Hyperthyroidism (hyperthyroidism) is a group of common endocrine disorders caused by excessive secretion of thyroid hormones from various causes. The main clinical manifestations of hyperthyroidism are: hyperphagia, lethargy, fever, excessive sweating, palpitations, agitation and other hypermetabolic syndromes, enhanced neurological and vascular excitability, as well as varying degrees of goiter, ophthalmoplegia, hand trespass and shin vascular murmur, etc. In severe cases, hyperthyroidism may lead to critical phase, coma or even life threatening. The most common type of hyperthyroidism is diffuse goiter with hyperthyroidism, which accounts for about 90% of all hyperthyroidism. The ratio of male to female is 1:4-6.
Hyperthyroidism is a common and frequent disease. It is divided into toxic diffuse goiter Graves’ disease (protrusive goiter or Barsetou’s disease, Basedow’s disease) and autonomous functional thyroid adenoma according to its etiology.
I. Clinical can be divided into.
1. primary: primary hyperthyroidism is the most common and is an autoimmune disease.
2. Secondary: Secondary hyperthyroidism is less common and is transformed by nodular goiter.
Hyperthyroidism is a difficult disease to cure, although it is not a persistent disease, but it is a hypermetabolic disease caused by excessive secretion of thyroid hormones.
At present, the prevalence rate of the female population in China is 2%, and the trend is increasing year by year. Due to the lack of awareness of prevention, people tend to ignore the treatable. The symptoms of hyperthyroidism are suddenly aggravated to a life-threatening state. The main manifestations are high fever, profuse sweating, extreme tachycardia, vomiting, diarrhea, restlessness, and in severe cases, coma, which can lead to death if not rescued in time.
There is another kind of hyperthyroidism that can be easily misdiagnosed and mistreated, namely Hashimoto’s hyperthyroidism, which often has symptoms of hyperthyroidism at the early stage of the disease.
II. Pathogenesis.
This disease is definitely an autoimmune disease, but its pathogenesis has not been fully elucidated. One of its characteristics is the presence of autoantibodies in the serum that can react with or stimulate the thyroid tissue, which can stimulate the thyroid gland in rodents, improve its function and cause tissue hyperplasia, but its effect is slow and long-lasting. This antibody is called thyroid-stimulating immunoglobulin (TSI) or thyroid-stimulating antibody (TSAb), and is clinically known as TSH receptor antibody (TRAb), which is an IgG secreted by the lymphocytes of the disease. When TSI binds to thyroid cells, the TSH receptor is activated, resulting in stimulation of thyroid function, causing hyperthyroidism and goiter, the effects of which are similar to those of TSH.
It is now believed that autoantibody production is mainly related to genetic defects associated with reduced function of suppressor T lymphocytes (Ts), which lead to inappropriate sensitization of helper T cells and the production of anti-self thyroid antibodies by B cells with the involvement of interleukin 1 and interleukin 2, possibly due to viral infection. Defective immune guardianship alone is not sufficient to explain some specific immune lesions and needs to be linked to genotypic ordination mechanisms.
III. Pathophysiology.
The pathophysiological role of hypothyroidism is multifaceted, but the rationale for its action has not been fully elucidated. Studies in recent years have found that thyroid hormone can promote phosphorylation, mainly by stimulating the Na-K-ATPase (i.e., Na-K pump) of the cell membrane, which requires a large amount of energy to promote active transfer of Na in the process of maintaining the Na-K gradient inside and outside the cell, resulting in increased ATP hydrolysis and thus promoting mitochondrial oxidative phosphorylation reactions, with the resultant increase in both oxygen consumption and heat production.
Although the effects of thyroid hormones are multifaceted, they are mainly reflected in the promotion of protein synthesis, thermogenesis, and mutual promotion with catecholamines, thus affecting various metabolic and organ functions. For example, thyroid hormones increase basal metabolic rate, accelerate the consumption of various nutrients, and muscle consumption. The synergistic effect of thyroid hormones and catecholamines enhances the excitation and stimulation of the latter in organs such as nerves, cardiovascular and gastrointestinal tract. In addition, thyroid hormones have a direct stimulatory effect on the liver, heart muscle and intestines. Non-infiltrative proptosis is caused by increased sympathetic excitability, while infiltrative proptosis is of unknown cause and may be related to autoimmune mechanism.
IV. Types of hyperthyroidism.
There are many types of hyperthyroidism, the most common of which is toxic diffuse goiter Graves’ disease. The development of toxic diffuse goiter is related to genetic and autoimmune factors, but whether or not symptoms of hyperthyroidism appear is also related to some triggering factors (environmental gonadotropin). If these triggers are avoided, it is possible to avoid, delay, or reduce the symptoms of hyperthyroidism.
Clinically, the following are common in addition to typical hyperthyroidism
1. T3 hyperthyroidism: T3 hyperthyroidism refers to a type of hyperthyroidism with clinical manifestations of hyperthyroidism, but normal or even low serum TT4 and FT4, and only elevated T3.
2, T4 hyperthyroidism: also known as thyroxine hyperthyroidism, refers to a type of hyperthyroidism with elevated serum TT4 and FT4 and normal TT3 and FT3. 1975 Turner first reported the name of T4 hyperthyroidism, whose clinical manifestations are the same as typical hyperthyroidism, which can occur in Graves’ disease, toxic nodular goiter or subacute thyroiditis, mostly in middle-aged and elderly people with poor general condition. The presentation is the same as typical hyperthyroidism, and can occur in patients with Graves’ disease, toxic nodular goiter or subacute thyroiditis, mostly in middle-aged and elderly patients in poor general condition, such as those with severe infections, surgery and malnutrition. Laboratory tests show elevated serum TT4 and FT4 and normal TT3 and FT3. The thyroid uptake rate of 131I is significantly increased, and the thyroid tablet or T3 suppression test is abnormal.
This disease needs to be differentiated from acute stress hyperthyroidism (pseudo-T4 hyperthyroidism). The so-called stress hyperthyroidism refers to patients suffering from various acute or chronic systemic diseases. As a result of these diseases, patients have increased serum TT4 and FT4, while TT3 and FT3 are normal or decreased, and there is no evidence of hyperthyroidism in other aspects except for a few patients with goiter, and when the primary disease is cured, the above laboratory indicators return to normal in a short period of time.
3. Childhood hyperthyroidism: The incidence of hyperthyroidism increases gradually after the age of 3 years, with the highest incidence between the ages of 11 and 16 years, and is more common in girls than boys.
4. Geriatric hyperthyroidism: Due to the physiological changes in the elderly, their whole body organ functions are decreasing to different degrees, the thyroid gland tissues appear some degree of fibrosis and atrophy, thyroid hormone secretion is reduced, and the peripheral tissues’ response to thyroid hormone is also changed. The symptoms of hyperthyroidism are not obvious, lack of hyperphagia, fear of heat and sweating, irritability, etc.; often combined with other heart diseases such as angina pectoris and even myocardial infarction, prone to arrhythmia and heart failure, mostly seen in persistent atrial fibrillation; the patient is indifferent with no desire, and in severe cases, drowsy or in wood stiffness and coma.
5. Apathetic hyperthyroidism: This type is a special type of hyperthyroidism. The symptoms are the opposite of those of typical hyperthyroidism, and it is a kind of hyperthyroidism that shows neurological depression. The clinical manifestations of indifferent hyperthyroidism include: loss of appetite, nausea, chilliness, dry skin, indifference and depression, indifference to surrounding things; sluggish mental thinking activities, slow answering of questions, sometimes difficulty in concentrating, lazy movement and few words; palpitations are common, often accompanied by heart enlargement, congestive heart failure, atrial fibrillation, sunken eyes, sluggish eyes, or even drooping eyelids.
6. Occult hyperthyroidism: Occult hyperthyroidism refers to a type of hyperthyroidism without typical hyperthyroid symptoms, but with a certain systemic disorder as the prominent manifestation. The clinical subtypes are
(1) Mental type: mental abnormality is the prominent manifestation. Patients show inattention, inattention, hallucination, delusion, depression, dementia, paranoia, mania, even suicidal concept, rage attacks, etc.
(2) Gastrointestinal type: often with diarrhea as the prominent manifestation. It is mostly seen in young and middle-aged patients, with the number of stools varying from several times a day to more than a dozen times a day, in the form of paste or watery, containing undigested food. Gastrointestinal hyperthyroidism is characterized by vomiting, diarrhea and water-electrolyte disorders. If the condition is not treated properly, hyperthyroidism may be triggered in serious cases and may endanger life.
(3) Myopathy, with myasthenia gravis and periodic paralysis as the main manifestations. The symptoms of hyperthyroidism are not obvious or appear late. The clinical manifestations are acute and chronic hyperthyroidism myopathy, periodic paralysis, myasthenia gravis and ocular muscle paralysis.
V. Main clinical manifestations of hyperthyroidism.
Clinically, it is a very common endocrine disease. It refers to a series of hypermetabolic syndromes of the body’s nervous system, circulatory system, digestive system, cardiovascular system and other systems, as well as hyperexcitability and eye symptoms, caused by various causes of enhanced thyroid function, excessive secretion of thyroid hormones or increased levels of thyroid hormones (T3, T4) in the blood.
The symptoms include panic attacks, tachycardia, fear of heat, excessive sweating, hyperphagia, weight loss, fatigue, emotional agitation, impatience, insomnia, lack of concentration, protruding eyes, trembling hands and tongue, goiter or enlargement, menstrual disorders or even amenorrhea in women, and impotence or breast development in men. The enlarged thyroid gland is symmetrical, while some patients have asymmetrical enlargement. The swollen or enlarged thyroid gland will move up and down with swallowing, and some hyperthyroid patients also have thyroid nodules.
1. Nervous system: Patients are easily agitated, hypersensitivity, fine tremor when tongue and second hand are held forward, talkative and hyperactive, insomnia and nervousness, lack of concentration, anxiety and irritability, suspicion, etc. Sometimes hallucinations occur, and even sub-mania, but there are also reticent and depressed patients, with active tendon reflexes and shortened reflex time.
2, hypermetabolic syndrome: the patient is afraid of heat and sweating, often with hypothermia, in the case of crisis, there may be high fever, more palpitations and rapid pulse, the appetite is obviously hyperactive, but weight loss, fatigue and weakness.
3. Goiter: Mostly diffuse symmetrical enlargement, a few asymmetrical, or obvious enlargement. At the same time, blood flow in the thyroid gland increases, and vascular murmurs can be heard and tremors can be felt in the upper and lower lobes, especially in the upper part of the gland. This sign is characteristic and has important diagnostic significance.
4, eye signs: infiltrative proptosis and non-infiltrative proptosis. The former is called malignant proptosis, which can be transformed from benign proptosis. Patients with malignant proptosis often have photophobia, lacrimation, diplopia, vision loss, eye swelling and pain, tingling, foreign body sensation, etc. Due to the high protrusion of the eye, the eye cannot be closed, and the conjunctiva and cornea are exposed and cause congestion, edema, corneal ulceration, and even blindness. Some patients with hyperthyroidism have no eye symptoms or the symptoms are not obvious.
5. Cardiovascular system: complaints of palpitations, shortness of breath, and marked increase with slight activity. There are often tachycardia (mostly sinus), arrhythmia, cardiomegaly, enlargement and congestive heart failure, as well as serious manifestations such as arrhythmia, heart enlargement and heart failure in severe cases.
6, digestive system: hyperphagia, but significant weight loss, both accompanied by often suggest the possibility of the disease or diabetes. Excessive thyroid hormone can excite intestinal peristalsis and increase the number of stools, and sometimes cause steatorrhea due to fat malabsorption. Thyroid hormone also has a direct toxic effect on the liver, causing hepatomegaly and BSP retention and increased GPT.
7, blood and hematopoietic system: the disease peripheral hematoma WBC total is low, lymphocyte percentage and absolute value and monocytes increased, platelet life is also shorter, sometimes can appear purpura, due to increased consumption, malnutrition and iron utilization disorders can lead to anemia.
8, motor system: mainly manifested as muscle weakness, a few visible hyperthyroidism myopathy
9, reproductive system: women have reduced menstruation, prolonged cycles or even amenorrhea. However, some patients can have pregnancy and childbirth. Men are more impotent.
10. Skin and extremities: A small number of patients have typical symmetrical mucinous edema, but it is not hypothyroidism, and it is mostly seen on the lower anterior tibial segment of the lower legs, sometimes on the dorsum of the feet and knees, upper extremities of the face and head. The lesions are initially dark red in color, with thickening of the skin followed by lamellar or nodular overlapping, and finally dendritic, with secondary infection and hyperpigmentation. In a few patients, swelling of the soft tissues of the fingertips in the shape of a pestle, new bone formation under the periosteum of the metacarpal phalanges, and separation of the adjacent free edge of the finger or toenail from the nail bed can be seen, which is called thickening of the fingertips.
Endocrine system: Excessive secretion of thyroid hormone affects gonadal function, and adrenal cortical function is often more active in the early stage of the disease, but in patients with severe disease (such as critical illness), its function is relatively reduced or even incomplete; pituitary secretion of ACTH is increased, and plasma cortisol concentration is normal, but its clearance rate is accelerated, indicating that its transport and utilization are increased.
Ocular changes caused in hyperthyroidism.
VII. Complications of hyperthyroidism.
1. Hyperthyroid heart disease
Main symptoms: palpitations, dyspnea, precordial pain, premature beats (premature contractions) or paroxysmal atrial fibrillation, and even persistent atrial fibrillation.
2. Hyperthyroidism ophthalmoplegia
Main symptoms: The acute phase of ophthalmoplegia is characterized by inflammatory reactions in the extraocular muscles and the tissues behind the eyes. The extraocular muscles may become significantly thicker, increasing 3 to 8 times more than normal, and the fat and connective tissue behind the ball, infiltrating and increasing in size up to four times. Chronic phase changes are dominated by hyperplasia. Similar pathological changes are seen in the lacrimal gland. Self-perceived symptoms include foreign body sensation in the eye, burning pain, photophobia and tearing. When the ocular muscle is partially paralyzed, eye rotation is restricted and diplopia occurs. Due to the protrusion of the eyeball, the eyelid can be closed with difficulty, so that the cornea and conjunctiva are stimulated and keratitis, corneal ulceration, conjunctival congestion, edema, etc. occur, affecting vision, and in severe cases, ulceration causes total ophthalmoplegia and blindness.
3. Hyperthyroidism liver damage.
Main symptoms: In addition to the symptoms of hyperthyroidism, mainly liver disease changes, liver enlargement, pressure pain, generalized itching, jaundice, dark yellow urine, increased number of stools, but appetite is still good, no aversion to oil.
4. Hyperthyroidism leukopenia symptoms / Ho hyperthyroidism anemia
It is related to immune regulation dysfunction of hyperthyroidism, increased consumption, malnutrition, iron metabolism disorder and liver function damage.
5. Hyperthyroidism combined with hypokalemic periodic paralysis (referred to as weekly palsy)
The occurrence of periodic palsy may be related to abnormal nail metabolism, immune factors, and mental factors. It is also easy to die from A – S syndrome or respiratory muscle paralysis.
Hyperthyroidism can cause diabetes or co-exist with diabetes
(1) Diabetes caused by hyperthyroidism: Thyroid hormones can antagonize the action of insulin. In hyperthyroidism, the supraphysiological level of thyroid hormone antagonizes insulin more strongly and promotes the absorption of intestinal glucose and glycogen xenobiogenesis, thus causing an increase in blood glucose and leading to diabetes mellitus. This type of diabetes is caused by hyperthyroidism, so it can be called secondary diabetes. Diabetes caused by hyperthyroidism can be completely normalized without hypoglycemic medication after the condition of hyperthyroidism is controlled.
(2) Coexistence of hyperthyroidism and diabetes mellitus: Both hyperthyroidism and diabetes mellitus are related to familial inheritance. The genetic defects of these two diseases often occur on the same pair of chromosomes, and therefore may be inherited together to the offspring. In clinical practice, it is not uncommon for both diseases to occur together in a single patient. This type of diabetes mellitus is primary and not secondary to hyperthyroidism. After the hyperthyroidism is controlled, the diabetes still exists and the blood glucose cannot be lowered to normal without the treatment of blood glucose rumbling drugs. However, hyperthyroidism can aggravate diabetes and increase blood glucose further, so it is important to control hyperthyroidism to reduce diabetes.
Can hyperthyroidism be hereditary?
Most of the clinical patients with hyperthyroidism are familial. The thyroid glands of the children of mothers with hyperthyroidism are more susceptible to hyperthyroid pathogens than those of other people. One is the exposure to hyperthyroidism and the other is the decrease in resistance to the disease due to overexertion or mental factors.
Hyperthyroidism refers to a clinical syndrome in which the thyroid gland increases its function and secretes too much thyroid hormone (TH) for a variety of reasons, resulting in increased excitability and hyper-metabolism in the nervous, circulatory and digestive systems of the body.
Hyperthyroidism is usually referred to as hyperfunctional toxic diffuse goiter Graves’ disease, which is the most common clinical condition. The immunological theory is that hyperthyroidism is an autoimmune disease. Recent studies have proved that the disease is induced by stress factors such as infection and trauma on the basis of heredity and is an organ-specific autoimmune disease caused by defective function of suppressive T-lymphocytes, and is an autoimmune thyroid disease together with autoimmune thyroiditis. A survey has shown that 60% of patients have a tendency to have familial qualities.
The human immune system includes cellular and humoral immunity, and it is the presence of these immune systems that protects the body from damage caused by various factors in nature. Autoimmunity is the process by which the body loses immune tolerance to its own tissue components or bacterial antigens, leading to the production of immune effector cells or autoantibodies and causing damage to itself. Autoimmunity is physiological in many cases, and in addition to defense against damage from nature, it also has an internal surveillance function within the organism that protects normal tissue cells and removes aging and mutated cells. When the autoimmune response exceeds the physiological limit or lasts too long, causing damage and dysfunction of its own tissues and leading to disease, it is called autoimmune disease. Some of these lesions are systemic, while others involve only certain organs, and hyperthyroidism belongs to the latter – organ-specific autoimmune disease.
Among the various types of hyperthyroidism, toxic diffuse goiter Graves’ disease has the most pronounced genetic predisposition, while other types of hyperthyroidism are generally not considered to have a significant genetic relationship. Family members of patients with toxic diffuse goiter are significantly more likely to develop the disease.
Human leukocyte antigens are a marker of heredity, and a number of studies have found a significant increase in one or more human leukocyte antigens in patients with toxic diffuse goiter, further suggesting a strong genetic association with this disease.