Catecholamine hypersecretion, also known as pheochromocytoma, originates in the adrenal medulla, sympathetic ganglion, parasympathetic ganglion (paraganglia) or other sites of chromophobic tissue. Due to the paroxysmal or persistent secretion of norepinephrine and epinephrine by the tumor cells, the clinical picture is one of paroxysmal or persistent hypertension, headache, sweating, palpitations and metabolic disorders. If treated early, it can be cured. Etiology of catecholamine hypersecretion: The age of onset of pheochromocytoma is 20-40 years old, and there is no difference in the incidence between men and women. Single tumors in the adrenal glands account for 60% to 80% of cases, while bilateral adrenal glands and multiple tumors account for about 10% each. The occurrence of pheochromocytoma is directly related to the growth and development of neural crest cells during the embryonic period, and may also be related to genetic factors. Multiple endocrine adenomas predispose to a variety of endocrine tumors such as thyroid, parathyroid or adrenal. There is also a proportion of cases associated with von Winkling’s disease, which presents with abnormal vascular growth and the formation of benign tumors (hemangiomas), and with von Recklinghausen’s disease, in which the tumor grows on a nerve. The pathology of catecholamine overproduction: Pheochromocytomas are mostly benign, round or ovoid, with intact envelope, tumor size varies, average around lOOg, heaviest up to 3800g. tumor cut surface pink or grayish white, may have hemorrhage, necrosis, cystic change and calcification. The tumor cells are polygonal in shape, varying in size, a few are spindle-shaped or columnar, with closely packed cells and abundant cytoplasm in a granular pattern. The nuclei were large, round, with obvious nucleoli and mostly heterogeneous nuclei. After fixed by chromate staining. There were brown or yellow granules in the cytoplasm of the tumor cells. Electron microscopy showed abundant organelles and neurosecretory granules in the cytoplasm, and the granule morphology was similar to that secreted by normal adrenal medullary cells. The diagnosis of malignant pheochromocytoma cannot be identified as benign or malignant based on pathomorphology. The diagnosis of malignant pheochromocytoma is based on extensive infiltration of the tumor into adjacent tissues and organs, especially metastases found in normal, chromophobic tissues or organs without chromophobic tissue. The pathophysiological changes of pheochromocytoma are mainly caused by the secretion of large amounts of catecholamines by the tumor. Under physiological conditions, catecholamines exert their physiological effects by binding to adrenergic receptors on the membranes of effector cells. Catecholamines are bound to ATP chromogranin and stored in chromophores and are released by diffusion and membrane fission secretion. Adrenergic receptors are divided into two classes, a and β, both of which can be divided into two subtypes. Epinephrine mainly excites beta receptors, causing increased heart rate, vasodilation and increased systolic blood pressure. Norepinephrine mainly excites alpha receptors, causing systemic vasoconstriction, increased peripheral resistance, elevated blood pressure, and enhanced myocardial contraction. Regarding the treatment of pheochromocytoma, patients with this disease need to be given intravenous phentolamine immediately when hypertensive crisis occurs, the first dose of Halo is first 1mg to avoid hypotensive shock due to the patient’s abnormal sensitivity to phentolamine, then 2-5mg is given intravenously every 5 minutes until the blood pressure is satisfactorily controlled, then phentolamine is given intravenously to maintain blood pressure stability; or the first dose of phentolamine can be given followed by continuous intravenous drip to control blood pressure.