All of this information can be found in the Merck Manual.
Symptoms and Signs
Most symptoms and signs of hyperthyroidism are the same for all types with some exceptions, such as infiltrative ophthalmopathy (common) and dermopathy (uncommon), which are autoimmune manifestations of Graves' disease and are not seen in other causes.
clinical presentation of hyperthyroidism may be dramatic or subtle. Common
signs and symptoms are goiter; tachycardia; widened pulse pressure; warm, fine,
moist skin; tremor; eye signs (see below); atrial
fibrillation; nervousness and increased activity; increased sweating;
hypersensitivity to heat; palpitations; fatigue; increased appetite; weight
loss; insomnia; weakness; and frequent bowel movements (occasionally diarrhea).
Many symptoms of hyperthyroidism are similar to those of adrenergic excess.
Older persons, particularly those with toxic nodular goiter, may present
atypically with apathetic or masked hyperthyroidism (see
Eye signs noted in patients with hyperthyroidism include stare, lid lag, lid retraction, and mild degrees of conjunctival injection. These eye signs are largely due to excessive adrenergic stimulation and usually remit with successful treatment. Infiltrative ophthalmopathy is a more serious development and is specific to Graves' disease. It is characterized by orbital pain, lacrimation, irritation, photophobia, increased retro-orbital tissue, exophthalmos, and lymphocytic infiltration of the extraocular muscles which can produce ocular muscle weakness frequently leading to double vision.
dermopathy, also called pretibial
myxedema (a confusing term, because myxedema suggests hypothyroidism), is characterized by nonpitting infiltration by proteinaceous
ground substance, usually in the pretibial area. It
rarely occurs in the absence of
The hyperthyroidism in molar pregnancy, choriocarcinoma, and hyperemesis gravidarum is transient, and normal thyroid function resumes when the molar pregnancy is evacuated, the choriocarcinoma is appropriately treated, or the hyperemesis gravidarum abates.
Patients with toxic nodular goiter have none of the autoimmune manifestations or circulating antibodies observed in patients with Graves' disease. Finally, in contrast to Graves' disease, which may remit spontaneously, toxic solitary and multinodular goiter usually do not remit.
Thyroid storm is characterized by the abrupt onset of more florid symptoms of hyperthyroidism, with some exacerbated symptoms and atypical signs. Included are fever; marked weakness and muscle wasting; extreme restlessness with wide emotional swings; confusion, psychosis, or even coma; and hepatomegaly with mild jaundice. The patient may present with cardiovascular collapse and shock. Thyroid storm, which is rare in children, results from untreated or inadequately treated hyperthyroidism and may be precipitated by infection, trauma, a surgical procedure, embolism, diabetic acidosis, or toxemia of pregnancy or labor. Thyroid storm is a life-threatening emergency requiring prompt and specific treatment (see Table 8–3 and Figure: Features of Thyrotoxic Storm).
Increases in serum T3 are usually somewhat greater compared to T4 in hyperthyroidism, probably because of both increased thyroidal secretion of T3 and increased peripheral conversion of T4 to T3. In some hyperthyroid patients, only T3 is elevated; this condition is called T3 toxicosis.
T3 toxicosis may occur in any of the usual disorders that produce hyperthyroidism, including Graves' disease, multinodular goiter, and the autonomously functioning solitary thyroid nodule. If T3 toxicosis is left untreated, the patient usually develops the typical laboratory abnormalities of hyperthyroidism, ie, elevated T4 and 123I uptake. This suggests that T3 toxicosis is an early manifestation of ordinary hyperthyroidism and should be treated as such.
The various forms of thyroiditis commonly have a hyperthyroid phase. Some have been discussed above and will be further discussed below under Thyroiditis.
Primary hypothyroidism, the most common form, is probably an autoimmune disease, usually occurring as a result of Hashimoto's thyroiditis and is associated often with a firm goiter or, later in the disease process, with a shrunken fibrotic thyroid gland with little or no function. The second most common form is posttherapeutic hypothyroidism, especially after radioactive iodine therapy or surgery for hyperthyroidism. Hypothyroidism during overtreatment with propylthiouracil, methimazole, and iodide usually abates after therapy ends. Mild hypothyroidism is common in elderly women.
patients with non-Hashimoto's goiters are euthyroid
or have hyperthyroidism, but goitrous hypothyroidism
may occur in endemic goiter. Iodine deficiency decreases thyroid hormonogenesis; TSH is released, the thyroid gland enlarges
under the TSH stimulus and traps iodine avidly, and goiter ensues. If iodine
deficiency is severe, the patient becomes hypothyroid, but this disease is
virtually extinct in the
inherited enzymatic defects can alter the synthesis of thyroid hormone and
cause goitrous hypothyroidism (see also Congenital
Secondary hypothyroidism occurs when there is failure of the hypothalamic-pituitary axis because of deficient TRH secretion from the hypothalamus or lack of TSH secretion from the pituitary.
Symptoms and Signs
(See Figure: Possible Clinical Manifestations of Hypothyroidism.)
The symptoms and signs of primary hypothyroidism are generally in striking contrast to those of hyperthyroidism and may be quite subtle and insidious in onset. The facial expression is dull; the voice is hoarse and speech is slow; facial puffiness and periorbital swelling occur due to infiltration with the mucopolysaccharides hyaluronic acid and chondroitin sulfate; cold intolerance may be prominent; eyelids droop because of decreased adrenergic drive; hair is sparse, coarse, and dry; and the skin is coarse, dry, scaly, and thick. Weight gain is modest and is largely the result of decreased metabolism of food and fluid retention. Patients are forgetful and show other evidence of intellectual impairment, with a gradual change in personality. Some appear depressed. There may be frank psychosis (myxedema madness).
There is often carotenemia, particularly notable on the palms and soles, caused by deposition of carotene in the lipid-rich epidermal layers. Deposition of proteinaceous ground substance in the tongue may produce macroglossia. A decrease in both thyroid hormone and adrenergic stimulation causes bradycardia. The heart may be enlarged, partly because of dilation but chiefly because of the accumulation of a serous effusion of high protein content in the pericardial sac. Pleural or abdominal effusions may be noted. The pericardial and pleural effusions develop slowly, and only rarely result in respiratory or hemodynamic distress. Patients generally note constipation, which may be severe. Paresthesias of the hands and feet are common, often due to carpal-tarsal tunnel syndrome caused by deposition of proteinaceous ground substance in the ligaments around the wrist and ankle, producing nerve compression. The reflexes may be very helpful diagnostically because of the brisk contraction and the slow relaxation time. Women with hypothyroidism often develop menorrhagia, in contrast to the hypomenorrhea of hyperthyroidism. Hypothermia is commonly noted. Anemia is often present, usually normocytic-normochromic and of unknown etiology, but it may be hypochromic owing to menorrhagia, and sometimes macrocytic because of associated pernicious anemia or decreased absorption of folic acid. In general, the anemia is rarely severe (Hb > 9 g/dL). As the hypometabolic state is corrected, the anemia subsides, sometimes requiring mo.
Myxedema coma is a life-threatening complication of hypothyroidism. Its characteristics include a background of long-standing hypothyroidism, coma with extreme hypothermia (temperatures 24 to 32.2° C [75.2 to 90° F]), areflexia, seizures, CO2 retention, and respiratory depression. Severe hypothermia may be missed unless special low-reading thermometers are used. Rapid diagnosis based on clinical judgment, history, and physical examination is imperative because early death is likely. Precipitating factors include exposure to cold, illness, infection, trauma, and drugs that suppress the CNS. (See also Figure: Specific Entities Causing Coma: A Differential Guide in Ch. 170.)