Endocrine hypertension

Introduction to endocrine hypertension Endocrine tissue hyperplasia or a variety of endocrine diseases caused by tumors, due to the excessive secretion of its corresponding hormones such as aldosterone, catecholamines, cortisol, etc., resulting in changes in the body's hemodynamics and elevated blood pressure. This type of hypertension caused by increased secretion of endocrine hormones is called endocrine hypertension, and it is also a common secondary hypertension. If the tumor can be removed, the cause can be removed, and hypertension can be cured or alleviated. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people. Mode of infection: non-infectious Complications: coronary heart disease, angina pectoris, cerebral infarction, cerebral thrombosis, cerebral hemorrhage, nephritis, proteinuria, cataract, multiple system organ failure

Etiology of endocrine hypertension

Usually secondary to some endocrine diseases, common Cushing syndrome (cortisolism), pheochromocytoma, primary aldosteronism, adrenal hypersensitivity syndrome, hyperthyroidism, hypothyroidism, parathyroid gland Hyperfunction, pituitary hyperfunction, menopausal syndrome, etc.

Therefore, early diagnosis can significantly improve the cure rate or prevent the progression of the disease.

Endocrine hypertension prevention

1. Hormone drugs: such as prednisone, dexamethasone and so on. These drugs can cause an increase in circulating blood volume and high blood pressure; thyroid hormone drugs can excite the nervous system and cause blood pressure to rise.

2. Analgesic drugs: such as indomethacin, phenylbutazone, etc., can inhibit the synthesis of prostaglandins, causing blood vessels to contract and cause high blood pressure.

3. Contraceptives: can cause blood vessels to contract, and stimulate the release of adrenocortical hormones to cause high blood pressure.

4. Antihypertensive drugs: such as commonly used methyldopa, guanethidine, etc., when taking antihypertensive drugs, when you eat tyramine-containing foods, such as cheese, animal liver, chocolate, etc., blood pressure will rise greatly High; and the sudden withdrawal of certain antihypertensive drugs, such as propranolol, methyldopa, etc., can also cause the same serious consequences.

5. Other drugs, as well as adrenaline, norepinephrine, Ritalin and Chinese herbal medicine licorice.

Endocrine hypertension complications Complications Coronary heart disease angina pectoris cerebral infarction cerebral thrombosis cerebral hemorrhage nephritis proteinuria cataract multisystem organ failure

1, heart problems; coronary heart disease, angina pectoris, myocardial infarction, heart rhythm disorder;

2, the brain; insufficient blood supply to the brain, cerebral infarction, cerebral thrombosis, cerebral hemorrhage, etc.;

3, kidney; proteinuria, nephritis, chronic renal failure;

4, eyes; decreased vision, fundus bleeding, cataract, blindness;

5, multiple organ failure, death.

Endocrine Hypertension Symptoms Common symptoms Hypertension Concentric obesity Aldosterone secretion Increase nausea and vomiting Full moon face Hypothyroidism Hypokalemia

Characteristics of hypothyroidism:

The cause of systolic hypertension (ISH), in addition to increased age and increased arterial stiffness, thyroid dysfunction is also an important cause of ISH.

Previous studies have suggested that hyperthyroidism is caused by increased heart rate, decreased systemic vascular resistance, increased cardiac output, and increased systolic blood pressure. The resulting hypertension is a highly dynamic hypertension with elevated systolic blood pressure. . Such patients are prone to atrial fibrillation, left ventricular hypertrophy, and heart failure. Hypothyroidism is mainly caused by volume change, and its blood pressure pattern may be different from hyperthyroidism. Some scholars reviewed the results of many previous clinical trials and found that only 40% of patients with hypothyroidism were mainly diastolic blood pressure, and more were still elevated systolic blood pressure. A 24-hour blood pressure monitor was performed on patients who had a clinical diagnosis of hypothyroidism (TSH) > 5 mU/ml and who had never received hypertension. The patients with hypothyroidism with an average TSH >25 mU/ml had the following characteristics.

1. Weight: Compared with the normal control group, the hypothyroidism group has more overweight or obese patients.

2. Distribution of blood pressure: According to the average arterial pressure of 24h>135/85mmHg or the blood pressure of the clinic>140/90mmHg, 20.2% of patients diagnosed with hypertension; 23.2% of white coat hypertension and recessive hypertension accounted for 23.2% and 8.1 respectively. %; normal blood pressure accounted for 48.5%.

3. Type of blood pressure increase: The increase of systolic blood pressure is greater than the increase of diastolic blood pressure, and the fluctuation of systolic blood pressure is increased at 24 hours.

4. Heart rate: Compared with the normal control group, the heart rate decreased little.

5. The effect of lesion severity on blood pressure: patients with mild to moderate hypothyroidism were mainly systolic blood pressure, and severe hypothyroidism was mainly mixed hypertension (increased systolic blood pressure and diastolic blood pressure).

The mechanism of hypothyroidism leading to elevated systolic blood pressure is currently considered to be the following: 1 by the concentration of triiodothyronine (T3), vascular resistance and stiffness increase; 2 plasma norepinephrine concentration is higher; 3 The level of vasopressin is increased; 4 the lack of thyroid hormone is associated with decreased renal blood flow and decreased glomerular filtration rate.

Compared with normal people, patients with hypothyroidism showed a significant increase in 24-hour systolic blood pressure, increased pulse pressure, and high volatility in 24-hour systolic blood pressure. The difference in systolic blood pressure between the night and the white sputum was reduced, suggesting that the nighttime patient had a higher systolic blood pressure load (non-sputum type), and the 24-hour diastolic blood pressure did not differ from the normal group.

Primary aldosteronism

The disease is caused by adrenal hyperplasia or excessive secretion of aldosterone by the tumor. Clinically, long-term hypertension with hypokalemia is characteristic, and a small number of patients have normal blood potassium. I often overlook the further examination of this disease. Due to electrolyte metabolism disorders, this disease may have symptoms such as muscle weakness, periodic paralysis, polydipsia, and polyuria. Most of the blood pressure is mild and moderate, and about one-third of the blood pressure is refractory hypertension.

Laboratory tests have hypokalemia, hypernatremia, metabolic alkalosis, decreased plasma renin activity, and increased urinary aldosterone. Increased plasma aldosterone/plasma renin activity ratio has higher diagnostic sensitivity and specificity. Ultrasound, radionuclide, C'r, and MRI can establish the nature and location of the lesion. Selective bilateral adrenal venous blood hormone determination has a high diagnostic value for patients with difficult diagnosis.

If the disease is caused by adrenal adenoma or cancer, surgical resection is the best treatment. If it is adrenal hyperplasia, it can also be used for adrenalectomy, but the effect is relatively poor, generally still need to use antihypertensive drugs, choose aldosterone antagonist spironolactone and long-acting calcium antagonist.

Pheochromocytoma

Pheochromocytoma originates from the adrenal medulla, sympathetic ganglia, and other parts of the body. The tumor intermittently or continuously releases too much adrenaline, norepinephrine and dopamine. Clinical manifestations vary widely, with typical episodes showing elevated paroxysmal blood pressure with tachycardia, headache, sweating, and pale complexion.

Blood or urine catecholamine or its metabolite 3-methoxy-4-hydroxylamarinic acid (VMA) can be measured during the onset, and if there is a significant increase, it suggests pheochromocytoma. Ultrasound, radionuclide, CT or magnetic resonance can be used for localization diagnosis.

Most of the pheochromocytoma is benign, about 10% of pheochromocytoma is malignant, and the surgical resection effect is good. Preoperative or malignant lesions have been transferred to multiple operations, the choice of a and 0 blockers combined with antihypertensive treatment.

Cortisol

Hypercortisolism, also known as Qmhing syndrome, is mainly caused by excessive secretion of adrenocorticotropic hormone (ACTH) leading to adrenal hyperplasia or adrenal adenoma, causing excessive glucocorticoids. 80% of patients have high blood pressure, and there are also manifestations of central obesity, full moon face, buffalo back, purple skin, increased hair, and elevated blood sugar.

The urinary 17-hydroxyl and 17-ketosteroids increased in 24 hours, and the dexamethasone inhibition test and the adrenocortical hormone stimulation test were helpful for diagnosis. Intracranial sellar X-ray examination, 'adrenal CT, radionuclide adrenal scanning can determine the lesion. Treatment mainly uses surgery, radiation and drug methods to cure the disease itself. Antihypertensive therapy can be used with diuretics or with other antihypertensive drugs.

Examination of endocrine hypertension

Examination of hypothyroidism

(1) Serum thyroid hormone spectrum: serum FT4 and FT3 are not affected by blood thyroid hormone binding globulin (TBG), which can directly reflect the thyroid function status, and its sensitivity and specificity are significantly higher than total T3 and total T4. Serum FT3 and FT4 were significantly elevated in GD hyperthyroidism. In addition to the inherent experimental error, the thyroid function test results vary depending on the region, patient age, and measurement method.

(2) Serum TSH: When thyroid function changes, TSH fluctuation is more rapid and significant than thyroid hormone, so TSH in blood is a sensitive index reflecting hypothalamic-pituitary-thyroid axis function. With the improvement of detection methods, the value of serum TSH in the diagnosis of hyperthyroidism was further confirmed. Serum TSH was significantly reduced, whether it was typical hyperthyroidism or subclinical hyperthyroidism. However, pituitary hyperthyroidism and certain non-endocrine system tumors caused a significant increase in hyperthyroidism TSH.

(3) thyroid iodine uptake rate (RAIU): typical GD hyperthyroidism increased RAIU, with peak advancement, and was not inhibited by thyroid hormone inhibition test. However, hyperthyroidism caused by hyperthyroidism, RAIU is often reduced, iodothyroid and drug-induced hyperthyroidism also see RAIU below normal. Therefore, all patients with hyperthyroidism should receive routine RAIU examination.

(4) Thyroid-specific antibodies: 80% to 100% of patients with Graves' disease are positive for thyroid stimulating hormone receptor antibody (TRAb), especially thyroid stimulating antibody (TSAb). 50%-90% of patients have positive thyroglobulin antibody (TGAb) and/or thyroid peroxidase antibody (TPOAb), but the titer is not as high as chronic lymphocytic thyroiditis.

(5) thyroid imaging examination: B-ultrasound and radionuclide scanning can determine the location, size and presence or absence of thyroid gland, which is of great value in the diagnosis of ectopic thyroid. The GD thyroid gland generally shows diffuse enlargement with no obvious nodules. MRI and CT examinations are not routine, and are considered only when the goiter is compressed, the corresponding symptoms of the trachea, esophagus, recurrent laryngeal nerve, or retrosternal goiter, and suspected malignant transformation and local metastasis.

Cortisol

(1) Erythrocyte count and hemoglobin content: A large amount of cortisol increases the total number of white blood cells and neutrophils, but promotes lymphocyte apoptosis, which redistributes lymphocytes and eosinophils. These two cells are in peripheral blood. Both the absolute value and the percentage in the white blood cell classification are reduced.

(2) hypercoagulable state of the blood: may be related to erythrocytosis, increased metabolism of vascular endothelial cells, elevated blood levels of factor VIII and VWF, and easy formation of thrombosis.

(3) Urine 17-OH, 17-KS, free cortisol (UFC) determination: 24-hour UFC measurement is widely used for screening of Cushing syndrome. Under normal circumstances, about 10% of cortisol in the human body is in a non-binding state and is biologically active. Normal free cortisol can be filtered through the glomerulus, most of which is reabsorbed in the renal tubules, while the amount of excretion through the kidneys is relatively constant. When excess cortisol in the blood saturates the circulating cortisol binding protein, the excretion of free cortisol in the urine increases. RIA determination of 24-hour UFC can reflect the body's cortisol secretion status, which is parallel with the Cushing syndrome. The normal upper limit fluctuation range is 220 to 330 nmol/24 h (80 to 120 g/24 h). When the excretion exceeds 304nmol/24h (110g/24h), it can be judged as elevated. The urinary creatinine excretion rate can be determined to determine whether the specimen is completely collected, thereby eliminating false negative results.

(4) Determination of blood and salivary cortisol and its circadian rhythm changes: Determination of cortisol concentration by blood sampling is a simpler method for the diagnosis of Cushing syndrome. Normal people have normal basal values and cortisol has a normal rhythm of diurnal secretion. Because cortisol is pulsed, and cortisol levels are highly susceptible to mood, venous puncture and other factors, the determination of single blood cortisol is limited in the diagnosis of Cushing syndrome. The concentration of cortisol in saliva is parallel to blood free cortisol and is not affected by the amount of salivary secretion. Therefore, the determination of cortisol concentration in saliva at 0:00 (valley) and 8:00 (peak) in the morning can also be used for Cushing synthesis. Diagnosis of the sign. At midnight saliva cortisol concentration increased, combined with 24-hour UFC excretion increased, the sensitivity of the diagnosis of Cushing syndrome can reach 100%.

(5) Determination of blood ACTH: Adrenal cortical tumors, benign or malignant, the blood ACTH level is lower than the normal low limit, due to a large amount of cortisol secreted by adrenal tumors, severely inhibit the secretion of pituitary ACTH. ACTH-dependent Cushing disease and elevated ACTH levels in patients with ectopic ACTH syndrome increased to varying degrees.

(6) Low-dose dexamethasone inhibition test (LDDST)

1) Standard low-dose dexamethasone inhibition test On the second day after the application of standard dexamethasone suppression in normal people, the urinary 17-OHCS decreased to 6.9 mol/24 h (2.5 mg/24 h) or below, and the UFC decreased to 27 nmol/24 h ( 10 g / 24 h) or less. This test is not inhibited by Cushing syndrome.

2) Midnight low-dose dexamethasone inhibition test After midnight dexamethasone 1 mg inhibition, blood cortisol levels were inhibited to below 140 nmol/L (5 g/d1), Cushing syndrome was ruled out.

(7) CRH excitatory test: In patients with pituitary Cushing disease, blood ACTH and cortisol levels increased significantly after intravenous bolus injection of CRH1-41 100IU or 1IU/Kg body weight, which was higher than that of normal people, and most of the ectopic ACTH Patients with syndromes have no response. This test is of great value in the differential diagnosis of these two ACTH-dependent Cushing syndromes.

(8) venous catheter segmentation blood test ACTH or ACTH-related peptides: the identification of ectopic ACTH syndrome and pituitary Cushing disease and the location of ectopic ACTH secretion tumors. For example, if the catheter is inserted into the drainage vein of the pituitary - bilateral subtalar veins, both sides of the blood or intravenous injection of CRH, both sides of the blood simultaneously taking ACTH, the identification of pituitary ACTH tumors (determination of the tumor on the left or right side) There's important meaning.

(9) Imaging examination is useful for identifying the cause and tumor location: 1) First, determine whether there is a tumor in the adrenal gland. At present, CT and B-mode ultrasound examination of the adrenal gland has been the first choice; 2) Adrenal radionuclide 131I-cholesterol scan is useful for distinguishing bilateral adrenal hyperplasia or unilateral adrenal gland tumor; 3) Coronal CT coronal, thin, sagittal and Coronal reconstruction and contrast enhancement can improve the detection rate of pituitary microadenomas. The current resolution of the best CT microadenomas is 60%; 4) Sella magnetic resonance (MRI) examination is superior to CT. In order to find ectopic ACTH secretory tumors, the thymus should be included in the routine; 5) If suspicious, further physical or chest CT should be performed. The ectopic ACTH secretory tumor located in the chest accounts for approximately 60% of the ectopic ACTH syndrome. Other areas that should be noted are the pancreas, liver, adrenal gland, gonads, etc., but the primary site of ectopic ACTH tumors is much more than that. The clinical examination should be combined with the examination site; 6) In order to understand the patient's osteoporosis, lumbar vertebrae should be used. X-ray examination of ribs. If it is a malignant adrenal tumor or an ectopic ACTH secretory tumor, you should also pay attention to whether there are other organs.

Pheochromocytoma

Blood or urine catecholamine or its metabolite 3-methoxy-4-hydroxylamarinic acid (VMA) can be measured during the onset, and if there is a significant increase, it suggests pheochromocytoma. Ultrasound, radionuclide, CT or magnetic resonance can be used for localization diagnosis.

Primary aldosteronism

Laboratory tests for serum potassium, sodium, plasma renin activity, and urinary aldosterone. Increased plasma aldosterone/plasma renin activity ratio has higher diagnostic sensitivity and specificity. Ultrasound, radionuclide, C'r, and MRI can establish the nature and location of the lesion. Selective bilateral adrenal venous blood hormone determination has a high diagnostic value for patients with difficult diagnosis.

Diagnosis and diagnosis of endocrine hypertension

According to the difference in blood pressure, hypertension is divided into 3 levels:

Grade 1 hypertension (mild) systolic blood pressure 140~159mmHg; diastolic blood pressure 90~99mmHg.

Grade 2 hypertension (moderate) systolic blood pressure 160~179mmHg; diastolic blood pressure 100~109mmHg.

Grade 3 hypertension (severe) systolic blood pressure 180 mmHg; diastolic blood pressure 110 mmHg.

Systolic hypertension with systolic blood pressure 140mmHg; diastolic blood pressure <900mmHg.

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