the relationship requires further study (Squizzato et al 2005). Preexisting hypothyroidism or subclinical hypothyroidism may be associated with milder clinical presentation and improved outcome (Alevizaki et al 2006; Baek et al 2010; Akhoundi et al 2011). Headaches. Many patients with hypothyroidism report headaches. In 1 series, 14% of patients had this complaint (Sanders 1962b). The headaches do not have any distinguishing characteristics; they are usually chronic, recurrent, and diffuse. Ataxia. Ataxia is present in 25% to 33% of patients with hypothyroidism (Cremer et al 1969). These patients all have an unsteady gait, and many of them also have limb incoordination. Dysarthria also occurs but is less common. There is 1 report of Hashimoto encephalopathy presenting with progressive ataxia (Nakagawa et al 2007). Movement disorders. Some features of hypothyroidism, such as bradykinesia and voice abnormalities, mimic parkinsonism, but no association has been documented between hypothyroidism and Parkinson disease (Munhoz et al 2004). One case has been reported of a 12-year-old girl in whom titubation and paroxysmal dyskinesia were the presenting symptoms of hypothyroidism due to lymphocytic thyroiditis (Hopkins et al 2007). Cranial nerve abnormalities. Hypothyroid patients frequently report hearing loss, but it is thought to be due to fluid accumulation in the inner ear rather than neurologic dysfunction. It improves after hormone replacement. Tinnitus and vertigo are less common complaints. Ptosis occurs in 50% to 75% of hypothyroid patients, apparently due to decreased sympathetic tone. Patients with autoimmune thyroid disease can develop thyroid ophthalmopathy, a condition in which infiltration of the extraocular muscles with glycosaminoglycans and inflammatory edema cause diplopia, exophthalmos, pain behind the eyes, and blurred vision (Hattori et al 2006). In primary hypothyroidism, secondary pituitary enlargement can cause chiasmal compression leading to visual field defects. Distortions of taste and smell are common in patients with hypothyroidism, and they are largely reversed with hormone replacement (McConnell et al 1975). Hoarseness and articulation defects are also common, but they are probably a result of mucopolysaccharide deposition in the larynx, vocal cords, and tongue, rather than cranial nerve dysfunction (Stollberger et al 2001; Kovacs et al 2010). Trigeminal neuralgia and facial palsy have been reported in patients with hypothyroidism but so rarely that the association may have been due to chance. Genis and colleagues reported 1 case of a patient with hemifacial spasm that resolved with thyroid replacement, reappeared when treatment was stopped, and disappeared again when treatment was resumed (Genis et al 1993). According to one group of investigators, Hashimoto thyroiditis is common among patients with benign paroxysmal positional vertigo, but the association is independent of thyroid status (Papi et al 2010). Sleep disorders. Obstructive sleep apnea was documented in 45% of successive hypothyroid patients in 1 prospective study (Hira and Sibal 1999). It can occur either on the basis of associated obesity or because of mucopolysaccharide deposition in the tongue and upper airway (Kaminski and Ruff 1989). Central sleep apnea has also been reported. The symptoms of idiopathic hypersomnia have also been reported to improve after initiating treatment with thyroxine in patients with subclinical hypothyroidism (Shinno et al 2009). Spastic paraparesis. Paraplegia and extensor plantar responses have been reported in hypothyroid patients but so infrequently that the association may have been fortuitous. A single case has been reported of a patient with hypothyroidism of hypothalamic origin who had spastic paraplegia that resolved with physiologic doses of thyroid replacement (Jackson et al 1978). However, the patient also received a small physiologic dose of prednisone. Peripheral nerve involvement. Hypothyroid patients commonly report limb paresthesias, but electrodiagnostic studies demonstrate a peripheral polyneuropathy in only a minority of patients (Rao et al 1980; Duyff et al 2000; El-Salem and Ammari 2006; Orstavik et al 2006; Nebuchennykh et al 2010). Elevated thermal thresholds have been described in patients with hypothyroidism and unexplained pain in the extremities, suggesting the possibility of small-fiber neuropathy (Orstavik et al 2006). Severe neuropathy is rare. The most common peripheral nerve manifestation of hypothyroidism is carpal tunnel syndrome, probably resulting from either obesity or mucopolysaccharide deposition within the nerve itself and in the surrounding tissue. Some hypothyroid patients have recurrent laryngeal nerve lesions as a result of prior thyroid surgery or because of compression by an enlarged thyroid gland. Thyroid enlargement can also compress the sympathetic chain in the neck to produce unilateral or bilateral Horner syndrome. Neuromuscular junction dysfunction. A few hypothyroid patients with myasthenic syndromes that responded to thyroid replacement have been reported (Norris 1966; Takamori et al 1972). The neuromuscular transmission abnormality was different from that seen in myasthenia gravis. Autoimmune thyroiditis may be associated with a myasthenic syndrome, but this is presumably due to the autoimmune disorder rather than a direct manifestation of hypothyroidism (Turker et al 2008). Muscle abnormalities. Proximal muscle weakness develops in about 25% of patients with hypothyroidism (Rao et al 1980). The weakness is usually mild, and most of the patients complain of associated pain, slowness, or stiffness. The weakness is slowly progressive over months to years. Serum creatine kinase measurement cannot be used as an indication of myopathy in hypothyroidism because creatine kinase levels are increased in about 90% of hypothyroid patients, most of whom do not have overt myopathy (Graig and Smith 1965; Finsterer et al 1999; Biondi and Cooper 2008). Conversely, markedly elevated creatine kinase levels do not exclude the diagnosis of hypothyroid myopathy (Scott et al 2002). Several abnormalities of muscle contraction are characteristic of hypothyroidism. Prolongation of both contraction and relaxation phases results in slow or "hung up" reflexes that normalize with thyroid hormone replacement. Measurement of reflex time was even used to assess adequacy of therapy before radioimmunoassays became readily available. Hypothyroidism can also lead to muscle enlargement, especially in children. The Kocher-Debre-Semelaigne syndrome refers to an "infant Hercules" appearance in some children with cretinism who manifest a striking increase in muscle bulk without an accompanying increase in muscle function (Salaria and Parmar 2004). Some hypothyroid adults have enlarged, firm muscles that become increasingly stiff and painful with exercise, forcing them to rest briefly before resuming activity, a condition known as Hoffman syndrome (Deepak et al 2004). Although this muscle activity bears a superficial resemblance to myotonia, it is not accompanied by electrical activity. Electrically silent contraction also occurs in myoedema, a local mound of contracting muscle induced by percussion or some other mechanical irritation of the muscle. Myoedema is present in about one third of hypothyroid patients. Hypothyroidism Pathophysiology Thyroid hormone deficiency affects different organs and body systems. Clinical data of hypothyroidism patophysiology usually depend on the degree of biochemical changes, however may occur that a person with a severe deficiency of hormones present mild symptoms while a person with a minor deficiency may show strong signs of hypothyroidism. Due to increase of medical information in all media, is possible to find welldocumented notes about hypothyroidism but in some cases it is also possible to find information only with a commercial purpose. This causes confusion among patients who consult their doctor wanting to know if they have a real hypothyroid problem even when their thyroid function is normal or if they have just some symptoms without laboratory values that support any thyroid disease and for which the physician may only catalog the problem as a probable thyroid dysfunction or thyroid imbalance. Symptoms fatigue, exhaustion feeling run down and sluggish depression difficulty concentrating, brain fog unexplained or excessive weight gain dry, coarse and/or itchy skin dry, coarse and/or thinning hair feeling cold, especially in the extremities constipation muscle cramps increased menstrual flow more frequent periods infertility/miscarriage Treatment Hypothyroidism is an easily treated disease. Several preparations for thyroid replacement are on the market. The most frequently prescribed is Synthroid (levothyroxine.) Other preparations include Liotrix, Desiccated Thyroid, and Levotriiodothyronine. Regulating the dose of thyroid replacement hormone may take a few weeks and several blood tests to determine if the correct amount of medication is being given. After thyroid function is back to normal the doctor will want to monitor therapy by checking serum free T4, TSH and T3 levels annually. Emergency Situations – What can go wrong? Symptoms of hypothyroidism develop slowly and acute emergency situations are very rare. Since we know now that individuals with developmental disabilities are more prone to thyroid disorders than other people, we hope that physicians are checking thyroid function every year as part of health maintenance of every individual with a developmental disability. Early diagnosis and treatment is the solution to avoiding the only potentially life threatening complication of untreated hypothyroidism that is myxedema coma. In myxedema coma the breathing slows, the person has seizures and blood supply to the brain is decreased. It can be triggered by cold exposure, infection, trauma or medications like sedatives or tranquilizers. What to do? 1. Suspect hypothyroidism long before any of these symptoms occur so it can be diagnosed and treated early. 2. If an individual presents to you with the symptoms of myxedema coma call 911 for immediate transport to a hospital emergency room. Hyperthyroidism Definition Hyperthyroidism is hyperthyroidism the thyroid gland is overactive and produces too much thyroid hormone. Over 2 ½ million Americans have hyperthyroidism. It is much more common in women than in men. There are several causes of hyperthyroidism. The most common include immunologic conditions (like Graves’ disease and thyroiditis,) toxic thyroid nodules (adenomas), and toxic multinodular (many nodules or adenomas) goiter (enlargement of the thyroid gland.) Graves disease is a syndrome of hypermetabolism, enlarged thyroid gland and exopthalmous (bulging of the eyeballs due to the collection of abnormal substances in the tissues of the orbit.) Autoimmune thyroiditis is an inflammation of the thyroid gland that may cause damage to the gland and eventually result in hypothyroidism. Thyroid nodules (one or many) are areas of abnormal thyroid tissue within the thyroid gland. They can be benign or malignant (cancer) but most are benign (not cancer.) Etiology Hyperthyroidism may result from increased synthesis and secretion of thyroid hormones (thyroxine [T4] and triiodothyronine [T3]) from the thyroid, caused by thyroid stimulators in the blood or by autonomous thyroid hyperfunction. It can also result from excessive release of thyroid hormone from the thyroid without increased synthesis. Such release is commonly caused by the destructive changes of various types of thyroiditis. Various clinical syndromes also cause hyperthyroidism. The most common causes overall include Graves' disease Thyroiditis Multinodular goiter Single, autonomous, hyperfunctioning "hot" nodule Graves' disease (toxic diffuse goiter), the most common cause of hyperthyroidism, is characterized by hyperthyroidism and one or more of the following: Goiter Exophthalmos Infiltrative dermopathy Graves' disease is caused by an autoantibody against the thyroid receptor for thyroid-stimulating hormone (TSH); unlike most autoantibodies, which are inhibitory, this autoantibody is stimulatory, thus causing continuous synthesis and secretion of excess T4 and T3. Graves' disease (like Hashimoto's thyroiditis) sometimes occurs with other autoimmune disorders, including type 1 diabetes mellitus, vitiligo, premature graying of hair, pernicious anemia, connective tissue disorders, and polyglandular deficiency syndrome. The pathogenesis of infiltrative ophthalmopathy (responsible for the exophthalmos in Graves' disease) is poorly understood but may result from immunoglobulins directed to the TSH receptors in the orbital fibroblasts and fat that result in release of proinflammatory cytokines, inflammation, and accumulation of glycosaminoglycans. Ophthalmopathy may also occur before the onset of hyperthyroidism or as late as 20 yr afterward and frequently worsens or abates independently of the clinical course of hyperthyroidism. Typical ophthalmopathy in the presence of normal thyroid function is called euthyroid Graves' disease. Inappropriate TSH secretion is a rare cause. Patients with hyperthyroidism have essentially undetectable TSH except for those with a TSH-secreting anterior pituitary adenoma or pituitary resistance to thyroid hormone. TSH levels are high, and the TSH produced in both disorders is biologically more active than normal TSH. An increase in the α-subunit of TSH in the blood (helpful in differential diagnosis) occurs in patients with a TSH-secreting pituitary adenoma. Molar pregnancy, choriocarcinoma, and hyperemesis gravidarum produce high levels of serum human chorionic gonadotropin (hCG), a weak thyroid stimulator. Levels of hCG are highest during the 1st trimester of pregnancy and result in the decrease in serum TSH and mild increase in serum free T4 sometimes observed at that time. The increased thyroid stimulation may be caused by increased levels of partially desialated hCG, an hCG variant that appears to be a more potent thyroid stimulator than more sialated hCG. Hyperthyroidism in molar pregnancy, choriocarcinoma, and hyperemesis gravidarum is transient; normal thyroid function resumes when the molar pregnancy is evacuated, the choriocarcinoma is appropriately treated, or the hyperemesis gravidarum abates. Nonautoimmune autosomal dominant hyperthyroidism manifests during infancy. It results from mutations in the TSH receptor gene that produce continuous thyroid stimulation. Toxic solitary or multinodular goiter (Plummer's disease) sometimes results from TSH receptor gene mutations causing continuous thyroid activation. Patients with toxic nodular goiter have none of the autoimmune manifestations or circulating antibodies observed in patients with Graves' disease. Also, in contrast to Graves' disease, toxic solitary and multinodular goiters usually do not remit. Inflammatory thyroid disease (thyroiditis) includes subacute granulomatous thyroiditis, Hashimoto's thyroiditis, and silent lymphocytic thyroiditis, a variant of Hashimoto's thyroiditis (see Thyroid Disorders: Silent Lymphocytic Thyroiditis). Hyperthyroidism results from destructive changes in the gland and release of stored hormone, not from increased synthesis. Hypothyroidism may follow. Drug-induced hyperthyroidism can result from amiodarone and interferon alfa, which may induce thyroiditis with hyperthyroidism and other thyroid disorders. Although more commonly causing hypothyroidism, lithium can rarely cause hyperthyroidism. Patients receiving these drugs should be closely monitored. Thyrotoxicosis factitia is hyperthyroidism resulting from conscious or accidental overingestion of thyroid hormone. Excess iodine ingestion causes hyperthyroidism with a low thyroid radioactive iodine uptake. It most often occurs in patients with underlying nontoxic nodular goiter (especially elderly patients) who are given drugs that contain iodine (eg, amiodarone , iodine-containing expectorants) or who undergo radiologic studies using iodine-rich contrast agents. The etiology may be that the excess iodine provides substrate for functionally autonomous (ie, not under TSH regulation) areas of the thyroid to produce hormone. Hyperthyroidism usually persists as long as excess iodine remains in the circulation. Metastatic thyroid cancer is a possible cause. Overproduction of thyroid hormone occurs rarely from functioning metastatic follicular carcinoma, especially in pulmonary metastases. Struma ovarii develops when ovarian teratomas contain enough thyroid tissue to cause true hyperthyroidism. Radioactive iodine uptake occurs in the pelvis, and uptake by the thyroid is usually suppressed. Clinical Manifestations The clinical consequences of thyroid endocrine excess are exaggerated expressions with the physiologic activity of T3 and T4. An extra of thyroid hormone brings about enough extra heat production to outcome inside a slight rise in body temperature and to activate heat-dissipating mechanisms, such as cutaneous vasodilation and a decrease in peripheral vascular resistance and elevated sweating. The increased basal metabolic fee leads to fat loss, especially in older sufferers with poor appetite. In younger patients, food intake usually increases, and some patients have seemingly insatiable appetites. The apparent increased catecholamine effect of hyperthyroidism is probably multifactorial in origin. Thyroid hormones improve -adrenergic receptors in many tissues, including center muscle, skeletal muscle, adipose tissue, and lymphocytes. They also decrease -adrenergic receptors in center muscle tissue and may amplify catecholamine action at a postreceptor site. Therefore, thyrotoxicosis is characterized by an elevated metabolic and hemodynamic sensitivity with the tissues to catecholamines. However, circulating catecholamine levels are normal. Drugs that block -adrenergic receptors reduce or eliminate the tachycardia, arrhythmias, sweating, and tremor of hyperthyroidism. When beta-blockers are used within the treatment of hyperthyroidism, it appears that "nonselective" -blockers (such as propranolol), which block each 1 and 2 receptors, have an advantage more than "selective" 1-blockers (for example metoprolol). Hyperthyroidism Pathophysiology The thyroid is a hormone that controls the metabolism of the body. The hypothalamus and the pituitary gland control the secretion of TSH which stimulates the secretion of the thyroid hormones, triiodothyronine, or T3 and thyroxine, or T4. When the body secretes an over abundance of these hormones it is referred to as hyperthyroidism. ("Hyperthyroidism", 2010) The most common form of hyperthyroidism is Graves Disease which occurs in 75% of all cases of hyperthyroidism. It is an autoimmune disorder in which the patient an enlarged thyroid which excretes excess amounts of thyroid hormone. “In this disease the patient develops antibodies to the TSH receptor. These antibodies attach to the receptors and stimulate the thyroid gland to release T3, T4, or both.” Another cause is toxic nodular goiters. These nodules will release thyroid hormones regardless of the TSH production of the body. (Lewis, et al., 2011)Other causes include, thyroiditis, tumors of the testes or ovaries, receiving too much iodine, or taking too much thyroid hormone. Symptoms Too much thyroid hormone speeds up metabolism and the symptoms can be dramatic. The heart pounds rapidly and may develop an irregular beat (arrhythmia.) Blood pressure goes up. The individual looses weight despite an increased appetite. There is usually heat intolerance and excess sweating, diarrhea, sleep disturbance, and muscle weakness. Many individuals feel nervous, tremulous (shaky) and emotionally labile. The skin feels smooth, warm and moist. With Graves’ disease there may be mild or marked bulging of the eyes that leads to irritation, drying, inflammation, and increased sensitivity to light. nervousness irritability increased perspiration thinning of your skin fine brittle hair muscular weakness especially involving the upper arms and thighs shaky hands panic disorder Treatment Treatment of hyperthyroidism depends upon the cause of the condition. Several options are available including medications, radioactive iodine therapy and surgery. Antithyroid medications used to treat hyperthyroidism include propylthiouracil (PTU) and methimazole (Tapazole.) They have several unpleasant side effects including rash, damage to white blood cell production (agranulocytosis,) liver damage and inflammation of blood vessels (vasculitis.) The doctor will monitor the white blood cell count (WBC) and liver function tests (LFTs) on a regular basis as long as the patient is taking one of these drugs. Very often treatment will be done in two stages. In the short-term, antithyroid drugs will be prescribed to decrease the production and release of thyroid hormone. Plenty of rest, good nutrition and stress management are also important pieces of the initial management of hyperthyroidism. Sometimes B-adrenergic blocking agents (like Propanolol) are prescribed to reduce the symptoms of hyperthyroidism during this phase of treatment. These medications slow down the heart rate, reduce the shakiness and control anxiety. Some patients (10-20%) may go into remission with this therapy. Most will need to be reassessed between 12-18 months and a decision made about long-term management Options for longterm management include continuation of antithyroid medication, surgery or radioactive iodine therapy. It is up to the individual and the physician to decide the best method of treatment in each case. Individuals with eye involvement will need to be followed by an ophthalmologist. Emergency Situations – What can go wrong? The most serious, life-threatening complication of hyperthyroidism is thyroid storm. This condition can be precipitated by infection or extra stress in an individual who has hyperthyroidism. Many of the symptoms of hyperthyroidism are exaggerated. 1. Racing heart 2. Palpitations 3. Excessive sweating 4. High fever 5. High blood pressure 6. Abdominal pain What to do? 1. When a marked increase in the symptoms noted above occurs in an individual with hyperthyroidism, suspect thyroid storm. 2. Notify the individual’s PCP or endocrinologist. 3. Call 911 for transport to the hospital. Thyroid storm requires intensive in-patient hospital treatment. Conclusion Abnormalities of thyroid gland function are more common among individuals with developmental disabilities than in the general population. Most will have either hypothyroidism (underactive thyroid function) or hyperthyroidism (over active thyroid function.) Both conditions are treatable. Onset of hypothyroidism can occur over a fairly long time and the symptoms can be subtle. In contrast, onset of hyperthyroidism is usually more rapid and the symptoms are often dramatic. If we can keep the possibility of abnormal thyroid function in mind we will not be likely to miss the diagnosis. Screening tests of thyroid function should be a part of routine health maintenance for all individuals with a developmental disability. In summary, a susceptible person develops Graves' disease because of one or more factors that trigger off thyroid overactivity. As thyroid function increases, more thyroid hormones are released into the blood stream, producing the symptoms of hyperthyroidism. Congenital hypothyroidism can result in profound cognitive and developmental delays in infants and children unless diagnosed within days of birth and treatment initiated. The incidence of congenital hypothyroidism may have doubled during the past decade, but variability of screening techniques and criteria for a positive newborn screening result vary across the United States. Pediatric primary care providers and pediatric nurses must monitor newborn screening results and make sure infants with a positive screen are seen by a pediatric endocrinologist for diagnosis and initiation of treatment. They must educate parents on the condition and importance of frequent serum monitoring of thyroid levels to assure optimal growth and development of the References Pathophysiology book ( N.K.SIMEONOVA) Huether, S., & McCance, K. (2007). Understanding Pathophysiology (4th ed.). St. Louis: Mosby. Guyton, A.C., & Hall, J.E. (2000). Medical Physiology. (10th ed.). Philadelphia: W.B. Saunders. drbrodabarnes.com Cecil Textbook of Medicine,19th Edition, W.B.Saunders Company, 1992 pp.1248-1271 Sharon Witemeyer MD (Pediatrician) Continuum of Care 2350 Alamo Avenue SE, Suite 155 Albuquerque, NM 87106 505.925.2350 Fax 505.925.2389 hsc.unm.edu/som/coc Douglas J Gelb MD PhD, author. Dr. Gelb of the University of Michigan has no relevant financial relationships to disclose. Zachary N London MD, editor. Dr. London of the University of Michigan has no relevant financial relationships to disclose.