There are many factors in the development of hyperthyroidism, but research on hyperthyroidism in recent years has revealed the following common factors that cause the occurrence of hyperthyroidism.
1, immune factors: In 1956, Adams and others found that long-acting thyroid sting (LATS) is similar to TSH, which is a kind of immunoglobulin (IgG) produced by B lymphocytes and is an autoantibody against the thyroid gland. LATS is also an IgG that excites only human thyroid tissue, also known as human thyroid-stimulating immunoglobulin (HTSI), which is positive in more than 90% of hyperthyroid patients.
Direct evidence for the immune mechanism of hyperthyroidism pathogenesis are.
① In humoral immunity a variety of antibodies against thyroid cell components are known, such as thyroid-stimulating antibodies against TSH receptors (TISI), or TSH receptor antibodies (TRAb), which bind to TSH receptors or their associated tissues, further activating cAMP and enhancing thyroid function. Such antibodies can pass through placental tissue and cause neonatal hyperthyroidism, or incomplete treatment of hyperthyroidism and The antibody continues to be positive, leading to recurrence of hyperthyroidism;
(2) In terms of cellular immunity, it is confirmed that these antibodies are produced by B-lymphocytes. In hyperthyroidism, the presence of sensitized T-lymphocytes against thyroid antigens in the blood of patients with hyperthyroidism, the activation of phytohemagglutinin (PHA) by lymphocytes in hyperthyroidism can produce LATS. Therefore, the immune response is a complex result of the interaction between T and B lymphocytes and phagocytes. It is now believed that the main cause of hyperthyroidism is the reduced function of suppressor T lymphocytes associated with genetic defects, and the defective function of Ts can lead to T cell sensitization, which causes B cells to produce TRAb. and cause hyperthyroidism, with indirect evidence of.
(1) A large number of lymphocytes and plasma cells infiltrate in the thyroid gland and behind the eyes;
(2) Increased number of lymphocytes in the peripheral blood circulation, which may be accompanied by hyperplasia of lymph nodes, reticuloendothelial tissue in the liver and spleen;
(3) Patients and their relatives may develop other autoimmune diseases at the same time or sequentially;
④Patients and their relatives may have positive blood anti-thyroid antibodies, TRAb, anti-gastric lining cell antibodies and anti-cardiac antibodies;
⑤ Elevated IgG, IgA and IgM in the thyroid and blood.
The cause of the initiation of Graves’ disease is thought to be due to a genetic defect in the immune guardianship and regulation of the patient’s Ts cells, and when there are factors such as external trauma or infection, the immune system is destroyed and the “forbidden” cells are out of control. In recent years, it has been found that HLA-B8 is 2 times higher than normal in Caucasians, HLA-BW35 is higher in Asian Japanese, and HIA-BW46 is higher in foreign Chinese, and B13 and B40 are more obvious, which have attracted attention.
2, genetic factors: clinically found that familial Graves disease is not uncommon, identical twins successively suffer from Graves disease up to 30% to 60%, heterozygotes only 3% to 9%, family history survey in addition to hyperthyroidism, but also other kinds of thyroid disease such as hypothyroidism, or family relatives in the TSI positive, which indicates that Graves disease has a family genetic tendency, this mode of inheritance It may be autosomal recessive, or autosomal dominant, or polygenic.
Environmental factors: Environmental factors mainly include various factors that trigger the onset of hyperthyroidism, such as trauma, mental stimulation, infection, etc. Although many triggers of hyperthyroidism are mainly related to autoimmune and genetic factors, the onset of hyperthyroidism is closely related to environmental factors. If you encounter triggering factors, you will develop hyperthyroidism, but if you avoid triggering factors, you will not develop hyperthyroidism. Thus, it is possible to prevent the onset of hyperthyroidism in some patients by avoiding the triggering factors.
(1) Infection: such as cold, tonsillitis, pneumonia, etc.
(2) Trauma: such as car accidents, trauma, etc.
(3)Mental stimulation: such as mental tension, apprehension, etc.
(4)Overexertion: such as overexertion, etc.
(5) Pregnancy: Early pregnancy may trigger or aggravate hyperthyroidism.
(6) Excessive iodine intake: such as eating large amounts of seafood such as kelp.
(7) Certain medications: such as acetaminophen iodofurone, etc.
Other causes.
(1) Hyperfunctioning nodular goiter or adenoma. In the past, it was thought that this disease was mostly not an autoimmune disease because immune corroboration such as IgG, TSI, and IATS were not detected in blood. In 1988, it was reported in China that serum thyroglobulin antibodies and microsomal antibodies were detected in single nodules with a positive rate of 16.9% (62/383) and 54.7% in multiple nodules (104/ 190), the hyperplastic thyroid tissue in these nodules is not regulated by TSI and becomes autonomously hyperfunctioning or hyperfunctioning thyroid nodules or adenomas, which are currently thought to be due to oncogenes.
(2) Increased TSH secretion by pituitary tumors causes pituitary hyperthyroidism, such as hyperthyroidism associated with TSH-secreting tumors or acromegaly.
(3) Subacute thyroiditis, chronic lymphocytic thyroiditis, painless thyroiditis, etc. can be accompanied by hyperthyroidism.
(4) Increased exogenous iodine can cause hyperthyroidism, called iodine hyperthyroidism, such as excessive iodine in patients with goiter, excessive thyroid tablets or levothyroxine sodium (L-T4) can cause hyperthyroidism, and in a few patients, it can also cause hyperthyroidism.
(5) Ectopic endocrine tumors can cause hyperthyroidism, such as ovarian tumors, choriocarcinoma, gastrointestinal tumors, respiratory system tumors and breast cancer, etc. The secretion of thyroid promoting glands can cause clinical hyperthyroidism.
(6) Albright syndrome is clinically manifested by multiple bone fibrous dysplasia, skin pigmentation and elevated AKP in blood, which may be accompanied by hyperthyroidism.
(7) Familial hyperglobulinemia (TBG) can cause hyperthyroidism, which can be due to familial with genetic defects or associated with the use of gourmand.
Clinical manifestations.
Clinically, it is a very common endocrine disease. It is a series of hypermetabolic syndromes in the nervous system, circulatory system, digestive system, cardiovascular system and other systems, as well as hyperexcitability and ocular 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.
Panic attacks, tachycardia, fear of heat, excessive sweating, hyperphagia, weight loss, fatigue and emotional agitation, impatience, insomnia, lack of concentration, protruding eyes, trembling hands and tongue, goiter or enlargement, menstrual disorders or even amenorrhea in women, impotence or breast development in men, etc. The enlarged thyroid gland is symmetrical, while some patients have asymmetrical enlargement. The swollen or enlarged thyroid gland moves up and down with swallowing, and some hyperthyroid patients also have thyroid nodules.
Patients with hyperthyroidism are easily agitated, hypersensitive, have fine tremors when the tongue and second hand are held flat and extended forward, talkative and hyperactive, insomnia and nervousness, lack of concentration, anxiety and irritability, suspiciousness, etc. Sometimes hallucinations occur, and even sub-mania, but there are also patients who are reticent and depressed.
Hypermetabolic syndrome Patients are fearful of heat and sweating, often with hypothermia, and may have high fever in the case of crisis, mostly with palpitations and rapid pulses, obvious hyperphagia, but weight loss, fatigue and weakness.
Goiter Mostly diffuse symmetric enlargement, a few asymmetric, or obvious enlargement. At the same time, blood flow to 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.
The latter is also called benign proptosis, in which the patient’s eyeballs protrude and the eyes stare or show frightened eyes; the former is called malignant proptosis, which can be transformed from benign proptosis, and patients with malignant proptosis often have photophobia, lacrimation, diplopia, vision loss, eye swelling, stinging pain, foreign body sensation, etc. Due to the high protrusion of the eyeballs, the eyes cannot be closed, and the conjunctiva and cornea are exposed and cause congestion, edema, and corneal ulceration. This can lead to blood congestion, edema, corneal ulceration, etc., and even blindness. Some patients with hyperthyroidism do not have eye symptoms or the symptoms are not obvious.
V. Cardiovascular system: Palpitations, shortness of breath, and shortness of breath may increase with slight activity. Tachycardia (mostly sinus), arrhythmia, cardiac hypertrophy, enlargement and congestive heart failure, as well as arrhythmia, heart enlargement and heart failure in severe cases.
6. Digestive system Hyperphagia with significant weight loss often suggests the possibility of the disease or diabetes. Excessive thyroid hormone can excite intestinal peristalsis, resulting in increased stool frequency, and sometimes lead to steatorrhea due to fat malabsorption. Thyroid hormone also has direct toxic effects on the liver, resulting in hepatomegaly, BSP retention, and increased GPT.
VII. Blood and hematopoietic system The total number of WBC in the peripheral hematoma of this disease is low, the percentage and absolute value of lymphocytes and monocytes are increased, the life span of platelets is also shorter, and sometimes purpura may appear.
VIII. Motor system The main manifestation is muscle weakness, and a few can be seen as hyperthyroid myopathy.
Reproductive system Women have reduced menstruation, prolonged cycles or even amenorrhea. However, some patients can have pregnancy and childbirth. Men are more impotent.
Skin and extremities A small number of patients have typical symmetrical mucinous edema, but it is not hypothyroidism. 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, formation of new bone 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 In addition to the effect of excessive secretion of thyroid hormones on gonadal function, adrenocortical function is often more active in the early stages of the disease, but in severe cases (e.g., 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 accelerated. Ocular changes caused in hyperthyroidism.
Differential diagnosis
Diagnosis must consider.
(1) Simple goiter. There are no signs and symptoms as described above except for an enlarged thyroid gland. Although the rate of 131I uptake is sometimes increased, T3 suppression tests mostly show suppressibility. Serum T3 and rT3 are normal.
②Neurosis.
③Autonomous hyperfunctional thyroid nodules with radioactivity concentrated at the nodule on scan: repeated scans after TSH stimulation show increased radioactivity at the nodule.
④Other. Tuberculosis and rheumatism often have hypothermia, hyperhidrosis tachycardia, etc. Those with diarrhea as the main manifestation are often easily misdiagnosed as chronic colitis. The manifestations of hyperthyroidism in the elderly are mostly atypical, often with apathy, anorexia, and marked wasting, which can easily be misdiagnosed as cancer. Unilateral infiltrative proptosis needs to be differentiated from intraorbital and low cranial tumors. Hyperthyroidism with myopathy needs to be differentiated from familial periodic paralysis and myasthenia gravis.
Complications
In addition to the typical clinical manifestations of hyperthyroidism, the electrocardiogram often shows sinus tachycardia, atrial fibrillation, atrial flutter, atrioventricular block, ventricular precontraction, myocardial injury and myocardial hypertrophy. Heart enlargement may be aortic valve type or right or left heart enlargement type. This disease should be diagnosed differently from myocarditis, coronary heart disease, rheumatic heart disease and other heart enlargement diseases.
2. Hyperthyroid periodic paralysis This disease occurs mostly in male young adults and is often confused with hyperthyroid myopathy, which has normal blood potassium and abnormal electromyography, while hyperthyroid periodic paralysis has.
(i) Blood potassium <3.5 mmol/L, which is an abnormality of potassium metabolism;
② abnormal potassium distribution: elevated blood glucose can cause potassium to move from extracellular to intracellular;
(3) Increased excitability of the central nervous system and increased insulin release from the vagus nerve may promote further abnormalities in potassium distribution;
④Immune factors may increase the levels of IATS, LATS-P, T3 and T4, and thyroid hormones may promote lower potassium levels;
(5) The hyperadrenergic state of hyperthyroidism may promote a decrease in potassium levels and lead to hyperthyroid periodic paralysis. This type should be distinguished from Bartter syndrome, familial periodic paralysis, hypomagnesemia, aldosteronism, myasthenia gravis and drug hypokalemia.
3, hyperthyroidism crisis type Occurrence accounts for 1% to 2% of hyperthyroidism, more common in the elderly, often associated with infection, trauma, surgery, childbirth, overexertion, sudden discontinuation of drugs, drug reactions and other co-morbidities, resulting in hyperthyroidism aggravated, sympathetic nerve activity to strengthen the crisis. Pre-critical phase can be fever of 39℃ or more, pulse rate of 120-160 times/min, restlessness, loss of appetite, nausea, vomiting, diarrhea, mental confusion, profuse sweating, drowsiness, and development to semi-coma or coma. Patients in coma are in critical condition and are very dangerous. Elevated white blood cells, abnormal liver function, GPT, GOT, and bilirubin may be elevated, and there may be dehydration, hypotension, electrolyte disturbances, acidosis, heart failure, and pulmonary edema. Serum T3, T4, FT3, FT4 can be elevated, and the morbidity and mortality rate is high, which must be rescued locally in time.
Internal drug treatment
(A) Treatment methods and indications
Including anti-thyroid drug therapy, adjuvant therapy and life therapy to enhance nutrition. Anti-thyroid drugs are based on thiourea compounds, and this method is the main method in internal medicine treatment. Adjuvant treatment is mainly symptomatic treatment such as insulin and reserpine. Life treatment is to take proper rest, give adequate nutrition and calories in diet, including sugar, protein, fat and B vitamins, and pay attention to avoid mental stimulation and excessive fatigue.
Drug therapy uses thiourea drugs to inhibit the organic iodine in the thyroid gland and reduce the synthesis of thyroid hormones, but this type of drug does not inhibit the iodine uptake by the thyroid gland and the release of already synthesized hormones, then beta-blockers should be added at the early stage of treatment, such as take-home pay and betalactam. However, they must be taken for a long period of time, and the dosage can be gradually reduced over a period of about one and a half to two years until the drug is discontinued.
However, about one-third to half of the patients will have recurrence, especially those with large necks or a diet with high iodine intake (such as frequent consumption of seaweed, seaweed, iodized salt). In addition, a small number of patients may experience drug allergies such as itchy skin, rash or reduced white blood cells (prone to fever and sore throat) and abnormal liver function within the first two or three months of taking the drug. If these phenomena occur, it is advisable to seek medical attention for further diagnostic treatment. Indications for drug therapy.
①Graves hyperthyroidism with mild disease and a small thyroid gland;
(2) Young age (under 20 years old), pregnant women, old and frail or combined with serious liver, kidney or heart disease and not suitable for surgery;
③Preparation for surgery;
④Recurrence after surgical treatment and not suitable for isotope treatment;
⑤ As adjuvant therapy to radioisotope therapy.
(2) Side effects of antithyroid drugs for hyperthyroidism
Anti-thyroid drugs for hyperthyroidism: propylthiouracil and tabazol can cause leukopenia, which usually occurs in the first few months after the drug is administered.
The most serious side effects of western anti-thyroid drug therapy for hyperthyroidism are leukopenia and granulocyte deficiency, which cause a significant decrease in systemic resistance due to low granulocyte count and subsequently lead to serious systemic infections, which are extremely life-threatening. Therefore, attention should be paid to the occurrence of granulocyte deficiency during the medication, and if it is detected in time, there is a better chance of cure. Granulocyte deficiency occurs mostly during the first 3 months of drug use, but can also be seen at any time after drug use. Therefore, special vigilance should be exercised during the first 3 months of drug use.
Granulocyte deficiency can develop in two ways, one is sudden and generally not preventable. The other is a gradual onset, usually preceded by leukopenia, which can turn into granulocyte deficiency if the medication is continued. The latter mode of onset can be prevented by regular leukocyte checks during drug administration. If the white blood cell count is less than 3×10^9/liter, it is usually necessary to discontinue the drug for observation. If the white blood cell count is 3-4×10^9/liter, it should be checked every 1-3 days and treated with leukocyte-raising drugs such as lisinopril and turmeric alcohol, and if necessary, hormone therapy, preferably with another antithyroid drug. After the above measures, if the white blood cells still drop, the anti-thyroid drugs should be stopped and other methods should be used to treat hyperthyroidism.
If granulocyte deficiency occurs, the antithyroid drug should be stopped immediately and the patient should be sent to hospital for resuscitation. Because the patient’s resistance is too weak, he should be resuscitated in a sterile isolation ward and given a large amount of glucocorticoids and antibiotics. After cure, the patient should not be treated with antithyroid drugs for hyperthyroidism.
(4) The question of whether a patient with hyperthyroidism or hypothyroidism can have a normal sex life. Whether a patient with hyperthyroidism or hypothyroidism can have a normal sex life depends on the condition of the disease. Generally speaking, patients with mild disease or medium or heavy patients can have sex in a controlled manner after treatment, symptoms disappear, and patients with normal functions of various vital activities.
However, the following problems should be brought to our attention.
①Patients with hyperthyroidism have a variety of neurological symptoms, such as excitability, paranoia, allergy, fear, anxiety, etc.; increased excitability of the vegetative nerves, heart panic, cardiac arrhythmia, etc. In addition, there are neuromuscular dysfunction, trembling and weakness of the limbs. Sexual excitement can often induce or aggravate the above symptoms.
②Some hyperthyroidism and hypothyroidism patients seriously affect the sexual harmony between husband and wife due to hypersexuality and impotence, and cannot have a normal sexual life, so they must actively carry out targeted treatment to restore their sexual function.
③Menstrual cycle of hyperthyroid patients is often irregular, the cycle is mostly prolonged, but there are also shortened cases, and the menstrual volume is also low, or even amenorrhea. Therefore, the chances of conception are low. If pregnancy occurs, there is a higher chance of miscarriage. In male patients, spermatozoa production is inhibited and the patient is azoospermic or oligospermic, which must be actively treated for the cause of the disease to achieve fertility.
When the condition of hyperthyroidism is stabilized, that is, when the clinical symptoms are basically controlled by treatment, the serum total triiodothyronine (T3) or tetraiodothyronine (T4) are normalized, and the iodine uptake rate of the thyroid gland reaches normal levels (4%-30% for 2 hours and 25-65% for 24 hours), and the medication is stopped for more than six months, you can generally If you stop taking the medication for more than six months, you can usually lead a normal sexual life. Some patients who have been taking medication for more than one year still have about 1/2-1/3 of relapses after stopping medication, so the resumption of sexual life must be supervised by a physician.
⑤ Hyperthyroidism patients take medication for a long time, and the drugs they take, such as tabazol, beta-blockers, reserpine, guanethidine, etc., all have teratogenic effects. Therefore, in order to avoid drug-induced fetal malformation, it is necessary to receive the physician’s guidance whether pregnancy is possible after resuming sexual life
Surgical treatment methods
(I) Treatment methods and indications
The recurrence rate after subtotal thyroidectomy is low, but surgery is a destructive irreversible treatment and can cause some complications, so it should be chosen carefully. The indications are.
(1) moderate or severe hyperthyroidism, long-term medication is ineffective, relapse after stopping medication, or those who cannot take medication unwillingly for a long time;
(2) Those with large thyroid gland or pressure symptoms;
③Post-thoracic goiter with hyperthyroidism; ④Nodular goiter with hyperthyroidism.
Those who are not suitable for surgical treatment methods are: ① those with infiltrative proptosis; ② those with severe heart, liver, kidney and lung comorbidities and poor systemic condition who cannot tolerate surgery; ③ those with early (first 3 months) and late (second 3 months) pregnancy; ④ those with mild cases who are expected to be relieved by pharmacological treatment methods.
(ii) Major postoperative complications.
1. postoperative dyspnea and asphyxia: this is the most critical postoperative complication, which mostly occurs within 48 hours after surgery. The common causes are
(1) Intra-incisional bleeding compressing the trachea. It is mainly caused by incomplete hemostasis during surgery, or by slipping of the vascular ligature.
②Laryngeal edema. It is mainly caused by trauma of surgical operation or tracheal intubation injury.
(③) Postoperative tracheal collapse. It is caused by long-term pressure on the tracheal wall, softening, and loss of surrounding tissue support after surgery.
The clinical manifestations are progressive dyspnea, irritability, cyanosis and even asphyxia. In cases caused by bleeding, there is also swelling of the neck and blood oozing from the drainage port. If the above situation occurs, the sutures should be removed immediately at the bedside, open the wound, and remove the hematoma; if the situation still does not improve, tracheotomy should be done immediately, and after the patient’s condition improves, the patient should be sent to the operating room for further examination and treatment.
2.Returning laryngeal nerve injury: mainly caused by direct injury from surgical operation, such as cutting, suturing, contusion clamping or excessive pulling; a few are caused by hematoma compression or scar tissue pulling. In the former case, symptoms appear immediately during the operation, and in the latter case, symptoms appear only a few days after the operation. If the laryngeal nerve is completely cut or sutured, the injury is permanent, while the injury caused by contusion, pulling or hematoma compression is mostly temporary and can be gradually recovered within 3 to 6 months after treatment with acupuncture and physical therapy. The hoarseness caused by injury to the recurrent laryngeal nerve on one side can be improved by excessive inversion of the vocal folds to the affected side, and the patient does not have significant hoarseness, although postoperative laryngoscopy still shows the vocal folds on the affected side to be abducted. Injury to the laryngeal nerve on both sides will occur paralysis of the vocal folds on both sides, causing loss of voice or breathing difficulties, requiring tracheotomy.
3, supraglottic nerve injury: mostly due to ligation, severing the upper thyroid artery, leaving the upper pole of the gland farther, without careful separation, together with the surrounding tissue caused by large bundle ligation. If the external branch of the superior laryngeal nerve is injured, the cricothyroid muscle will be paralyzed, causing relaxation of the vocal cords and a decrease in pitch. When the upper pole of the thyroid gland, which extends very high upward, is separated, sometimes the inner branch of the superior laryngeal nerve can be injured. Due to the loss of sensation in the laryngeal mucosa, the patient loses the reflex cough of the larynx, and when eating, especially when drinking water, it can cause choking by mistake. Generally, it can recover by itself through acupuncture and physiotherapy.
4. Hand and foot twitching: When the parathyroid glands are mistakenly removed together during surgery, contusions or involvement of their blood supply can cause insufficient parathyroid function and cause hand and foot twitching.
The symptoms mostly appear 1 to 2 days after surgery. In mild cases, there is only tonicity or numbness of the face or hands and feet, often accompanied by heavy pressure in the precordial area; in severe cases, twitching of the facial muscles and hands and feet (a spasm with pain) occurs. It can occur several times a day for 10 to 20 minutes or even several hours. In severe cases, it is accompanied by laryngeal and diaphragmatic spasms, which can cause death by asphyxia. Late onset is often followed by cataracts in both eyes.
If the facial nerve is tapped in front of the ear, short spasms of the facial muscles occur (chrostek sign), and if the upper arm nerve is compressed, it causes hand twitching (Trousseau sign).
Blood calcium decreases and blood phosphorus rises, while urinary calcium and phosphorus excretion decreases.
Treatment: 10-20 ml of 10% calcium gluconate or calcium chloride should be injected intravenously immediately at the time of seizure. Oral calcium gluconate or calcium lactate 2 to 4 grams, 3 to 4 times a day. Also add vitamin D2 at 50,000 to 100,000 units daily to promote its absorption in the intestine. The most effective method is to take dihydrotestosterone (AT10) oil orally, which has the special effect of raising blood calcium, thus reducing nerve and muscle stress. In recent years, the same conductor parathyroid gland transplantation, also has efficacy, but not lasting.
5, thyroid crisis: the cause of the pathogenesis has not been confirmed so far. In the past, it was thought that thyroid crisis was the result of excessive squeezing of thyroid tissue during surgery, which prompted a large amount of thyroid hormones to suddenly enter the bloodstream. However, the level of thyroid hormones in the patient’s blood is not necessarily high. Therefore, it cannot be simply assumed that thyroid crisis is simply the result of too much thyroid hormone in the blood. In recent years, it is believed that thyroid crisis is caused by insufficient secretion of adrenocorticotropic hormones, and that the synthesis, secretion and catabolism of adrenocorticotropic hormones are accelerated in hyperthyroidism. Over time, the adrenal cortical function is reduced, and surgical trauma stress induces crisis. It is also caused by inadequate preoperative preparation and failure to control the symptoms of hyperthyroidism well.
Clinical manifestations mostly occur within 12 to 36 hours after surgery with high fever, fast and weak pulse (more than 120 beats per minute), patient agitation, delirium, and even coma, and often vomiting and watery diarrhea. If not actively treated, the patient often dies rapidly. Therefore, once the crisis occurs, it should be promptly rescued and treated.
6. Postoperative recurrence: The common causes of postoperative recurrence are: failure to remove the isthmus or cone lobe of the thyroid gland; or not enough glands removed, to too many glands remaining, or failure to ligate the inferior thyroid artery. Reoperation for recurrent thyroid often poses incalculable difficulties and tends to damage the recurrent laryngeal nerve and parathyroid glands. Therefore, for recurrent hyperthyroidism, non-surgical treatment is generally preferred.
7. Hypothyroidism: caused by excessive removal of the gland. Mucinous edema of varying severity: edema of the skin and subcutaneous tissues, especially of the face, which does not leave indentations when pressed, dry skin, sparse hair, fatigue, indifference, mental retardation, slow movement, and decreased libido. In addition, the pulse rate is slow, the body temperature is low, and the basal metabolic rate is reduced.
Isotope therapy
This is called “internal thyroid surgery”, which uses radioactive iodine to destroy the thyroid tissue for therapeutic purposes. This treatment uses the thyroid gland’s ability to concentrate iodine and the biological effect of beta radiation emitted by 131 iodine to destroy and atrophy thyroid follicular epithelial cells and reduce secretion. Usually the patient only needs one dose, and if the result is not good, an additional dose can be given after three months or six months. After treatment, the size of the thyroid gland will gradually decrease, and some patients may suffer from hypofunction due to excessive destruction of the thyroid gland. Indications for this therapy are.
①Moderate hyperthyroidism, age 20 years or older, should be preferred to this therapy;
(2) Those who are ineffective in long-term treatment with anti-hyperthyroid drugs, or those who have relapsed after stopping the drugs, or those who are allergic to the drugs;
③ Combined with heart, liver and kidney diseases who are not suitable for surgery, relapsed after surgery or unwilling to operate;
④Some high-functioning nodular hyperthyroidism.
The following conditions are not suitable for this treatment.
①Pregnancy, lactation;
② peripheral blood white blood cells <3000/mm3 or neutral <1500/mm3, severe heart, liver and kidney failure, severe infiltrative proptosis; hyperthyroidism crisis.
There is no etiological treatment for this disease, the course of drug therapy is long; permanent hypothyroidism may occur after isotope therapy; surgery is a destructive irreversible treatment, cut less postoperative hyperthyroidism recurrence, cut more hypothyroidism. Therefore, strictly speaking, all three treatment methods are unsatisfactory. The majority of patients with this disease have an extremely benign course, and the appropriate choice of treatment plays an important role in achieving a significant remission of the disease.
Complications
1. Hyperthyroid heart disease
Main symptoms: palpitations, dyspnea, precordial pain, premature beats (premature contractions) or paroxysmal atrial fibrillation, or 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 palsy (referred to as weekly palsy)
The occurrence of periodic paralysis may be related to abnormal nail metabolism, immune factors, and psychological 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) Hyperthyroidism causes diabetes: Thyroid hormones can antagonize the action of insulin. In hyperthyroidism, the supraphysiological thyroid hormone content antagonizes insulin more strongly and promotes intestinal glucose absorption and glycogen isogenesis, thus causing an increase in blood glucose and leading to diabetes. 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 in some way. The genetic defects of both diseases often occur on the same pair of chromosomes and may therefore be interlocked and passed on to offspring. In clinical practice, it is not uncommon for both diseases to occur together in a single patient. This type of diabetes 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 sugar further, so it is important to control hyperthyroidism to reduce diabetes.
Hyperthyroidism and heredity
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, although their susceptibility to hyperthyroidism is higher, not everyone will develop hyperthyroidism. 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 genetic predisposition and is an organ-specific autoimmune disease caused by defective function of suppressive T lymphocytes. A survey has shown that 60% of patients have a tendency to have familial qualities.
The immune system of the human body includes cellular and humoral immunity, and it is due to the presence of these immune systems that the body is protected from the 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, Graves’ disease, a toxic diffuse goiter, has the most pronounced genetic predisposition, while the 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 close genetic relationship.
Diet taboos In the process of hyperthyroidism maintenance, the patient’s diet is particularly important. Because hyperthyroidism increases the demand for nutrients due to hyper-metabolism, if the nutrition is not sufficient, the wasting will be more obvious and even the symptoms similar to late stage cancer will appear.
Patients should pay attention to the following aspects of diet: daily calorie intake should be at least 2400 kcal for men and 2000 kcal for women. Eat more high-protein foods, and young patients should also eat more fatty foods, more vitamin-rich fruits and vegetables, and less spicy foods, such as chili, onion, ginger and garlic. Eat less iodine-containing foods, such as kelp, sea shrimp, sea fish, etc. Patients should pay special attention to the self-regulation of their mental and emotional state and spiritual life level, keep their mood relaxed, happy and emotionally stable, avoid getting wind and cold, overwork and high fever.
Hyperthyroidism patients should pay attention to the following during medication and diet
l. Avoid spicy food: spicy, raw onion, raw garlic;
2, avoid seafood: kelp, sea shrimp, scallops;
3, avoid strong tea, coffee, tobacco and alcohol;
4. Keep a calm mood and avoid exertion.
Life precautions for hyperthyroidism patients
(1) Learn to relax, do not give yourself too much pressure and burden. Perhaps it is because you do not know how to cherish yourself that your body is prone to protest.
(2) For women who are planning to get pregnant, they should discuss with their physician to decide the timing and whether they need to adjust their treatment.
(3) Reduce the consumption of stimulating foods, especially coffee and tea, to avoid aggravating symptoms such as palpitations and hand tremors.
(4) Reduce the intake of iodine-containing foods, such as seaweed, seaweed, and nori. Avoid using iodized salt or switch to non-iodized salt.
(5) Be cautious of using warm supplements and prescriptions with high iodine content.
(6) Be careful with hairy food, such as small rooster and old goose.
(7) Check thyroid function regularly.