What is Hyperthyroid disease?

Hyperthyroidism Meaning: Hyperthyroid (Thyroid disease)  referred to as hyperthyroidism. It is clinically characterized by increased basal metabolic rate, increased nerve excitability, and enhanced organ and tissue function. This may be accompanied by goiter. The cause of hyperthyroidism is very complex, and its causes are classified in: 

Graves’ disease Struma ovarii

Graves’ disease in newborns Subacute thyroiditis

Toxic multinodular goiter painless and postpartum thyroiditis

(Toxic multinodular goitre) fetal hyperthyroidism

Sporadic autonomic thyroid adenoma pituitary TSH adenoma hyperthyroidism

Iodine-induced hyperthyroidism (Jod-Basedow disease) or pituitary resistance to thyroid hormones

Exogenous hyperthyroidism thyroid carcinoma hyperthyroidism

 

The incidence of hyperthyroidism varies across the world. In iodine-deficient areas, toxic multinodular goiter and sporadic spontaneous adenoma of thyroid function are relatively increased. Graves disease is most common in high-iodine areas. In other areas, subacute thyroiditis and painless thyroiditis are not uncommon. This section focuses on Graves’ disease.

 

Graves’ disease has diffuse goiter with hyperfunction, ophthalmia, and anterior tibial myxedema. A few patients also have thyroid clubbing fingers. Neonatal Graves disease refers to hyperthyroidism in newborns, whose mothers are often patients with Graves disease.

 

What are the causes of hyperthyroidism?

Hyperthyroidism causes: Graves’ hyperthyroidism and goiter are the result of antithyroid-stimulating antibodies acting on the thyroid gland. This stimulating antibody has a similar TSH effect. It is an antibody against the abundant TSH receptor of thyroid cells and works through the adenylate cyclase mechanism. Therefore, it is also called thyroid stimulating hormone antibody (TRAb). Or thyroid-stimulating antibody (TSAb), or thyroid-stimulating immunoglobulin (TSI). These antibodies are also known as Longacting thyroid stimulator (LAST) due to their long-lasting and long-lasting effects. They are 7S IgG molecules. In the serum of some patients with Graves´ disease where LATS cannot be detected, another immunoglobulin can also be detected, that is, the comparison between LATS and TSH.

 

Graves’ disease’s autoimmune abnormality is also manifested in:

  •  Lymphocytes and plasma cell infiltration in the thyroid and posterior eyeball tissue
  • IgG, IgM, and IgA infiltration in thyroid tissue
  • The absolute value and percentage of lymphocytes in peripheral blood circulation increase, often Accompanied by lymph node, thymus and spleen lymphoid hyperplasia.
  • Patients or their families often have other autoimmune diseases Corticosteroids and immunosuppressants can alleviate Graves’ hyperthyroidism and eye signs.

 

Graves disease is closely related to HLA-A1, B8, DR3, and BW40, and the susceptibility and relative risk of those who are positive are increased. Traumatic trauma and high iodine food can cause hyperthyroidism in individuals with a genetic predisposition to Graves disease, which are important inducements, but the pathogenesis has not yet been elucidated.

 LATS TSH

Source Lymphocytes Anterior pituitary

Biological interaction peak

Structure and molecular weight IgG, 150,000 proteins, about 28,000

Inhibition of activity Anti-IgG serum Anti-TSH serum

Decrease in circulating levels High-dose corticosteroids Thyroid hormones

Overproduction of antithyroid drugs

Graves disease pituitary resistance to thyroid hormones

 

The cause of the eye signs is still unclear, and may be parallel and different immune mechanisms. Exophthalmic immunoglobulin (OIgG) can be detected in the serum of two-thirds of patients with active Graves’ eye sign, and its activity can cause exophthalmos in fish. OIgG can also be directed against one or several antigens of the tibialis anterior muscle membrane. OIgG was not present in the serum of patients without exophthalmos.

 

What are the Clinical manifestations of Hyperthyroidism?

Graves’ disease can be seen at any age, up to 30-50 years. Onset is generally slow, and a few can be acute onset of mental stimulation or infection. Elderly patients and pediatric patients are mostly atypical.

 

The clinical manifestations of Graves disease can be divided into three main aspects:

  1. Abnormalities in the main gland
  2. Increased thyroid hormones
  3. Abnormalities outside the thyroid:
  •   eye signs
  •   local mucosal edema and thyroid pestle State means.

 

I. Thyroid gland Graves’ disease often has goiter, especially in women. Goiter is usually milder in men. You can’t even touch it. Most of the thyroid tumors are diffusely symmetrical and soft in texture. A small number of patients can be single-nodular or multi-nodular swollen, asymmetric, and sometimes even difficult to distinguish between multi-nodular goiter and typical Graves disease goiter. Vascular signs of the thyroid gland are systolic fine tremors and systolic murmurs in the thyroid region, which are mainly seen in severe patients. Thyroid murmur should be distinguished from murmurs that are transmitted to the neck by certain large blood vessels, such as aortic or pulmonary stenosis, carotid stenosis, and venous ying.

 

What are the Effects of increased thyroid hormones?

 (A) Syndrome with increased metabolic rate: As T3 and T4 increase, catabolism is enhanced, oxidative phosphorylation is decoupled, the body’s oxygen consumption is increased, and the heat production and heat dissipation are out of balance. The patient is afraid of heat and sweat, and the skin can be found warm and moist when examined, especially on the palms, feet, face, neck, chest, and underarms.

The skin appears ruddy due to the expansion of capillaries, and the surface temperature rises. Low fever. High metabolic rate and excessive heat production can also cause patients to lose weight sharply, burn out, lose concentration at work, and reduce efficiency. Excessive thyroid hormones can promote intestinal absorption and restore liver glycogen breakdown, so often after meals urine glucose is positive, blood sugar is elevated and glucose tolerance is impaired.

If the patient has pre-existing diabetes, it can make diabetes worse, or make hidden Sexual diabetes becomes clinical diabetes. Excessive oxidation and decomposition of fats cause body fat loss, and cholesterol synthesis and conversion to bile acids increase in speed and increase in excretion, so blood cholesterol is often reduced. Protein has a negative nitrogen balance due to the influence of high generation, which causes excessive consumption of muscles and other soft groups, resulting in weight loss and weakness.

 

(B) Gastrointestinal system Patients with increased digestive function, often have anorexia, increased appetite and meals, but significantly reduced weight. Elderly patients have no significant increase in appetite, or even decline, and accompanied by weight loss, the cachet showed cachexia. A small number of young patients also significantly increase the edible amount, while maintaining the same weight, intestinal peristalsis too fast, indigestion and malabsorption can also lead to diarrhea, increased stool frequency, stool-like, containing more indigestible food. Sometimes fat indigestion is fat puppet. Due to nutritional disorders and the toxic effects of excessive thyroxine, the liver is slightly enlarged, GPT and AKP are increased, and occasionally jaundice. Sometimes accompanied by vitamin B deficiency.

 

(C) Cardiovascular system Due to hypermetabolism, toxic effects of excessive thyroid hormones, and increased sensitivity of cardiac blood vessels to catecholamines, patients feel palpitations and shortness of breath, exacerbated after activity. The elderly can develop symptoms of angina and heart failure. On examination, tachycardia can be found, which can reach 90 to 130 times per minute, and the pulse rate during sleep can still be more than 80 times per minute, and the pulse is strong and powerful. The blood pressure can be systolic hypertension, which can reach more than 22.7KPa (170mmHg), while the diastolic blood pressure can drop below 9.33KPa (70mmHg), the pulse pressure difference increases, capillary pulsations can be seen, and water flushes the pulse upon palpation.

Paroxysmal supraventricular tachycardia, atrial flutter, atrial fibrillation, and heart failure can occur in elderly patients. Premature beats are more common in young patients. The heart can be enlarged, the first heart sounds are strong, the anterior heart area can be heard and mild systolic murmurs, and diastolic murmurs are rare.

 

(D) The neuromuscular system has the following manifestations:

i. chronic chronic thyrotoxic myopaty is more common, the onset is slow, often involving the proximal large muscles and the shoulder or hip belt muscle groups, showing progressive muscle weakness Ineffective for neostigmine, urinary creatine excretion increased (> 456 μmol / 24h for males,> 760 μ / 24h for females). The relationship between myopathy and hyperthyroidism is unknown. It is generally believed that the mitochondria of myocytes are damaged and energy metabolism is impaired. The proximal large muscle is mainly composed of mitochondria-rich red muscle.

ii. Hyperthyroidism with periodic paralysis (thyrotoxicosis associated withperiodic paralysia) is more common in the races of Eastern countries. It occurs in young men, has a rapid onset, lower limbs are heavier than upper limbs, and can be accompanied by hypokalemia. The pathogenesis is unknown, which may be related to the dysfunction of Na-K pump and the transfer of potassium ions into cells.

iii. Thyrotoxicosis associated with myasthenia gravis mainly affects the eye muscles and manifests as drooping eyelids, eye movement disorders, and diplopia. He responded well to neostigmine. Hyperthyroidism and myasthenia gravis are both autoimmune diseases.

iv. Acute thyrotoxic myopathy or hyperthyroidism with acute bulbar palsy is rare and has an acute onset. Speech and swallowing difficulties can occur within a few weeks, and respiratory muscle paralysis can occur, which can also occur simultaneously with the hyperthyroidism crisis.

 

In addition to the above-mentioned special forms of neuromuscular abnormalities, patients generally exhibit muscle weakness, burnout, hand tremor, and hypertenoid reflexes. Dyskinesia can occur in children.

 

(E) Mental system Irritability, arguing with others, nervousness, anxiety, insomnia, suspicion, etc. Occasionally, hallucinations, mania or depression may occur.

 

The clinical manifestations of hyperthyroidism in the elderly are mostly inconsistent with the above, showing atypical manifestations, which should be paid attention to, and are prominently manifested as indifferent, lethargic, unresponsive, markedly wasted, and even cachexia. Symptoms are usually atypical, sometimes only anorexia, diarrhea, and other digestive symptoms, or there may be only unexplained arrhythmias, especially paroxysmal or persistent atrial fibrillation. Elderly patients may have angina pectoris, myocardial infarction with heart failure. Hypermetabolism group is not obvious, easily lead to systemic organ failure and induce crisis. This type of elderly hyperthyroidism is called occult or leisurely hyperthyroidism, or indifferent hyperthyroidism.

 

III. Abnormalities outside the thyroid

(1) Eye Signs: Eye signs of Graves’ disease include eyelid edema, conjunctival irritation, protruding eyeballs, and upper eyelid contracture. The above-mentioned signs may occur alone, or several kinds of signs may appear simultaneously. Among them, exophthalmos can occur simultaneously with hyperthyroidism, can also occur when hyperthyroidism is controlled, thyroid function is normal or even hypothyroidism, can also occur before hyperthyroidism, exophthalmos occurs in a few patients, and hyperthyroidism only occurs after several years.

 

Eye protrusion can be divided into two types, namely non-invasive eyes and invasive exophthalmos. Non-invasive exophthalmos are also known as benign exophthalmos. Patients are often asymptomatic, with only ocular symptoms:

i. Widening of the fissure of the eye, anterior protrusion of the eye, measured by sweating, and the degree of exophthalmos is generally <18mm (normal <16mm).

ii. Upper eyelid contracture, when looking down the upper eyelid can not follow the downward movement of the eyeball

iii. the inside of the eyeballs weakened polymerization

iv. when looking up, the forehead does not wrinkle. The above eye signs are mainly caused by sympathetic excitement of the extraocular muscles and the upper eyelid muscle (Muller muscle), and the pressure behind the ball may not change significantly. Such exophthalmos have good prognosis and good treatment effect.

 

Infiltrative exophthalmos are also called malignant exophthalmos. Patients often have significant ocular symptoms such as photophobia, diplopia, vision loss, foreign body sensation, limited eye movement, and even fixation. Eyeballs are more prominent. Generally, the degree of exophthalmos is> 18mm, and the sides can be asymmetric. The reading difference can be ≥2mm, but rarely exceeds 5mm. Due to the high exophthalmos, the eyelids cannot be closed, and the conjunctiva and cornea are often exposed, especially during sleep, which can cause congestion, edema, and infection, leading to conjunctivitis, keratitis, and even pancreatitis, and blindness. Infiltrative exophthalmos are caused by an increase in the volume of the orbital contents and an increase in pressure, mainly due to increased fat, muscle thickening, lymphocyte infiltration, and increased water and mucopolysaccharide content. Exophthalmos in this group have a poor response to treatment. Exophthalmos in a few patients are progressively exacerbated, and blindness can be caused if effective treatment is not given.

 

(2) Local myxedema: About 5% of Graves’ disease patients have localized myxedema. It is more common in front of the tibia, but can also be affected by other parts of the body, such as the face, back of the foot, and toes. The skin of the myxedema area becomes darker and rougher, and the pores become thicker. It is orange peel-like, with rough hairs, thickened and hard skin, and sometimes plaque-like nodules of various sizes, round or oval, brown-red , Raise the surrounding skin. It is usually asymptomatic and sometimes has a slight itching and burning sensation. Pathological biopsy showed mucopolysaccharide hyaluronic acid deposition in superficial skin, increased colloids, connective tissue fibrosis, hypertrophy and increased phagocytic cells. The pathogenesis is related to autoimmunity.

 

(3) Thyroid acropathy: Thyroid acropathy can occur in both men and women, thick finger skin, finger (toe). Enlargement, swelling of the soft tissue, and hypertrophy of the terminal fingers (toes) are clubbing. X-ray pictures show new bone formation under the periosteum of the finger (toe), which is rare.

 

 

Laboratory and other inspections for Hyperethyroidism

Any patient with suspected hyperthyroidism needs to undergo at least two more laboratory tests. The choice of examination depends on the hospital’s equipment and the experience of the doctor.

 

Firstly, about 85% of patients with basal metabolism are higher than the normal range (-10 to + 15%), and the degree is consistent with the condition. Generally, + 15 ~ + 30% is classified as light, + 30 ~ 60% is medium, and> + 60% is heavy. When judging basal metabolism, you should pay attention to the following factors that affect the increase of basal metabolism, such as pregnancy, fever, cardiopulmonary insufficiency, leukemia, malignant tumors, mood, drugs (adrenaline, ephedrine, caffeine, aminophylline, etc.) and Metabolic disorders. Clinically, the following formula can also be used to estimate, the method is to fast for 12 hours, sleep for 8 hours, fast in the morning, measure pulse rate and blood pressure while resting, and then use the following formula to calculate for reference.

 

Basal metabolic rate (%) = (pulse rate + pulse pressure difference)-111

 

Basal metabolic rate (%) = 0.75 [pulse rate + (0.74 × pulse pressure difference)]-72

 

Secondly, the measurement of circulating thyroid hormone levels The current measurement methods mainly include radioimmunoassay (RIA) and competitive protein binding analysis (CPBA).

 

(1) Serum total thyroid hormone: (TT4) and total triiodothyronine (TT3) T4 concentration in normal human blood is 30 times higher than T3. Most of T3 and T4 are combined with serum proteins. Less (free T4 accounts for 0.03 to 0.05% of total T4, free T3 accounts for 0.05 of total 3). The bound and free T3, T4 are in dynamic equilibrium. TT4 and TT3 can more accurately reflect thyroid function. Both TT4 and TT3 can increase during hyperthyroidism. Among them, TT3 is of great significance in the diagnosis of hyperthyroidism. If TT4 is normal, only TT3 is elevated, which can be diagnosed as “T3 hyperthyroidism”. Normal TT4 is about 580 ~ 1608nmol / L (45 ~ 125ng / ml), and TT3 is about 12.3 ~ 14pmol / L (0.7 ~ 2.1ng / ml).

The determination of TT4 and TT3 is affected by alpha gland binding globulin (TBG), such as pregnancy, estrogen, perphenazine, hereditary TBG and viral hepatitis can increase TT4 and TT3 due to the increase in TBG On the other hand, in nephrotic syndrome, severe liver failure, active acromegaly, reduced hereditary TBG, TBG decreases when taking prednisone or androgen, which lowers TT4 and TT3, which must be noted during analysis.

 

(2) Serum free thyroid hormone: (FT4) and free triiodothyronine (FT3) FT4 and FT3 are biologically active parts of thyroid hormone, which can directly reflect thyroid function; they are not affected by TBG. Normal values ​​are FT4 of 9.11 to 25.47 pmol / L (7.08 to 19.79 pg / ml) and FT3 of 3.19 to 9.15 pmol / L (2.08 to 5.96 pg / ml).

 

(3) Serum anti-triiodothyronine: (rT3) rT3 is an inactive thyroid hormone in normal human serum, namely 3,3 ‘, 5’-triiodothyronine. Its concentration is very low, only 1/5 to 1/4 of T3, and the normal value is 0.559 to 0.882nmol / L (0.364 to 0.574ng / ml). During hyperthyroidism, rT3 also increased, and the rT3 / T3 ratio remained unchanged.

 

Thirdly, the indirect determination of blood thyroid hormone concentration

 

(A) Thyroid hormone binding test: (THBT) or 125I-triiodothyronine absorption test (125I-T3U). Most of thyroid hormones (T4) are combined with TBG. T3 and TBG are not as strong as T4 and are easily replaced by the latter. The amount of T3 and TBG binding depends on how much TBG is saturated with T4 or the remaining binding capacity of unbound TBG. Add a certain amount of 125I-T3 to the patient’s serum. 125I-T3 is bound to the remaining binding capacity of TBG in the serum.

The unbound 125I-T3 can be adsorbed by adsorbents such as red blood cells, resin or activated carbon. Determination of free 125I-T3 (absorption test) or determination of plasma TBG binding 125I-T3 (binding test), we can understand the remaining binding capacity of TBG, which indirectly reflects the concentration of T4 in the blood circulation. Such as the absorption test, the absorption rate of 125I-T3 increased during hyperthyroidism. If the binding rate of TBG combined with 125I-T3 was measured, it decreased during hyperthyroidism. The domestic 125I-T3 red blood cell absorption rate varies from unit to unit. The normal value is usually 13 ± 4.6%, and> 17% can diagnose hyperthyroidism.

It is also possible to use the ratio of 125I-T3 binding rate to normal. The normal value is 0.99 ± 0.10, and <0.83 is hyperthyroidism. The disadvantage of this test is that the accuracy is not high enough, and the coincidence rate with clinical diagnosis is not high enough, and it can be affected by the concentration of TBG.

 

(B) Free T4 Index (FT4I) The remaining binding capacity of serum TBG is determined by two variables, blood TT4 and TBG concentration. When the TBG concentration is normal, the 125I-T3 absorption rate (or uptake ratio) is parallel to the serum TT4 concentration, but when the TBG concentration is abnormal, the two results change in the opposite direction. For example, during pregnancy, because the blood TBG concentration increases. When TT4 is increased, the 125I-T3 absorption rate (or uptake ratio) is correspondingly reduced, but its free thyroxine (FT4) is not affected by the change in TBG. If you multiply the 125I-T3 uptake ratio (or the inverse of the binding ratio) by The value of serum TT4 is called “free thyroxine index” (FT4I). This index is directly proportional to the serum FT4 level and can represent the relative value of FT4, thereby eliminating the abnormal impact of TBG. The calculation of FT4I is as follows.

 

FT4I = 125I-T3 uptake value × TT4 (or PBI) or FT4I = TT4 (or PBI) / 125I-T3 plasma binding ratio

 

The normal value of FT4I is about 2.23 to 8.08, which increases during hyperthyroidism.

 

(C) Determination of thyroxine in urine FT4 and FT3 can be filtered out by the glomerulus, so the discharge of T3 and T4 in urine can indirectly reflect the concentration of FT4 and F3 in the blood, and it is not affected by the concentration of TBG. Protein-bound thyroxine cannot be filtered out by the glomeruli. Normal value, urine T4 is 4.3 ~ 12.7 μg / 24h urine, T3 is 2.0 ~ 4.5μg / 24h urine, which is higher than the above value in hyperthyroidism.

 

(D) The thyroid 131 iodine rate was measured. Fasting after oral administration of 2μciNa 131I. 3 and 24 used radioisotope counters to measure the number of radioactive pulses in their thyroid gland, compared with the standard source, and calculated the relative percentage. Its normal value is 5 to 25% in 3 hours, 20 to 55% in 24 hours, and the peak appears in 24 hours. Patients with hyperthyroidism have 3 hours> 25% and 24 hours> 45%, and the peak can be advanced to 3 hours. The coincidence rate of this test for the diagnosis of hyperthyroidism can reach 90%, but it has no significance in observing the effect. The 131I rate of iodine-deficient goiter can also be increased, and it must be identified by T3 inhibition test. Foods containing iodine, sulphur-containing drugs, antithyroid drugs, bromide, reserpine, butepine, parasalin, and melbendazole can all reduce the 131I rate; female contraceptives can increase it, Such drugs should be discontinued for more than 1 to 2 months before testing. Pregnant women and lactating women are not allowed to make this test.

 

(E) Thyroxine Inhibition Test (T3 Inhibition Test) A certain amount of thyroid hormone in normal people can inhibit the release of TSH and reduce the thyroid’s iodine uptake. Patients with hyperthyroidism are autonomous, so thyroid iodine uptake is not inhibited by thyroid hormones.

 

Methods: The thyroid iodine 131 iodine rate was measured first, then 180 mg oral glandular tablets were taken orally daily (sodium triiodothyronine sodium salt 20 μg / 8 hours), for 7 consecutive days, the thyroid 131I rate was repeated on the 8th day Determination.

 

Inhibition rate (%) = 131I rate for the first time-131I rate for the second time / 131I rate for the first time × 100

 

Results: The normal inhibition rate was> 50%; the patients with hyperthyroidism were <50%.

 

(F) Thyroid stimulating hormone (TRH) stimulation test TRH can promote the synthesis and release of TSH. In patients with hyperthyroidism, T3 and T4 increase, and TSH secretion is inhibited by feedback, so TSH secretion is not excited by TSH. The method is to first measure the serum TSH level, then intravenously inject 400 μg TRH (dissolved in physiological saline), and take the serum TSH concentration at 15, 30, 60 and 120 minutes after injection.

 

In normal people, serum TSH peaked at 30 minutes after TRH injection, reaching 10-30 μIU / ml. Women have a higher response than men. Patients with hyperthyroidism are unresponsive, and if there is a response, hyperthyroidism can be ruled out. This test is safe, rapid, and convenient, and has a tendency to replace the T3 inhibition test in the clinic.

 

Diagnosis and Differential Diagnosis of Hyperthyroidism

In addition to the above clinical symptoms and related signs, the diagnosis should be confirmed by two or more thyroid function tests or tests. There are sometimes post-contradictions between the clinic and the laboratory, and the two may not be completely consistent. This may be caused by a variety of factors, such as laboratory errors, mastery of diagnostic criteria, disease type, course of disease, drugs, and catecholamine receptor sensitivity. Wait. The following diseases should be noted in the differential diagnosis.

 

1. Simple goiter: Goiter, but without hyperthyroidism, various thyroid function tests are within the normal range.

 

2. Neurosis: The neuropsychiatric syndrome is similar to hyperthyroidism, but there is no hyperthyroidism with hyperthyroidism. The appetite is not hyperactive, and the hands are flat tremor. The pulse rate after falling asleep is normal. There is no goiter and eye signs. The thyroid function test is normal.

 

3. Other causes of hyperthyroidism, such as pituitary hyperthyroidism, autoimmune thyroiditis, subacute thyroiditis, heterogenic TSH hyperthyroidism, etc., can be identified through corresponding special examinations.

 

4. Miscellaneous Loss of weight and fever must be distinguished from tuberculosis and cancer; diarrhea must be distinguished from chronic colitis; arrhythmia must be distinguished from rheumatic heart disease, myocarditis and coronary heart disease. Unilateral exophthalmos must be distinguished from intraorbital tumors.

 

What is the Treatment for Hyperthyroidism?

 There are three standard treatment options for hyperthyroidism:

 1. Antithyroid drugs All patients can be controlled by antithyroid drugs. Should be used as the preferred treatment for hyperthyroidism. Commonly used are methylthiouracil and propylthiouracil in thioureas; dibazole in imidazole is equal to hyperthyroidism. The pharmacological effects of thiourea and imidazole antithyroid drugs are to inhibit the peroxidase system in the thyroid gland, inhibit the conversion of iodine ions into new ecological iodine or reactive iodine, thereby hindering the combination of iodine and tyrosine and inhibiting the thyroid gland. Synthesis.

Propylthiouracil can also inhibit the conversion of T4 to T3 in peripheral tissues. This class of drugs is easily absorbed by mouth. After absorption, it is distributed in the whole body tissue and can pass through the placenta. The concentration in milk sweat is 3 times the blood concentration. The drug is mainly metabolized in the dirty, with a single oral half-life of 1 to 2 hours. About 60% of the drug is destroyed in the body, and the rest is mostly excreted from the urine in a combined form. For liver and kidney dysfunction, the dose should be reduced.

 

(I) Indications (Hyperthyroidism)

i. Patients with mild disease and mild to moderate thyroid enlargement

ii. Adolescents, children and elderly patients under 20 years of age

iii. Pregnant women

iv. Subtotal thyroidectomy, recurrence after surgery, and unsuitable for radioactive 131 iodine Healers

v. Preparation before surgery

vi. Adjuvant radioactive 131 iodine treatment; sacral exophthalmia.

 

(II) Dosage and the initial stage of treatment (hyperthyroidism)

The dose should be determined according to the severity of the disease, methyl or propylthiouracil is 150-450mg / d, tabazole or methypine is 10-45mg / d, divided 2 ~ 3 times orally, until the symptoms are relieved, BMR drops below + 20%, or T3 and T4 return to normal can be reduced. Each time methylthiouracil is reduced by 50 to 100 mg, and tabazol or hyperthyroidism is reduced by 5 to 10 mg. 2 to 3 times a day. Symptoms are completely eliminated, and when the BMR is normal, you can switch to the smallest dose to continue treatment.

The methyl or propylthiouracil is 50 to 100 mg per day, and the tazobazole or hyperthyroidism is 5 to 10 mg per day. Maintain at least 1 to 3 / 2 years, can be extended to 2 years or more, and the dose can be smaller. During treatment, symptoms may disappear and exophthalmos may worsen. This may be the result of the decrease in blood T3 and T4 and the increase in TSH. At this time, the release of thyroid hormone can be appropriately added and stored in the thyroid acinar. , Thereby delaying the marked effect of antithyroid drugs. And the relapse rate is high after discontinuation.

 

(III) Side effects of Dose

i. General adverse reactions are headache, joint pain, salivary gland enlargement, lymph node enlargement and gastrointestinal symptoms. Treat symptomatically or reduce the dosage appropriately. Excessive application may be in favor of hypothyroidism, causing chills, fatigue, and myxedema, and most of them can heal after stopping treatment.

ii. Granulocytopenia and agranulocytosis, usually within 1 to 3 months after initial administration or 1 to 2 weeks after re-administration. Patients should pay attention to fever, sore throat, myalgia, weakness, and infection symptoms during medication.

Once found The above performance should be discontinued immediately for white blood cell examination. In general, white blood cells should be checked regularly, such as when the white blood cells are as low as 3 × 109 / L (3000 / mm3) or the granulocytes are less than 15 × 109 / L (1500 / mm3). Drug therapy should be discontinued and switched to other antithyroid drugs after recovery.

iii. Drug rash, mostly mild, rarely exfoliative dermatitis. General drug eruption can be treated with antihistamines, if necessary, stop or switch to other antithyroid drugs. If exfoliative dermatitis occurs, the drug should be stopped immediately and treated accordingly.

 

After 1 to 2 years of treatment, if a small dose of antithyroid drugs can maintain the effect, the thyroid gland shrinks, vascular sounds disappear, exophthalmia is reduced, serum T3 and T4 are normal, 131 iodine uptake by the thyroid can be suppressed by thyroid hormones, and TSAb in the blood circulation turns Negative or significantly lower titers can be discontinued and observation continued. On average, patients who relapse after treatment usually occur within one year after discontinuation of the drug. Therefore, they should be reviewed regularly after discontinuation of the drug, especially for thyroid autoantibodies in the blood circulation. If necessary, a TRH test can be performed.

 

Antithyroid drugs work slowly and cannot quickly control many symptoms of hyperthyroidism, especially the increase in sympathetic nerve excitability. Therefore, in the early stage of treatment, β-blocker propranolol, 10-20 mg, 2 to 3 times a day can be combined to improve the symptoms of palpitations, tachycardia, hyperhidrosis, tremor, and nervousness. Propranolol is also suitable for preparations for hyperthyroidism crisis and thyroid surgery or radioactive iodine treatment; it also has a certain effect on acute hyperthyroidism myopathy. For patients with bronchial asthma, atrioventricular block, dyscardia and pregnancy are contraindicated.

 

1. At the beginning of the reducing period, a small dose of thyroid preparations such as thyroid tablets 20 to 40 mg, once a day, or thyroxine 50 to 100 μg, once a day can be appropriately added to stabilize the hypothalamic-pituitary-thyroid axis relationship. Avoid exacerbation of goiter and exophthalmos.

 

2. Radioactive 131 iodine has a high concentration of 131 iodine in the treatment of thyroid. When 131 iodine decays, β and γ rays (99% of which are β rays) are emitted. The range of β rays in the tissue is only 2mm, so the ionization effect is limited to the thyroid gland. Local without affecting adjacent tissues. In patients with hyperthyroidism, the effective half-life of 131 iodine staying in the thyroid gland is about 3 to 4 days on average, so some thyroid epithelial tissue can be damaged, thereby reducing thyroid function and achieving the purpose of treatment.

 

Although radioactive 131 iodine treatment is effective, the difficulty is to accurately calculate the dose taken to restore thyroid function to just the right level. The radiation dose given depends on several factors:

i. The radiation intensity of the 131 iodine given

ii. the intensity and dose of 131 iodine taken by the thyroid

iii. The length of time that radioactive 131 iodine stays in the gland

iv. The sensitivity of thyroid to radioactive iodine varies from person to person and cannot be measured.

 

(1) Indications 

i. Age over 35 years

ii. Patients with hyperthyroidism who have relapsed after subtotal thyroidectomy

iii. Those who are allergic to antithyroid drugs, or those who cannot adhere to long-term medication

iv. They also suffer from other diseases, such as liver, Heart and kidney diseases are not suitable for surgery

v. functional autonomic thyroid adenoma.

 

(2) Contraindications

i. Pregnant or lactating women

ii. Those under 20 years of age

iii. Those with severe liver and kidney dysfunction

iv. Number of peripheral blood leukocytes <3.0 × 109 / L (3000 / mm3), or number of granulocytes <1.5 × 109 / L (1500mm3)

v. patients with severe hyperthyroidism and crisis of hyperthyroidism

vi. Severe invasive exophthalmos; nodular goiter with hyperthyroidism with hyperthyroidism.

 

(3) Dose and usage: Based on the estimated thyroid weight, the maximum oral dose of 131 iodine can be calculated as follows:

 

131 doses of iodine (MBq) = weight of thyroid (g) × amount of 131I per gram of thyroid tissue (MBq / g) / maximum 131 iodine rate of thyroid (%) where 131 iodine per gram of thyroid tissue is 2.6 ~ 3.7MBq (70 ~ 100μCi / g). Moderate thyroid enlargement, moderate disease, effective half-life of more than 4 days, generally give 2.96MBq (80μCi / g. The following conditions should be increased:

i. The thyroid is large and hard

ii. Long duration, long-term drug treatment is not effective

iii. Short effective half-life

iv. Older

v. The first course of treatment is not satisfactory, the second course of treatment should be increased as appropriate. Conversely, the dose of those who have a short course of disease, no drug treatment, young age, small thyroid and recurrence after surgery should be The radiation absorbed dose calculated according to the above formula is about 60 to 100 Gy (6000 to 10,000 rad).

 

(4) Treatment side effects A small number of patients had mild reactions within 1 to 2 weeks after taking 131 iodine, mainly as fatigue, dizziness, decreased appetite, stomach discomfort, nausea, itching of the skin, local thyroid swelling and slight pain, etc. It usually disappears after a few days. After taking 131 iodine, the permeability of thyroid blood vessels increases, and a large amount of thyroxine can enter the blood circulation, so that the symptoms of hyperthyroidism can be exacerbated in the first two weeks.

 

(5) Therapeutic effect: After taking the medicine for 2 to 3 weeks, the symptoms of hyperthyroidism gradually reduced, the thyroid gland shrank, and the weight gained. The therapeutic effect of 131 iodine generally lasts 3 to 6 months, so those who are not satisfied with the effect of the first course of treatment must wait at least 6 months before the second treatment.

The cure rate of one treatment is about 50-80%, the total effective rate is more than 90%, and the recurrence rate is 1-4%. Some patients may have transient hypothyroidism 2 to 6 months after treatment, and most symptoms are mild. It can resolve spontaneously within 6-9 months, and some patients can develop permanent hypothyroidism. Individual patients can induce crisis, therefore, attention must be paid to the prevention and treatment of antithyroid drugs before taking 131I. Infiltrative exophthalmos can worsen after 131 iodine treatment, but it also improves.

 

3. Surgical treatment Subtotal thyroidectomy is one of the effective methods for treating hyperthyroidism. Most patients can be cured, and the autoimmune response can be weakened, and the recurrence rate is low.

 

(I) Indications

i. The drug treatment is not effective, especially in patients who have been ineffective for more than 2 years

ii. The goiter is obvious, especially those with nodular or compression symptoms

iii. Recurrent hyperthyroidism

iv. Patients who have a toxic drug reaction and cannot adhere to medication.

 

(II) Contraindications

i. Those with insignificant goiter and mild symptoms

ii. Patients with hyperthyroidism who are uncontrolled and who may have a crisis during or after surgery

iii. Recurrence after subtotal thyroidectomy

iv. Height Exophthalmos, those who may be aggravated after surgery

v. Aged and frail, with heart, liver, kidney and other diseases, can not tolerate surgery.

 

(III) Preoperative preparations

Antithyroid drugs must be used to control hyperthyroidism before surgery, so that the heart rate is <80 beats / min, and the serum T3, T4 and BMR are basically normal. The compound iodine solution should be taken two or three times a day before surgery, 3 to 5 drops each time. Now use the compound iodine solution plus propranolol for preoperative preparation, less intraoperative bleeding, and less prone to crisis after surgery. The propranolol dose is 10-20 mg, which is taken orally every 8 hours.

 

(IV) Surgical complications

Postoperative complications mainly include wound bleeding, infection, thyroid crisis, recurrent laryngeal nerve injury, tetany of hand and foot, hypothyroidism (about 10-15%), and exophthalmos.

 

Treatment of Comorbidities

 (I) Infiltrative exophthalmos: The eye signs of most patients with Graves disease do not need special treatment. When the thyroid function gradually normalizes, the eye signs gradually improve. However, a small number of eye signs do not improve with the recovery of thyroid function, but they are getting worse. Therefore, when choosing a treatment plan, care should be taken to prevent exophthalmos from worsening. Severe exophthalmos are generally not suitable for surgical treatment and radioactive 131 iodine treatment. It is safer to use antithyroid drugs to control hyperthyroidism supplemented with other necessary treatment measures

 

1. Protect the eyes, wear black glasses to prevent strong light and dust from irritating the eyes, use antibiotic eye ointment and wear eye masks during sleep to avoid corneal exposure and keratitis. Unilateral eye mask can relieve complex vision. A high-pillow, low-salt diet or supplemented with diuretics can reduce edema. 0.5% methylcellulose or 0.5% hydrocortisone has a better effect on reducing irritation. For severe diseases such as severe corneal exposure, eyelid suture can be considered. In severe cases, intraorbital decompression can be used when various treatments fail.

 

2. Prednisone 10 ~ 40mg, 3 times a day, has a certain effect on early cases. After the symptoms are improved, it can be gradually reduced and changed to a maintenance amount, 5 ~ 20mg daily, or the minimum dose can be given every other day, and finally discontinued.

 

3. Other immunosuppressive agents, such as cyclosporin A, cyclophosphamide, nitrobutyric acid mustard (Linconine, CB1348), 6-MP, etc. can be tried.

 

4. Thyroid tablets, 40 to 120 mg daily, are used in combination with antithyroid drugs to adjust pituitary-thyroid axis function.

 

5. Post-bulbar or pituitary radiotherapy Radiation suppresses sensitive lymphocytes and reduces post-orbital infiltration. After the above-mentioned hormone therapy is ineffective, we can consider that the efficacy of this method is not certain, and there is a risk of hypopituitarism, so it is rarely used.

 

(II) Local myxedema does not require treatment for small areas or mild myxedema, extensive and severe myxedema that affects walking or discomfort can be topically applied with betamethasone and then wrapped with polyethylene. Better, treatment needs to be maintained for one year, and may relapse after stopping treatment. If you are resistant to betamethasone, you can use anti-inflammatory pine (fluroxydehydrocortisol, fludroprednisolone, fludroprednisolone). In addition, erythema doses of ultraviolet radiation may improve symptoms.

 

(III) Thyroid crisis: This disease should focus on prevention, especially preparation before surgery and preventive measures after infection, the general prevention effect is better. If it happens, it should be dealt with urgently:

 

1.   Decrease the concentration of thyroid hormones in the blood circulation:

   1.  Drugs that inhibit the synthesis of T3 and T4 and the conversion from T4 to T3. Take propylthiothiouracil as the first. The first dose is 600 mg orally or through a gastric tube. 600 mg of methylthiouracil or 60 mg of tazobazole and methypine, 200 mg of the former two or 20 mg of the latter two, three times a day.

    2.  After applying the above medicine, add compound iodine solution, the first dose is 30 to 60 drops, and then every 6 to 8ihjf 5 to 10 drops, or 0.5 to 1.0 g of sodium iodide is added to the liquid for 12 to 24 hours. Iodine preparations can inhibit the release of T3 and T4 from the thyroid into the blood.

     Reduce the response of surrounding tissues to thyroid hormones and catechins

   i. β adrenergic blockers, propranolol 40 to 80 mg, once every 6 to 8 hours, or 1 mg intravenously, and then repeat as appropriate, or 5 mg dissolved Slowly drip in liquid. Used with caution or disabled in patients with heart and lung diseases.

   ii. Catecholamine depletion agent, intramuscular injection of reserpine 1 to 2 mg, once every 6 to 8 hours.

   iii. Norepinephrine release inhibitor, guanethidine 25 to 50 mg orally, every 6 to 8 hours, the effect reached a peak after 2 to 3 days.

3. Antagonistic stress: Hydrocortisone 100mg or dexamethasone 15-30mg can be added to the liquid for intravenous drip, once every 4-6 hours. After the condition is improved, it can be reduced.

4. Others If there is high fever, you can cool the physical temperature or the drug, you can try promethazine. Duolidine was given in drops of 50 mg each. At the same time, give oxygen, actively prevent infection, pay attention to the protection of heart and kidney function and peripheral circulation function.

 

Hyperthyroidism Hypothyroidism Chart 

 

 Chronic Lymphocytic Thyroiditis

Chronic lymphocytic thyroiditis, also known as Hashimoto thyroiditis, is a common type of autoimmune thyroiditis.

 

What are the causes of chronic Lymphocytic Thyroiditis?

The disease is characterized by high titer antithyroid antibodies that can be detected in the blood and is therefore considered to be an autoimmune disease. In addition, the main evidence is that:

i. A large amount of plasma cells and lymphocytes infiltrate in the thyroid tissue of the patient, and can form lymphoid follicles

ii. Lymphocytes can form lymphoblasts after contact with thyroid antigen, and inhibit migration Factors and lymphotoxin suggest that the patient’s T cells have sensitizing activity, and the corresponding antigens are components of thyroid cells

iii. About 50% of relatives of patients can detect similar thyroid autoantibodies in blood.

iv. Patients or their relatives are susceptible to autoimmune diseases of other organs or tissues, such as Graves disease, autoimmune Addison disease, malignant anemia, atrophic gastritis, insulin-dependent diabetes mellitus, systemic lupus erythematosus, etc.

v. Have a good response to immunosuppressive agents.

 

Pathology for Lymphocytic Thyroiditis

 The thyroid gland often presents with moderate diffuse lymphocytic infiltration, with the formation of lymphatic follicles, plasma cell infiltration, and thyroid follicle rupture. Some follicular cells show swelling and eosinophilia, so-called “Askanazy cells”. Some patients may be accompanied by myxedema, whose thyroid is small and cannot even be touched. The histological changes of the thyroid are similar to the above, but the fibrous changes are obvious and the cell infiltration is reduced.

 

Clinical Manifestations of Lymphocytic Thyroid

Chronic lymphocytic thyroiditis is more common in middle-aged people, but can be affected in any age group. The incidence of women is significantly higher than that of men, about 20: 1. The onset is hidden and slow. Often, goiter is found inadvertently, of medium size. A few patients may have local discomfort or even pain, which is easily confused with subacute thyroiditis.

Most goiter is symmetrical, accompanied by the enlargement of the pyramidal lobe, the surface of the gland can be lobulated, tough as rubber, and the thyroid function is more normal, but some patients may be accompanied by hyperthyroidism, seen in young patients, called Hashimoto’s hyperthyroidism (Hashitoxicosis), hypothyroidism may occur in the later stage, and a few are myxedema.

 

Slow lymphocytic thyroiditis is diffusely enlarged in adolescents with a smooth surface. Most middle-aged patients have only moderately enlarged thyroid glands, medium hardness, less uniformity, and less smooth surfaces. TGA and TMA increase significantly. A small number of patients have a hard thyroid texture that is difficult to distinguish from thyroid cancer or medullary thyroid cancer.

 

Laboratory inspection for Lymphocytic Thyroid

1. The red blood cell sedimentation rate often increases, serum globulin increases, and albumin decreases.

 2. About 60 to 80% of patients with antithyroid antibodies are positive for TGA, and about 95% for TMA are significantly positive.

 3. Potassium perchlorate excretion test: About 40% of the patients showed abnormal reactions, indicating that there is a disorder of organic iodine in the thyroid.

4. Thyroid function can be normal, hyperactive or diminished according to different clinical types.

5. Thyroid scans showed uneven distribution or changes in cold nodules.

6. The needle needle biopsy biopsy can show corresponding histological changes.

 

Diagnosis of Lymphocytic Thyroid

Middle-aged women with diffuse goiter, especially with pyramidal lobes, should be suspected of this disease regardless of thyroid function. Further determination of TMA and TGA can assist diagnosis. Potassium perchlorate excretion test is of reference value. Thyroid puncture can be used for histological examination to confirm the diagnosis. It can also be treated with thyroid hormone test. Give thyroid tablets 80 to 160 mg daily. Diagnosis helps. The diagnosis of this disease should be distinguished from patients with thyroid disease such as thyroid cancer, subacute thyroiditis, simple goiter and nodular goiter.

 

Treatment of Lymphocytic Thyroid

1. Thyroid hormone preparations: Thyroid function is normal or low, thyroid preparations can be used, the effect is good. 80 to 160 mg of thyroid tablets can be taken daily. Or L-thyroxine 0.2-0.4mg, the specific dose should be based on thyroid function, the degree of goiter, the age of the patient and the state of the cardiovascular system. Generally, after 2 to 4 weeks of medication, the symptoms can be improved and the thyroid gland shrinks. At this time, the dose can be appropriately reduced and maintained for 1 to 2 years or even longer.

 

2. Antithyroid drugs If accompanied by hyperthyroidism, antithyroid drugs can be appropriately applied, the dose should not be too large, and monitor thyroid function, adjust the dose or discontinue the drug in time. In addition, according to the degree of hyperthyroidism, an appropriate amount of thyroid tablets can be added to improve the symptoms of goiter and compression.

3. Adrenocortical hormone is obvious in patients with goiter, significant compression symptoms, and rapid progress of the disease. It can be considered for the purpose of obtaining better results in the short term. The general medication period is 1 to 2 months. After the condition is stable, it is maintained with thyroid tablets.

If the treatment fails, the diagnosis should be re-examined, excluding thyroid tumors or lymphomas, and surgical treatment can be used if necessary.

 

Hypothyroidism (Hypothyroidism)

Hypothyroidism is a systemic disease caused by insufficient thyroid hormone synthesis and secretion, or poor physiological effects of thyroid hormones. If the hypofunction begins in the fetus or neonatal period, it is called Cretinism; children who begin before sexual development are called juvenile hypothyroidism; and adults who start are called adult hypothyroidism.

What are the causes of Hypothyroidism?

 1.  the primary hypothyroidism caused by the disease of the thyroid itself, patients with elevated serum TSH. Mainly seen in:

i. Congenital thyroid atrophy

ii. thyroid atrophy

iii. Diffuse lymphocytic thyroiditis

iv. Subacute thyroiditis

v. After thyroid destructive treatment (radioactive iodine, surgery)

vi. thyroid hormone synthesis disorder (congenital Enzyme deficiency, iodine deficiency or iodine excess)

vii. Drug inhibition

viii. invasive lesions (lymphatic cancer, amyloidosis, etc.).

2. Serum TSH decreased in patients with secondary hypothyroidism. It is mainly seen in pituitary disease, pituitary tumor, and solitary TSH deficiency; hypothalamic syndrome, hypothalamic tumor, and solitary TRH deficiency.

3. Peripheral hypothyroidism It is rare. It is a family inherited disease. The function of uptake of hormones in peripheral target tissues is good, but the dysfunction or lack of receptors in the nucleus, so the physiological effects on thyroid hormones are weakened.

 

Clinical Manifestations of Hypothyroidism

 1. Adult type hypothyroidism is more common in middle-aged women. The ratio of male to female is 1: 5. The onset is hidden and the disease develops slowly. Typical symptoms are as follows:

I. General performance: Afraid of coldness, dry skin and less sweat, thick, yellowing, cold hair, thinning and dry hair, brittle nails, cracks, fatigue, lethargy, poor memory, mental retardation, slow response, mild anemia. Gain weight.

(2) Special face: The face is pale and yellow, the face is swollen, the eyes are dull, the eyelids are swollen, the expression is indifferent, the words are hoarse, the words are hoarse, and the words are vague.

(3) The heart rate of the cardiovascular system is slow, the heart sounds are weak, and the heart is generally enlarged, often accompanied by pericardial effusion, myocardial fiber swelling, mucus glycoprotein (positive PAS staining) deposition, and interstitial fibrosis after chronic illness, Called hypothyroidism cardiomyopathy. Patients may have significant lipid metabolism disorders, showing hypercholesterolemia, hypertriglyceridemia, and hyperbeta-lipoproteinemia, often accompanied by atherosclerosis.

The incidence of coronary heart disease is higher than that of the general population, but due to the surrounding the tissue’s low metabolic rate, reduced cardiac output, and reduced myocardial oxygen consumption, rarely cause angina pectoris and heart failure. Sometimes high blood pressure, but more common in diastolic blood pressure. The electrocardiogram showed a low voltage, the T wave was inverted, the QRS wave was widened, and the P-R interval was prolonged.

(4) Digestive system: Patients have decreased appetite, constipation, abdominal distension, and even paralytic intestinal obstruction. About half of the patients have complete gastric acid deficiency.

(5) Muscle and joint system: Muscle contraction and relaxation are slowly delayed, and muscle pain and stiffness are often felt. Bone metabolism is slow, and bone formation and absorption are reduced. Joint pain, inability to move, anxiety, exacerbation after cold, like chronic arthritis. Occasionally, joint cavity effusion.

(6) Endocrine system: Males have impotence, women have more menstrual periods, and those who have not been cured for a long time can also have amenorrhea. Tight adrenal cortex function is low, blood and urinary cortisol are reduced. Primary hypothyroidism can sometimes be accompanied by autoimmune adrenal insufficiency and / or type I diabetes, called Schmidt syndrome.

II. Dementia in children with Creutzfeldt-Jakob disease, poor appetite, difficulty feeding, no sucking power, quiet, less crying, drowsiness, less spontaneous movements, muscle relaxation, pale skin, dry skin, cold, thick, hoarse, tendon Weak reflection. There is a delay in development.

III. Juvenile type hypothyroidism: Young patients behave like cretinism. Older children have symptoms such as adult hypothyroidism, affected growth and development, delayed pubertal development, and poor intelligence and academic performance.

No matter what type of hypothyroidism patients, when the symptoms are severe and cannot be treated reasonably, under certain circumstances, such as infection, cold, surgery, anesthesia or sedation can induce coma, special myxedema coma. Patients have drowsiness first, body temperature does not rise, even below 35ºC, blood pressure decreases, shallow breathing, slow and slow heartbeat, muscle relaxation, disappearance of tendon reflexes, can be associated with shock, heart and kidney failure and life-threatening.

 

Laboratory inspection

 A. General inspection

i. blood routine often has mild and moderate anemia, is positive cell positive pigmentation, small cell low pigmentation or large cell type.

ii. Normal or low blood sugar, low glucose tolerance curve.

iii. Increased blood cholesterol, triglycerides and β-lipoprotein.

 

B. Thyroid function test

i. The basal metabolic rate decreases, often below -30-45%

ii. The thyroid iodine uptake rate is lower than normal, showing a flat curve

iii. Serum T4 decreases, often at 38.6nmol / L (30ng / ml) Below, FT4 is often <9.11 pmol / L (7.08pg / ml); serum T3 and FT3 can also be reduced to varying degrees, but mild to moderate patients are sometimes normal, and serum rT3 can be less than 0.3nmol / L (0.2ng / ml). ).

 

C. Hypothalamus-pituitary-thyroid axis function test

i. Serum TSH measurement, normal people are mostly <10mu / L (10μu / ml), in primary hypothyroidism, TSH> 20mu / L (20μu / ml). Secondary Hypothyroidism is significantly reduced, can be <0.5mu / L (0.5μv / ml)

ii. TSH excitation test, after subcutaneous injection of 10 units of TSh, such as thyroid 131 iodine rate significantly increased, suggesting a secondary hypothyroidism, such as Not elevated, suggesting primary hypothyroidism.

iii. In the TRH excitation test, after intravenous injection of TRH 200-500 μg, if the serum TSH showed a delayed elevation response, it suggests that the lesion may be at the level of the hypothalamus. If there is no increased response, the lesion may be in the pituitary. Prompt the lesion in the thyroid.

 

D. X-ray examination

Make plain skull, CT, magnetic resonance or ventricular angiography to exclude pituitary tumors, hypothalamus or other intracranial tumors that cause hypothyroidism. Primary hypothyroidism, pituitary and sphenoid saddle can be secondary increase.

 

E. Thyroid autoantibody examination

The cause is related to thyroid autoimmunity. The blood of patients with antithyroid microsomal antibodies (TMA) and antithyroglobulin antibodies (TGA) can increase.

 

Treatment of Hypothyroidism

Hypothyroidism requires replacement therapy with thyroid hormones and is often treated for life. Thyroid preparations include levothyroxine sodium (L-T4), triiodothyronine (L-T3), and thyroid tablets. The strength ratio of the three is about 0.1mgT4 = 25μg, T3 = 40mg thyroid tablets. Each tablet contains T40.06mg, T315μg), and Thyrolar contains T40.05mg, T312.5μg). Commonly used preparations in China are thyroid tablets.

Dosage and usage

i. Thyroid tablets, starting dose of 20 ~ 40mg / day, increase 20mg / day every week until Qinxiao. Generally, the swelling subsides first, and then other symptoms improve or disappear. After obtaining satisfactory results, explore the appropriate maintenance amount and take it for a long time.

ii. L-T4 0.05-0.1 mg / day, 0.05 mg every 4 to 6 weeks, the complete replacement dose is 0.1 to 0.2 mg / day.

iii. L-T350 ~ 100μg / day, divided into 2 to 3 times, the drug is quickly absorbed, the effect is strong, it is not good for sensitive patients with hypothyroidism, it is generally not used alone.

iv. The daily dose for children over 1 year old should be taken orally according to T42.8 ~ 4.4μg / kg, or a thyroid tablet with equivalent dose (0.1mgT4 equivalent to 40mg thyroid tablet). Infants under 1 year of age need to increase the dose and take T410 μg / kg daily.

In addition to thyroid preparation replacement therapy, patients with anemia should be supplemented with iron, vitamin B12, folic acid or liver preparations according to the type of anemia. Stomach acid deficiency should be supplemented with dilute hydrochloric acid.

Patients with myxedema and coma should be injected intravenously with L-T340 ~ 120μg immediately, then 50μg daily, divided into 2 or 3 times, or immediately with L-T4200μg, 50μg daily, if there is no injection, the medicine can be dissolved and injected. Gastric tube, once every 4 to 6 hours, with the same dose as above. In addition, we should pay attention to keep warm, give oxygen, keep the breathing unobstructed, and the infusion should not be too fast. Infection can be infused with 200 ~ 300mg of hydrocortisone, and antibiotics infection.

 

Subacute Thyroiditis

 Also known as giant cell thyroiditis, granulomatous thyroiditis, pseudonodular thyroiditis, DeQuervain thyroiditis, etc., was first described by De Quervain in 1904.

 

What are the causes of Subacute Thyroiditis?

 It is generally believed to be related to viral infection:

i. Most patients have upper respiratory tract infection before the onset of disease.

ii. Mumps can also cause epidemic thyroiditis

iii. Patients often have high titers of viral antibodies in the serum, the most common Coxsackievirus antibodies, followed by adenovirus antibodies, influenza virus antibodies, and mumps virus antibodies.

iv. Mumps virus was directly cultured in the affected thyroid tissue.

 

Pathology for Subacute Thyroiditis

 Goiter, mostly diffuse, can reach 1 to 3 times the normal, or nodular, cross-section visible transparent gelatinous, scattered gray lesions. More giant cells and granulation tissue can be seen under the light microscope, with fibrosis and chronic inflammatory cell infiltration, and the lesions are similar to tuberculous nodules.

 

Clinical manifestations of Subacute Thyroiditis

Patients often have symptoms of acute onset, systemic symptoms include fever, night sweats, fatigue, and loss of appetite. Mild hyperthyroidism symptoms may appear in the early stages of onset: palpitation, fear of heat, sweating, tremor, and nervousness.

Thyroid pain can be severe or faint, and can radiate along the neck to the submandibular, the root of the ear and behind the occipital, and also to the chest and shoulders. A few patients may have headaches, tinnitus, nausea, and vomiting. Female patients may be accompanied by menstrual abnormalities, menstrual flow is scarce. Symptoms of hypothyroidism are occasional during the recovery period.

Most goiters are bilateral and a few are unilateral. Tenderness in the thyroid area, smooth surface, firm texture, can move with phagocytosis, no obvious adhesion and fixation with surrounding tissues. The compression depends on the condition of the goiter and is usually not obvious.

The duration of the disease varies, ranging from weeks to months, and even repeated and delayed to 1 to 2 years.

 

Laboratory inspection of Subacute Thyroiditis

White blood cell count and neutrophils are normal or high, red blood cell sedimentation rate increases, serum protein bound iodine or serum T3, T4, FT3 and FT4 concentrations increase, thyroid iodine uptake decreases, thyroid scan shows thyroid enlargement, but If the development is uneven or defective, there are also those that are not developed at all. Protein electrophoresis showed a decrease in albumin and an increase in globulin, mainly an increase in r and α1 globulin.

 

Treatment Subacute Thyroiditis

1. Adrenal cortex hormone, suitable for persistent fever, fatigue, weakness, severe systemic symptoms, obvious thyroid enlargement or pain. Prednisone is commonly used at a dose of 30 mg / day. Fever and pain often ease quickly after 1 to 3 days of administration, and goiter often shrinks quickly after one week. After the condition improves, the hormone dosage can be gradually reduced according to the red blood cell sedimentation rate, the whole process is about 1 to 2 months. Those with hypothyroidism should take thyroid tablets to eliminate symptoms.

2. Anti-inflammatory analgesics such as indomethacin, aspirin can be used as appropriate, the course of treatment is generally more than two weeks.

 

 

Refer also:

 

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