Clinical presentation.
Hyperthyroidism can occur at any age, mostly between the ages of 20 and 40, and is generally more common in women than in men, with a prevalence of about 4:1, but in endemic goiter areas, it is slightly more common in women than in men, with a prevalence of about 4:3. Young women can often develop adolescent hyperthyroidism with mild symptoms, and some may resolve themselves after puberty without treatment.
Older patients are more likely to have “insidious” or “indifferent” hyperthyroidism than younger patients, and their neurotic and emotional symptoms are milder, and the incidence of proptosis is also less. The clinical manifestations of hyperthyroidism are variable, with multi-system involvement. The onset of the disease is slow and there is a history of trauma and family history. After the onset of the disease, the course of the disease is prolonged and does not heal for several years, and the recurrence rate is high, and a variety of complications can occur.
1. Abnormal energy metabolism, sugar, protein and fat metabolism: In hyperthyroidism, the basal metabolic rate (BMR) increases, resulting in irritable heat, sweating, weight loss, low work efficiency, muscle wasting, weakness and easy fatigue. Negative balance of protein metabolism, decreased or normal cholesterol, disappearance of subcutaneous fat, and accelerated fat metabolism. Liver glycogen and muscle glycogen decomposition increases, glycogen isogenesis increases, blood glucose may rise or postprandial hyperglycemia, and diabetes may occur in severe cases of abnormal sugar metabolism.
2, water and salt metabolism and vitamin metabolism disorders: thyroid hormone can promote diuresis, potassium and magnesium excretion, so when hyperthyroidism is prone to hypokalemic cycle paralysis and hypomagnesemia. Calcium and phosphorus run faster, often with high urinary calcium, high urinary phosphorus and high urinary magnesium; after a long time, bone decalcification and osteoporosis may occur, and when there is low blood calcium, patients have insufficient calcium intake, and a few patients may have secondary hyperparathyroidism. At the same time, due to the poor absorption, fast metabolism and consumption of hyperthyroidism, vitamin B1, C, D and other vitamin deficiencies and trace element deficiencies can occur.
3. Symptoms of abnormal skin and muscle metabolism: negative metabolic balance of protein, negative creatine balance, negative nitrogen balance, reduced ATP, reduced creatine phosphate, prone to hyperthyroidism myopathy, ocular muscle weakness, myasthenia gravis, or frequent flaccidity. Mucinous edema of the skin occurs, mostly in the eyelids and anterior tibia. The nails become soft or deformed and infected.
4, cardiovascular system symptoms: thyroid hormone excites the sympathetic nerve of the heart muscle, enhancing the effect of catecholamines, appearing tachycardia, arrhythmia, increased heart sound, increased pulse pressure, and even heart enlargement, systolic murmur in the apical part of the heart. The elderly are prone to atrial fibrillation, angina pectoris and even hyperthyroid cardiac heart disease and coronary heart disease at the same time, resulting in heart failure.
5. Mental and neurological symptoms: Thyroid hormone can excite the nerve muscles, resulting in nervousness, impatience, agitation, insomnia, dizziness, anxiety, irritability, talkativeness, hand trembling, hyperreflexia, and in severe cases, hyperthyroidism and autonomic dysfunction may occur.
6. Digestive system symptoms: Thyroid hormone can increase intestinal peristalsis, resulting in easy hunger, hyperphagia, increased stool frequency, dyspeptic diarrhea, malnutrition and malabsorption, and in severe cases, hypoproteinemia and ascites, resulting in a cachectic state and bedridden, mostly in the elderly.
7. Endocrine and reproductive system symptoms: In hyperthyroidism, the function of the endocrine system may be disturbed, the most common being the involvement of gonadal function, amenorrhea and menstrual irregularities in women and impotence in men, but pregnancy in women is not affected.
8. Enlarged thyroid gland: Generally symmetrical, some are asymmetrical, with Ⅰ°, Ⅱ° and Ⅲ° enlargement, most are diffusely enlarged, often with vascular murmur and tremor. The thyroid gland may not be enlarged, or there may be cystic or nodular enlargement of the thyroid gland, but the symptoms of hyperthyroidism are not reduced.
9. Proptosis: protrusion of the eyeball beyond 16 mm is known as proptosis. Generally, there are benign proptosis and malignant proptosis (infiltrative proptosis), the former is common. In the past, it was thought that proptosis was due to the secretion of proptosis-causing substances by the pituitary gland. Currently, it is believed that proptosis is due to autoimmune factors. Namely.
(1) deposition of thyroglobulin and antithyroglobulin complexes in the ocular muscle cell membrane causing edema and lymphocyte infiltration, hypertrophy of the extraocular muscles, resulting in proptosis and extraocular muscle paralysis.
(2) Immune reactions occur in retrobulbar fat and connective tissue cells. In severe cases, the upper and lower lids cannot be closed, the eye is poorly regulated, and the vergence reflex is dysregulated. Sympathetic hyperactivity causes upper lid retraction, widening of the eyelid fissure and gaze. In malignant proptosis, the intraocular pressure rises and corneal ulceration, perforation, conjunctival congestion, edema, and even blindness can occur.
10. Restricted mucinous edema: symmetrical infiltrative skin lesions occur mostly in front of the tibia, but also in the fingers, dorsum of the palm and ankle joints. The skin is thickened and toughened, and brownish-red plaque-like skin nodules of various sizes appear, which are uneven and gradually expand and fuse in size, resembling elephant skin legs.
11. Indifferent hyperthyroidism: opposite to typical hyperthyroidism symptoms in general, indifferent and not easily agitated. Features are.
(1) More elderly women than men.
(2) Dullness, drowsiness, depression.
(3) Wasting, weakness, emaciated and premature aging.
(4) Dry, rough and less sweaty skin.
(5) Edema and drooping eyelids, but marked protrusion of the eyes is less common.
(6) Nodular or adenomatous or cystic adenomatous changes of the thyroid gland are more common.
(7) Muscle atrophy, thin stature and more cachectic state.
(8) More arrhythmias, atrial fibrillation or sinus arrhythmia, generally with a heart rate of 90 to 120 beats/min, with enlarged heart, inadequate blood supply or chronic heart failure.
(9) The condition is more severe with atypical manifestations, easily misdiagnosed and not properly treated, and hyperthyroid crisis may occur.
(10) The disease is often complicated by anemia, gastric disease, hypertension, hyperlipidemia, hyperviscosity and immune dysfunction.
(12) T3 hyperthyroidism: proposed in 1957, this type of hyperthyroidism refers to the clinical manifestation of hyperthyroidism, while serum T4, FT4, TSH, 131Ⅰ, PBI levels are normal, only T3 and FT3 are elevated. It is mostly seen in the prelude to the onset of hyperthyroidism, relapsing hyperthyroidism, iodine deficiency regional hyperthyroidism and response in treatment, also seen in diffuse goiter, nodular goiter or thyroid adenoma hyperthyroidism, T3 type hyperthyroidism is not inhibited by exogenous T3.
13. T4 hyperthyroidism: Clinical manifestations of hyperthyroidism, while serum T3, FT3, TSH, PBI and 131Ⅰ uptake are normal, T4 and FT4 are elevated, mostly seen in Graves’ disease and nodular goiter. Poor general nutrition, history of medication, increased T4 synthesis after iodine loading, or peripheral tissues with impaired T4 deiodination, resulting in reduced T3 and increased rT3.
14. Hyperthyroidism with abnormal T4, T3 and TBG: Graves’ disease can be accompanied by elevated TBG, mostly familial or genetically related, due to increased synthesis or slow degradation of TBG. increased TBG can also be related to medication, such as fenadine, estrogen and drug use, etc. Certain diseases such as myeloma, infectious hepatitis, connective tissue disease and porphyria can all increase TBG. The TBG value can be increased or decreased when T3/T4 is elevated, resulting in changes in the thyroid hormone profile, with T3 hyperthyroidism accounting for about 12%, T4 hyperthyroidism accounting for 3 or 5%, and typical hyperthyroidism accounting for about 84 or 5%. The blood is also caused by infection, surgical stress, nephrotic syndrome, application of androgens, glucocorticoids and phenytoin sodium.
15.Familial goiter with hyperthyroidism: 2 or more members of the family have the disease, which can be the same generation or relatives of the next generation, mostly due to family heredity, but also due to environmental factors or immune factors, and their thyroid function is mostly hyperthyroidism, but can also be normal.
16, recurrent hyperthyroidism: clinically seen hyperthyroidism, the general course of treatment for 2-3 years, most can be cured. A few patients may have relapsing hyperthyroidism, i.e., relapsing once in several years, with the longest duration of illness being nearly 30 years. Patients with this type are reluctant to undergo surgery and 131Ⅰ radiotherapy, but are related to their own medication history, i.e., they stop medication for six months to one year, and come back to the clinic when they relapse.
17. Pregnancy with hyperthyroidism: In hyperthyroidism, menstruation is disrupted or amenorrhea is present, but pregnancy is possible. Pregnancy can aggravate hyperthyroidism, so it is not good for mother and child, so those with moderate to heavy hyperthyroidism should try to avoid pregnancy. Mild hyperthyroidism can continue pregnancy, because the fetus after 12 weeks its thyroid gland gradually develops, has the function of iodine absorption and hormone synthesis, and has the function of response to TSH, so the diagnosis and treatment of 131Ⅰ or 125Ⅰ should be prohibited. Small amounts of anti-thyroid medication should be applied, and surgical treatment is not advisable. Postpartum medication users should not breastfeed.