History
The clinical presentation of hyperthyroidism ranges from an array of nonspecific historical features to an acute life-threatening event. Historical features common to hyperthyroidism and thyroid storm are numerous and represent a hypermetabolic state with increased beta-adrenergic activity.
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Weight loss
Patients typically report an average loss of approximately 15% of their prior weight.
Basal metabolic rate is increased with a stimulation of lipolysis and lipogenesis.
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Palpitations
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Chest pain - Often occurs in the absence of cardiovascular disease
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Psychosis
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Menstrual irregularity
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Disorientation
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Tremor
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Nervousness, anxiety, or emotional lability
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Heat intolerance
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Increased perspiration
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Fatigue
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Weakness - Typically affects proximal muscle groups
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Edema
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Dyspnea
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Frequent bowel movements
Physical
See the list below:
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Fever
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Tachycardia (often out of proportion to the fever)
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Diaphoresis (often profuse)
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Dehydration secondary to GI losses and diaphoresis
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Warm, moist skin
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Widened pulse pressure
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Congestive heart failure (may be a high output failure)
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Thyromegaly
Nontender, diffuse enlargement in Graves disease
Tender, diffusely enlarged gland in thyroiditis
Thyroid nodules, either single or multinodular goiter
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Exophthalmos
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Shock
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Atrial fibrillation
Typically in elderly patients
May be refractory to attempted rate control with digitalis
Converts after antithyroid therapy in 20-50% of patients
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Myopathy
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Thyroid bruit - Relatively specific for thyrotoxicosis
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Fine, resting tremor
Causes
Hyperthyroidism results from numerous etiologies, including autoimmune, drug-induced, infectious, idiopathic, iatrogenic, and malignancy.
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Autoimmune
Graves disease
Chronic thyroiditis (Hashimoto thyroiditis) - Although the primary cause of hypothyroidism, the disease process occasionally presents initially with thyrotoxicosis
Postpartum thyroiditis - Presents similarly to subacute thyroiditis 2-6 months postpartum but typically painless with mild symptoms
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Drug-induced
Iodine-induced - Occurs after administration of either supplemental iodine to those with prior iodine deficiency or pharmacologic doses of iodine (contrast media, medications) in those with underlying nodular goiter
Amiodarone - Its high iodine content is primarily responsible for producing a hyperthyroid state, though the medication may itself induce autoimmune thyroid disease.
Antineoplastic agents - Agents may cause thyroid dysfunction in 20-50% of patients. Symptoms of thyrotoxicosis may be mistaken for sepsis or an adverse drug effect, so monitoring of thyroid function must be considered. [13]
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Infectious
Suppurative thyroiditis - Often bacterial, results in a painful gland commonly in those with underlying thyroid disease or in immunocompromised individuals
Postviral thyroiditis
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Idiopathic
Toxic multinodular goiter - The second most common cause of hyperthyroidism, characterized by functionally autonomous nodules, typically after age 50 years
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Iatrogenic
Thyrotoxicosis factitia - A psychiatric condition in which high quantities of exogenous thyroid hormone are consumed
Surgery - Now uncommon secondary to preventative measures, manipulation of the thyroid gland during thyroidectomy historically caused a flood of hormone release, often resulting in highly toxic blood levels
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Miscellaneous
Toxic adenoma - A single, hyperfunctioning nodule within a normally functioning thyroid gland commonly among patients in their 30s and 40s
Thyrotropin-producing pituitary tumors
Struma ovarii - Ovarian teratoma with ectopic thyroid tissue
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Thyroid storm can be triggered by many different events, classically in patients with underlying Graves disease or toxic multinodular goiter.
Infection
Surgery
Cardiovascular events
Toxemia of pregnancy
Diabetic ketoacidosis, hyperosmolar coma, and insulin-induced hypoglycemia
Thyroidectomy
Discontinuation of antithyroid medication
Radioactive iodine
Vigorous palpation of the thyroid gland in hyperthyroid patients