139. Symptomatic arterial hypertension: causes, mechanisms of development, complications, causes of death in patients.

Symptomatic hypertension - appears a second time in diseases of the nervous and endocrine systems, pathology of the kidneys and blood vessels. Symptomatic hypertension leads to: 1) Central – injuries, tumors, encephalitis, polio of the brain stem.

2) Endocrine tumors (basophilic pituitary adenoma, pheochromocytoma, adrenal aldosteroma, paraganglioma), menopausal

3) Renal – glomerulonephritis, tubulopathy, pyelonephritis, diabetic nephropathy, amyloidosis, polycystic

4) Vascular – atherosclerosis of the aorta, coarctation of the aortic mouth, vasculitis. Pathogenesis - Depletion of the centers of vascular regulation with the involvement of reflex and humoral factors in the process - Off of the depressant effects of the carotid sinus and aortic arch, act of simp HC - Hyperplasia of the pituitary gland, act of the renin-hypertensive system - Renal factor (Vasoconstrictor hypertension - with high plasma renin; Hypervolemic - with reduced renin act (increased BCC) - Hereditary factors

Classification:

Complications and causes of death in hypertension:

140. Changes in the brain in arterial hypertension and related complications.

Cerebrovascular diseases are acute disorders of cerebral circulation against the background of atherosclerosis and hypertension.

Acute cerebrovascular accident, which is the basis of cerebrovascular disease, is divided into transient cerebral ischemia and stroke. Stroke is an acute (sudden) local disorder of cerebral circulation, accompanied by damage to the substance of the brain and a violation of its function. There are hemorrhagic and ischemic strokes. Hemorrhagic stroke is a hematoma or hemorrhagic impregnation of brain matter, it also includes subarachnoid hemorrhage. The morphological expression of an ischemic stroke is a heart attack.

The morphology of transient cerebral ischemia is represented by vascular disorders (spasm of arterioles, plasma impregnation of their walls, perivascular edema and small single hemorrhages) and focal changes in brain tissue (edema, dystrophic changes in cell groups). These changes are reversible; perivascular deposits of hemosiderin are determined at the site of small hemorrhages.

When a brain hematoma is formed, which occurs in 85% of those who die from hemorrhagic stroke, there is a pronounced alteration of the walls of arterioles and small arteries with the formation of microaneurysms and rupture of their walls. At the site of the hemorrhage, the brain tissue is destroyed with the formation of a cavity filled with blood clots and detritus of brain tissue. A stroke with a breakthrough into the ventricles of the brain ends in death. In patients who have suffered from a cerebral form of hypertension for a long time and died of a stroke, along with fresh hemorrhages, cysts are often found as a result of hemorrhages.

Ischemic cerebral infarction is the most common (75%) manifestation of ischemic stroke, it is formed with thrombosis of atherosclerotically altered precerebral or cerebral arteries, and has a diverse localization. An ischemic heart attack looks like a focus of gray softening of the brain. Microscopic examination of necrotic masses can reveal dead neurons.

Hemorrhagic cerebral infarction looks like a focus of hemorrhagic impregnation, but the mechanism of its development is different. Ischemia of brain tissue develops primarily, and hemorrhages into ischemic tissue develop secondarily.

In mixed infarction, which occurs in the gray matter of the brain, areas of both ischemic and hemorrhagic infarction are found.

A complication of stroke (hemorrhages and cerebral infarction), as well as its consequences — paralysis. Cerebral stroke is a common cause of death in patients with atherosclerosis and hypertension.