Read more about this disease, some with Classification – Types – Signs and symptoms – Genetics – Pathophysiology – Diagnosis – Screening – Prevention – Treatment and management – Cures and much more, some including pictures and video when available.
Hyperthyroidism is the term for overactive tissue within the thyroid gland, resulting in overproduction and thus an excess of circulating free thyroid hormones: thyroxine (T4), triiodothyronine (T3), or both. Thyroid hormone is important at a cellular level, affecting nearly every type of tissue in the body. It functions as a stimulus to metabolism, and is critical to normal function of the cell. In excess it overstimulates, causing “speeding up” of various body systems, and thus symptoms: Fast heart beat results in palpitations; a fast nervous system, in tremor and anxiety symptoms; a fast digestive system, in weight loss and diarrhea. Lack of functioning thyroid tissue results in a symptomatic lack of thyroid hormone, termed hypothyroidism.
Functional thyroid tissue producing an excess of thyroid hormone occurs in a number of clinical conditions.
The major causes in humans are:
High blood levels of thyroid hormones (most accurately termed hyperthyroxinemia) can occur for a number of other reasons:
Major clinical signs include weight loss (often accompanied by an increased appetite), anxiety, intolerance to heat, fatigue, hair loss, weakness, hyperactivity, irritability, apathy, depression, polyuria, polydipsia, delirium, and sweating. Additionally, patients may present with a variety of symptoms such as palpitations and arrhythmias (notably atrial fibrillation), shortness of breath (dyspnea), loss of libido, nausea, vomiting, and diarrhea. Long term untreated hyperthyroidism can lead to osteoporosis. In the elderly, these classical symptoms may not be present.
Neurological manifestations can include tremors, chorea, myopathy, and in some susceptible individuals (particularly of asian descent) periodic paralysis. An association between thyroid disease and myasthenia gravis has been recognized. The thyroid disease, in this condition, is autoimmune in nature and approximately 5% of patients with myasthenia gravis also have hyperthyroidism. Myasthenia gravis rarely improves after thyroid treatment and the relationship between the two entities is not well understood. Some very rare neurological manifestations that are dubiously associated with thyrotoxicosis are pseudotumor cerebri, amyotrophic lateral sclerosis and a Guillain-Barré-like syndrome.
Minor ocular (eye) signs, which may be present in any type of hyperthyroidism, are eyelid retraction (“stare”) and lid-lag. In hyperthyroid stare (Dalrymple sign) the eyelids are retracted upward more than normal (the normal position is at the superior corneoscleral limbus, where the “white” of the eye begins at the upper border of the iris). In lid-lag (von Graefe’s sign), when the patient tracks an object downward with their eyes, the eyelid fails to follow the downward moving iris, and the same type of upper globe exposure which is seen with lid retraction occurs, temporarily. These signs disappear with treatment of the hyperthyroidism.
Neither of these ocular signs should be confused with exophthalmos (protrusion of the eyeball) which occurs specifically and uniquely in Graves’ disease. This forward protrusion of the eyes is due to immune mediated inflammation in the retro-orbital (eye socket) fat. Exophthalmos, when present, may exacerbate hyperthyroid lid-lag and stare.[1]
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