upright=1.4 The precise mechanism for the development of<unk>  is poorly understood. In the human body, thyroid hormone may be free (biologically active T3/T4) or bound to thyroid binding hormone (biologically inactive) to be transported. The release of thyroid hormone is tightly regulated by a feedback system involving the hypothalamus, pituitary gland, and thyroid gland. Hyperthyroidism results from a dysregulation of this system that eventually leads to increases in levels of free T3/T4. The transition from simple hyperthyroidism to the medical emergency of<unk>  may be triggered by conditions (see Causes) that lead to the following: Increases in free thyroid hormone Individuals with<unk>  tend to have increased levels of free thyroid hormone, although total thyroid hormone levels may not be much higher than in uncomplicated hyperthyroidism. The rise in the availability of free thyroid hormone may be the result of manipulating the thyroid gland. In the setting of an individual receiving radioactive iodine therapy, free thyroid hormone levels may acutely increase due to the release of hormone from ablated thyroid tissue. Decrease in thyroid hormone binding protein A decrease in thyroid hormone binding protein in the setting of various stressors or medications may also cause a rise in free thyroid hormone. Increased sensitivity to thyroid hormone Along with increases in thyroid hormone availability, it is also suggested that<unk>  is characterized by the body's heightened sensitivity to thyroid hormone, which may be related to sympathetic activation (see below). Sympathetic activation Sympathetic nervous system activation during times of stress may also play a significant role in<unk> . Sympathetic activation increases production of thyroid hormone by the thyroid gland. In the setting of elevated thyroid hormone, the density of thyroid hormone receptors (esp. beta-receptors) also increases, which enhances the response to catecholamines. This is likely responsible for several of the cardiovascular symptoms (increased cardiac output, heart rate, stroke volume) seen in<unk> .<unk>  as allostatic failure According to newer theories,<unk>  results from allostatic failure in a situation where thyrotoxicosis hampers the development of non-thyroidal illness syndrome, which would help to save energy in critical illness and other situations of high metabolic demand. Usually, in critical illness (e.g. sepsis, myocardial infarction and other causes of shock) thyroid function is tuned down to result in low-T3 syndrome and, occasionally, also low TSH concentrations, low-T4 syndrome and impaired plasma protein binding of thyroid hormones. This endocrine pattern is referred to as euthyroid sick syndrome (ESS), non-thyroidal illness syndrome (NTIS) or thyroid allostasis in critical illness, tumours, uraemia and starvation (TACITUS). Although NTIS is associated with significantly worse prognosis, it is also assumed to represent a beneficial adaptation (type 1 allostasis). In cases, where critical illness is accompanied by thyrotoxicosis, this comorbidity prevents the down-regulation of thyroid function. Therefore, the consumption of energy, oxygen and glutathione remains high, which leads to further increased mortality. These new theories imply that<unk>  results from an interaction of thyrotoxicosis with the specific response of the organism to an oversupply of thyroid hormones.
Thyroid storm
Euthyroid sick syndrome
Adrenal crisis
Pseudo-Cushing's syndrome
Postpartum thyroiditis
Subacute thyroiditis
Cushing's syndrome
Drug-induced hyperthermia