With the changes in diet and lifestyle, hypertension has become a common disease, and people have a general understanding of hypertension. However, most people's understanding of hypertension is limited to the fact that high blood pressure is harmful to the heart, brain and kidneys, and once discovered, they must take antihypertensive drugs regularly for life. This type of hypertension we often talk about is called primary hypertension. Because the cause is unknown, it cannot be cured. We can only control blood pressure by taking long-term medication to reduce its damage to important target organs. Another type of hypertension is often overlooked and confused by us. That is secondary hypertension. Unlike primary hypertension, secondary hypertension is caused by a clear cause of high blood pressure, so it can be cured. Once the primary disease disappears, hypertension as a secondary symptom will also decrease or return to normal. Although secondary hypertension only accounts for 5% of all hypertension diseases, the absolute number and misdiagnosis rate are still very high. Therefore, it is very necessary to be familiar with the knowledge related to secondary hypertension. At present, kidney diseases such as renal artery stenosis and renal parenchymal disease, endocrine diseases such as hypercortisolism, hyperaldosteronism, pheochromocytoma, and obstructive sleep apnea are the main causes of high blood pressure. It is the most important cause of secondary hypertension, so let’s start with the kidney. Renovascular hypertension is caused by stenosis of the main trunk of the unilateral or bilateral renal artery or the large branches of the renal artery in the patient’s kidney, which leads to an increase in the patient’s blood pressure. It is called renovascular hypertension. Renal artery atherosclerosis, large arteritis and fibromuscular dysplasia are common causes of stenosis. Therefore, for patients with renovascular hypertension, routine color ultrasound examinations of the renal arteries in the bilateral kidney area or abdomen, as well as more sensitive angiography examinations, should be performed during examination and diagnosis. Improving stenosis, controlling blood pressure, and improving and protecting kidney function are the treatment principles of renovascular hypertension. At present, patients with stenosis ≥75% are treated with stent implantation or percutaneous renal artery balloon angioplasty. Renal parenchymal hypertension, chronic glomerulitis, diabetic nephropathy, chronic pyelonephritis and polycystic kidney disease are the main causes of renal parenchymal diseases that cause high blood pressure. Since hypertension itself has no typical symptoms, the diagnosis of hypertension is generally discovered and diagnosed when the above diseases are diagnosed. Renal parenchymal diseases require a kidney puncture biopsy for diagnosis in clinical practice. Usually, they can be diagnosed through renal function tests, imaging tests and urine routine tests. When treating renal parenchymal hypertension, the primary disease is usually treated first, and then various antihypertensive treatments are actively carried out on this basis to control the patient's blood pressure as much as possible and maintain it below 130/80 mmHg. For some patients whose urine protein excretion exceeds 1.5g within 24 hours, the patient's blood pressure must be controlled below 125/75 mmHg during treatment. Drugs that inhibit the renin-angiotensin system are the first choice for antihypertensive treatment of patients with renal parenchymal hypertension with proteinuria. This type of drug can not only effectively lower the patient's blood pressure level, but also effectively protect the patient's kidneys, thereby successfully delaying the patient's progress into end-stage renal disease. These drugs are also of great help to patients with moderate to severe renal insufficiency. For those with severe renal insufficiency, dialysis treatment can also be used. Endocrine hypertension is also a major cause of secondary hypertension. The most common is primary aldosteronism. It is caused by an abnormal increase in aldosterone secretion due to adrenal cortical tumors or hyperplasia, with hypokalemia, increased blood pressure and alkalosis as typical clinical manifestations. In the past, it was generally believed in medicine that the incidence of primary aldosteron in patients with hypertension was relatively low, but in recent years, through the use of new screening methods, it has been found that the proportion of primary aldosteron in patients with hypertension is still relatively high. Assuming that you are diagnosed with unilateral adrenal hyperplasia or unilateral aldosterone-producing tumor, you can consider laparoscopic unilateral adrenalectomy. If the patient has other problems that prevent surgery, such as bilateral adrenal hyperplasia, mineralocorticoid receptor antagonists such as eplerenone and spironolactone should be used for treatment. The patient's blood potassium level should be closely monitored during treatment. Pheochromocytoma is caused by excessive secretion of catecholamines by tumors in the adrenal medulla or extra-adrenal nerves. The diagnosis of pheochromocytoma requires a combination of clinical manifestations, genetic testing, functional diagnosis, and accurate tumor localization. Magnetic resonance imaging and CT examinations can detect tumors near the abdominal aorta or in the sympathetic ganglia of the adrenal glands, but the sensitivity for certain types of cell tumors is low. The main method used in clinical diagnosis of pheochromocytoma is to detect the content of catecholamines (dopamine, norepinephrine and adrenaline) in the patient's blood and urine. At present, there has been great progress in the genetic diagnosis of pheochromocytoma in medicine. For pheochromocytoma, surgical resection is the most effective method, because most pheochromocytomas are benign tumors. Before surgery, the patient's blood pressure should be actively and effectively controlled to prepare for the surgery. Open surgery or laparoscopic surgery is a common surgical treatment. Hypercortisolism, also known as Cushing's syndrome, is a clinical syndrome caused by hyperfunction of the adrenal cortex leading to increased cortisol secretion. The reasonable treatment of Cushing's syndrome depends on its cause. Generally, surgical treatment is the first choice, and drug treatment or other treatments are used as appropriate for those who cannot undergo surgery or fail surgery. Finally, let's talk about obstructive sleep apnea syndrome. As the name suggests, it means that the collapse of the pharyngeal muscles during sleep blocks the patency of the airway, causing the patient to repeatedly experience apnea during sleep or the patient's oral and nasal airflow is obvious. Daytime sleepiness, snoring during sleep, and frequent apnea are its clinical manifestations. In recent years, an important cause of high blood pressure is obstructive sleep apnea syndrome. The standard method currently used in clinical diagnosis of obstructive sleep apnea syndrome is multi-lead sleep monitoring, fingertip blood oxygen monitoring and simple nasal cannula ventilation can also be performed. Once the indicators are found to be abnormal, we should go to the otolaryngology department for treatment in time. Through the above popular science, it is not difficult to find that in addition to its special clinical symptoms, the treatment of secondary hypertension is completely different from that of primary hypertension. Therefore, when we find that our blood pressure is high, we should first rule out secondary factors and then carry out conventional treatment with antihypertensive drugs. References [1] Hirsch AT.Haskal ZJ.Herder NR.et al.ACC/AHA guidelines for management of patients with peripheral anterial discharge[]J Am Coll Cardiol.2006.47(6):1239-1312. [2]Pemrson JC.Adler S.Bmkart JM.et al.Blood pressure control. proteinuria.and the prosTession of renal disease|JJ.Ann Intem Med.1995.123(10):754-762. [3] Altar L.Bherat J.Ihuclia E.et al.Genetic testillg in pheocbomocy- toma or functional paraganglioma[J]JClin Oncol.2005.23(34) |
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