Hypothyroidism clinical symptoms

Many of the manifestations of thyroid hyperactivity resemble sympathetic nervous system overactivity (especially in the cardiovascular system), although catecholamine levels are not increased. Changes in catecholamine-stimulated adenylyl cyclase activity as measured by cAMP are found with changes in thyroid activity. Possible explanations include increased numbers of 13 receptors or enhanced amplification of the 13 receptor signal. Other clinical symptoms reminiscent of excessive epinephrine activity (and partially alleviated by adrenoceptor antagonists) include lid lag and retraction, tremor, excessive sweating, anxiety, and nervousness. The opposite constellation of effects is seen in hypothyroidism (Table 38-4). 

There are numerous thyroid gland function tests, each designed to determine the etiology of thyroid dysfunction. In general, though, when hypothyroidism is present, circulating T3 and T4 levels are down and TSH is up. The opposite is true of hyperthyroidism. In addition, free (non-protein-bound) T4 and TBG may be determined to clarify inconclusive results. In hyperthyroidism, free T4 is increased but total T4 may be normal. It is the free serum T4 that has been correlated with clinical symptoms rather than total T4. 

Suboiinioai hypothyroidism is defined as a bioohemioal abnormality charaoterized by an elevated serum level of serum thyroid-stimulating hormone (TSH) with normal thyroid hormones and no clinical symptoms. 

Primary hypoparathyroidism can be due to atrophy of the parathyroid gland, possibly by an autoimmune process. Another cause is removal of the glands during thyroidectomy. Primary hypothyroidism can result in hypocalcaemia with its associated clinical symptoms. 

Iodine deficiency currently affects more than eight hundred million human beings all over the world. It presents in the form of clinical symptoms of hypothyroidism, generally caxising impairment of intellectual development and is usually responsible for obvious signs such as goitre. 

A TSH level of 4.5 to 10 milliunits/L constitutes mild or sub-clinical hypothyroidism, and some patients with a TSH level of 2.5 to 4.5 milliunits/L also may be mildly hypothyroid. A TSH level greater than 10 milliunits/L signifies overt hypothyroidism." The free T4 level will be normal (0.7-1.9 ng/dL or 9.0-24.5 pmol/L) in mild or subclinical hypothyroidism and low (less than 0.7 ng/dL or 9.0 pmol/L) in patients with obvious signs and/or symptoms. 

LT4 is indicated for patients with overt hypothyroidism.22 However, the need for treatment is controversial in patients with mild or subclinical disease (TSH less than 10 milli-units/L). There are no large clinical trials that show an outcome benefit with treating these patients, and the therapeutic decision must be individualized.1,23 Many patients with subclinical hypothyroidism do, in fact, have subtle symptoms that improve with LT4 replacement. If the patient s serum cholesterol is elevated,24 or if serum anti-TPOAbs are present, many clinicians recommend LT4 therapy. 

Many of the signs and symptoms seem to be related to autonomic hyperactivity. As with hypothyroidism, the clinical... 

BW, a 50-year-old woman with a history of osteoarthritis and hypothyroidism, presents to the clinic complaining of hot flashes, vaginal dryness, and insomnia. She states that she experiences approximately two hot flashes per day and is awakened from sleep at least three to four times a week in a "pool of sweat" requiring her to change her clothes and bed linens. Her symptoms began about 3 months ago, and over that time, they have worsened to the point where they have become very bothersome. On questioning, she states her last menstrual period was 1 year ago. 

This point of view overlooks the fact that every well and normal individual is potentially an ill individual, and the roots of disease may be present in his make-up years before there is any overt disease. A dozen young men used as normal controls may each have metabolic peculiarities that point toward a different metabolic derangement gout, multiple sclerosis, diabetes, anemia, atherosclerosis, hypertension, nephrosis, hypothyroidism, rheumatoid arthritis, rheumatic heart disease, liver cirrhosis, and myasthenia gravis, for example, and yet at the time of their use as controls these young men may show no symptoms of the disease which is to appear later in life. It seems far from safe to assume that because an individual on clinical examination seems well, all of his blood values, for example, are normal and meaningless so far as disease susceptibilities are concerned. 

The most extreme manifestation of untreated hypothyroidism is myxedema coma, which even if detected early and appropriately treated, carries a mortality rate of 30 to 60%. Myxedema coma is a misnomer. Most patients exhibit neither the myxedema nor coma. Patients with myxedema coma usually have longstanding hypothyroidism with the classic symptoms of hypothyroidism. Decompensation into myxedema coma may occur when the homeostatic mechanisms of the severely hypothyroid patient are subject to a stressful precipitating event (e.g., infection, trauma, some medications, stroke, surgery). The principal manifestation of myxedema coma is a deterioration of mental status (apathy, confusion, psychosis, but rarely coma). Other common clinical features include hypothermia, diastolic hypertension (early), hypotension (late), hypoventilation, hypoglycemia, and hyponatremia. If myxedema coma is suspected, the patient is usually admitted to an intensive care unit for pulmonary and cardiovascular support... 

Treatment is thyroid hormone replacement. The goal of the therapy is to relieve the symptoms of hypothyroidism by normalizing the levels of circulating thyroid hormones. In addition to the amelioration of symptoms, the clinical effectiveness of the thyroid hormone replacement may be monitored by periodically measuring the serum TSH concentration. The lowest dose of thyroid hormone that is needed to normalize the serum TSH concentration is usually the appropriate dose. Most or all of the symptoms of hypothyroidism should improve with appropriate thyroid hormone replacement, but this may require weeks or months of therapy. 

Thyroid dysregulation has also been reported in depressed patients. Up to 25% of depressed patients are reported to have abnormal thyroid function. These include a blunting of response of thyrotropin to thyrotropin-releasing hormone, and elevations in circulating thyroxine during depressed states. Clinical hypothyroidism often presents with depressive symptoms, which resolve with thyroid hormone supplementation. Thyroid hormones are also commonly used in... 

Failure of the thyroid to produce sufficient thyroid hormone is the most common cause of hypothyroidism and is known as primary hypothyroidism. Secondary hypothyroidism occurs much less often and results from diminished release of TSH from the pituitary. Treatment of hypothyroidism is achieved by the replacement of thyroid hormone, primarily T4. A synthetic preparation of T4 is available, levothyroxine (Synthroid ), which has been a popular choice for hypothyroidism because of its consistent potency and prolonged duration of action. No toxicity occurs when given in physiological replacement doses. Desiccated animal thyroid is also available at a lesser cost. Overdoses cause symptoms of hyperthyroidism and can be used as a guide in clinical management. Hypothyroidism is not cured by the daily intake of thyroid hormone it is a life-long regimen. 

No patients with depression had clinical hypothyroidism and the sole patient with overt hypothyroidism had no depressive symptoms. 

The clinical, biochemical, and thyroid imaging characteristics of thyrotoxicosis resulting from interferon alfa treatment have been retrospectively analysed from data on 10 of 321 patients with chronic hepatitis (75 with chronic hepatitis B and 246 with chronic hepatitis C) who developed biochemical thyrotoxicosis (161). Seven patients had symptomatic disorders, but none had ocular symptoms or a palpable goiter. Six had features of Graves disease that required interferon alfa withdrawal in four and prolonged treatment with antithyroid drugs in all six. Three presented with transient thyrotoxicosis that subsequently progressed to hypothyroidism and required interferon withdrawal in one and thyroxine treatment in aU three. 

Thyroid hormones are frequently affected by lithium, but rarely in a clinically significant way. Changes in certain laboratory tests of thyroid function are common but seldom require discontinuation of treatment. However, approximately 5 percent of patients develop hypothyroidism, which some clinicians elect to treat with thyroid supplementation while continuing lithium (Weber, Saklad, and Kastenhol 1992). Periodic thyroid function monitoring is important, not only from a safety standpoint but to rule out (in the bipolar individual with depressed or mixed-state features), that hypothyroidism is not the cause of symptoms. 

The clinical signs and symptoms of thyroid hormone excess or deficiency are generally vague and nonspecific (see Box 52-4). Therefore when hypothyroidism or hyperthyroidism is suspected, confirmation with laboratory tests is generally required. Guidelines for the selection of appropriate laboratory tests for thyroid function have been published... 

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