Pheochromocytomas originate from chromaffincell (chromophobe) cells. During the embryonic period, the distribution of chromaffincells is associated with the sympathetic ganglia of the body. As the embryo matures, the vast majority of chromaffincells degenerate and their remnants form the adrenal medulla. Thus the vast majority of pheochromocytomas occur in the adrenal medulla. Extra-adrenal pheochromocytomas can occur anywhere from the carotid body to the pelvis, but are seen mainly in the paraspinal sympathetic ganglion (predominantly posterior to the mediastinum) and in the abdomen mainly in the para-aortic apparatus at the bifurcation. Renal hypertension is a type of secondary hypertension, which is mainly due to high blood pressure caused by substantial renal lesions and renal artery lesions. For the development of this disease is mainly due to glomerular vitreous degeneration, interstitial tissue and connective tissue hyperplasia, tubular atrophy, and narrowing of the small renal arteries, resulting in both substantial damage and inadequate blood supply to the kidney; mucinous myofibers proliferation in the middle layer of the renal artery wall, forming most small aneurysms, causing a bead-like protrusion of the inner wall of the small renal arteries, resulting in segmental narrowing of the renal arteries; nonspecific aortitis that causes inadequate renal blood perfusion; under the combined effect of the above factors, it leads to the development of hypertension. In turn, hypertension can cause damage to the kidney, and the two promote each other, which will further develop the disease; therefore, renal hypertension should be treated actively. Pathological changes Pheochromocytoma is more than 90% benign tumor. The tumor is brownish-yellow in cut and rich in blood vessels, with little interstitium and often bleeding. The tumor cells are large, irregular and polygonal, with more particles in the cytoplasm; the cells can be stained with chromium salts, so it is called chromophobe cell tumor. According to statistics, 80% to 90% of pheochromocytomas occur in the chromophores of the adrenal medulla, and about 90% of them are unilateral single lesions. Multiple tumors, including those occurring in both adrenal glands, account for about 10% of cases. Pheochromocytomas originating from outside the adrenal glands account for about 10%; this statistic is slightly higher in China. Malignant pheochromocytoma accounts for about 5% to 10% and can cause metastasis to lymph nodes, liver, bone and lung. A small number of pheochromocytomas may be accompanied by multiple subcutaneous neurofibromas, about 25% of which are interlocked with Hippel-Lindau syndrome. Pheochromocytoma is also a major lesion of multiple endocrine neoplasia type II (MEN II), which is familial, autosomal dominant, and accounts for approximately 5% to 10% of pheochromocytoma cases; patients with bilateral adrenal pheochromocytoma should be particularly alert for the presence of MEN II. Pheochromocytomas autonomously secrete catecholamines, including epinephrine, norepinephrine, and dopamine. Adrenaline and norepinephrine act on adrenergic receptors, such as alpha and beta receptors, affecting the corresponding tissues and organs, causing a range of clinical manifestations. All pathophysiological bases of pheochromocytoma patients are directly related to this secretory function of the tumor. Clinical manifestations Pheochromocytoma is mostly seen in young adults, with a high incidence age of 30-50 years old, and there is no significant difference between the sexes of patients. 1. Cardiovascular system manifestations: As a large amount of catecholamines intermittently enter the blood circulation, vasoconstriction, end resistance increases, heart rate accelerates and cardiac output increases, leading to paroxysmal and sudden increase in blood pressure, systolic pressure can reach 26,6kPA (200mmHg) or more, diastolic pressure also increases significantly. The attack may be accompanied by palpitations, shortness of breath, chest depression, headache, pale face, profuse sweating, blurred vision, etc. In severe cases, hypertensive crisis such as cerebral hemorrhage or pulmonary edema may occur. The patient is extremely fatigued and debilitated after the attack subsides, and skin flushing such as facial flushing may occur. Seizures can be triggered by sudden changes in body position, emotional excitement, strenuous exercise, coughing and urinary and fecal activities. The frequency and duration of seizures vary greatly among individuals and do not correlate positively with the size of the tumor. Some patients may present with persistent hypertension. Persistent hypertension has been reported in about 90% of pediatric patients and in about 50% of adults. The difference lies in the presence of adrenaline or norepinephrine hypersecretion. A small number of patients may present with episodes of hypotension and shock. A few patients may present with episodic hypotension and shock, which may be related to tumor necrosis, intra-tumor hemorrhage that stops the release of catecholamines, or serious cardiac accidents. The prognosis is often poorer when this occurs. In 1958, Szakas introduced the concept of catecholamine cardiomyopathy, characterized by myocardial hypertrophy, edema, focal hemorrhage, intimal hypertrophy, and inflammatory cell infiltration due to the direct toxic effects of catecholamines on the myocardium. Clinical manifestations resemble myocarditis, and in severe cases, heart failure and severe arrhythmias may occur. 2, metabolic disorders: catecholamines stimulate pancreatic α-receptors, resulting in decreased insulin secretion, acting on liver α and β receptors and muscle β receptors, resulting in increased gluconeogenesis and glycogenolysis, and decreased utilization of sugar by peripheral tissues, resulting in increased blood glucose or decreased glucose tolerance. Catecholamines also promote the secretion of TSH and ACTH in the pituitary gland and increase the secretion of thyroxine and adrenocorticotropic hormone, resulting in increased basal metabolism, increased blood fluids and accelerated lipolysis, causing wasting. A small number of patients may have hypokalemia. 3, other manifestations: catecholamines can relax the gastrointestinal smooth muscle, so that the gastrointestinal demand is weakened, so it can cause constipation, sometimes very stubborn. Severe contraction and spasm of small gastrointestinal arteries can cause ischemia of gastrointestinal mucosa and occasionally necrosis and perforation. Due to the compression of adjacent organs by tumor growth, corresponding clinical manifestations may appear.