The severity of symptoms depends on the severity and duration of the disease.
Cardiovascular system and thyrotoxicosis. Direct exposure to thyroid hormones on the conduction system of the heart causes supraventricular tachycardia, the main symptom of thyrotoxicosis. Atrial fibrillation or atrial flutter can be caused by both heart disease and thyrotoxicosis itself. With prolonged thyrotoxicosis, cardiomegaly often develops. leading to heart failure with high cardiac output. The first tone of the heart is strengthened, a loud systolic noise is heard. With cardiomegaly, non-cardiac murmurs are heard. This complex of symptoms is called the thyrotoxic heart.
Musculoskeletal and thyrotoxicosis. Increased catabolism leads to muscle weakness and atrophy (thyrotoxic myopathy). Patients look exhausted. Muscular weakness manifests itself when walking, climbing uphill, getting up from the knees or lifting weights. In rare cases, there is a transient thyrotoxic paralysis. lasting from several minutes to several days. Thyrotoxicosis aggravates the course of myasthenia gravis and familial hypokalemic periodic paralysis. Resorption of bone tissue predominates over its formation, so the concentration of calcium in the urine is increased. Sometimes there is hypercalcemia. With prolonged untreated hyperthyroidism, osteopenia may develop.
Gastrointestinal tract and thyrotoxicosis. Consumption of food increases, some patients have an unquenchable appetite. Despite this, patients are usually thin. Because of the increase in peristalsis, the stool is frequent, but diarrhea is rare. Biochemical parameters of liver function may be violated.
Vision and thyrotoxicosis. The eye slits are greatly expanded. the look becomes intimidated or frightened. At a sight directly sometimes the scleral striae between an upper eyelid and an iris (a sign of Dalrymplea) is visible. When looking down, lowering the upper eyelid lags behind the movement of the eyeball (Gref's symptom). These symptoms are caused by an increase in the tone of smooth muscles lifting the upper eyelid. A rare blinking (symptom of Stellwag) is characteristic. Graves' ophthalmopathy occurs in 15-18% of patients with diffuse toxic goiter. Graves' ophthalmopathy is an autoimmune organ-specific disease accompanied by lymphocytic infiltration of all orbital structures and retroorbital edema. The main symptom of Graves' ophthalmopathy is exophthalmos. Edema and fibrosis of the oculomotor muscles lead to a limitation of the mobility of the eyeball and diplopia. Patients complain of pain in the eyes, photophobia, lacrimation. Due to the lack of continuity of the eyelids, the cornea dries up and can ulcerate. The compression of the optic nerve and keratitis can lead to blindness. Graves' ophthalmopathy occurs in 3-20% of patients with chronic lymphocytic thyroiditis and in patients with other autoimmune pathologies. Graves' ophthalmopathy can also develop as an independent disease.
Skin and thyrotoxicosis. Skin is warm, moist and velvety, like in children; palms sweaty, hot. Onycholysis indicates a prolonged untreated thyrotoxicosis. Occasionally there are local mucous edema, mainly - the anterior surface of the shins (pretybial myxedema). The skin is thickened, with protruding hair follicles, hyperpigmented, resembles an orange peel.
Metabolism and thyrotoxicosis. Patients are usually thin. For the elderly, anorexia is characteristic. On the contrary, some young patients have an increased appetite. so they add weight. Since thyroid hormones increase heat production, heat loss is also enhanced by sweating, which leads to mild polydipsia. Many people do not tolerate heat. In patients with IDDM with thyrotoxicosis, the need for insulin increases.
Thyroid gland and thyrotoxicosis. The thyroid gland is usually enlarged. The size and consistency of goiter depends on the cause of thyrotoxicosis. In the enlarged and hyperfunctioning gland, the blood flow increases, which causes the appearance of local vascular noise.