Main Clinical Forms
Depending on etiology and pathogenesis, several variants of the condition are distinguished:
- Diffuse Toxic Goiter (Graves' disease / Basedow's disease). The most frequent cause of the pathology. It is based on an autoimmune process: thyroid-stimulating antibodies (markers) and immunoglobulins directed against thyrocyte antigens, such as thyroid peroxidase, circulate in the blood.
- Nodular Toxic Goiter (Plummer's disease). Less common, typically seen in older patient populations.
- Inducted Toxic Goiter. Arises from external interventions: uncontrolled intake of thyroid hormone medications or excessive iodine intake (the Jod-Basedow phenomenon).
Neonatal hyperthyroidism holds a special place. It develops in newborns due to the transplacental transfer of thyroid-stimulating antibodies from a mother suffering from active Graves' disease during pregnancy. This condition is transient and resolves 2–3 months after maternal antibodies are cleared.
Metabolic Shifts
An excess of $T_3$ and $T_4$ radically alters all types of metabolism. Energy metabolism is shifted toward increased heat production (patients complain of sweating and heat intolerance), and the basal metabolic rate rises.
- Protein metabolism: catabolism begins to prevail over anabolism. A negative nitrogen balance develops due to massive protein breakdown (proteolysis) and active utilization of amino acids for gluconeogenesis.
- Carbohydrate metabolism: hormone excess inhibits glycogen synthesis and accelerates its breakdown. Carbohydrates are absorbed more intensively in the gut. The result is moderate hyperglycemia, further supported by an activated sympathoadrenal system.
- Lipid metabolism: active mobilization of fats from depots (lipolysis) occurs. Cholesterol synthesis increases, but its transport, utilization, and hepatic elimination accelerate even more, leading to hypocholesterolemia.
Nervous System and Visual Impairment
Patients experience a significant increase in nervous and mental excitability, along with tremors. Unmotivated feelings of fear, emotional instability, and impaired sequential thinking and concentration are characteristic.
A significant portion of patients develop Graves' ophthalmopathy (a result of immune autoaggression).
- Exophthalmos: eyeballs are displaced forward due to retroorbital tissue edema, lymphocyte infiltration, and fibrosis of extraocular muscles. This leads to diplopia (double vision) and restricted eye movement.
- Corneal involvement: occurs due to the inability to fully close the eyelids. Keratitis, dryness, erosions, and photophobia develop.
- In severe cases, compression of the optic nerve by edematous tissues can lead to blindness.
The patient's appearance acquires specific features: an "angry" stare during fixation, a startled facial expression, and increased ocular shine due to infrequent blinking.
Laboratory Diagnostics and Complications
Blood serum tests show elevated total fractions of $T_4$ and $T_3$. The level of thyroid-stimulating hormone (TSH) depends on the level of the lesion: in primary hyperthyroidism, it is suppressed via negative feedback, whereas in secondary (pituitary) or tertiary (hypothalamic) forms, it is elevated.
Radioactive iodine uptake by the gland is typically increased, though it may be reduced in the Jod-Basedow phenomenon or subacute thyroiditis.
An acute critical rise in hormone levels leads to a severe condition accompanied by:
- Loss of consciousness and delirium.
- Hyperthermia.
- Acute heart failure, tachycardia, and arrhythmias.
- Respiratory disturbances and progressive renal failure (uremia).