Many diseases of the adrenal cortex are accompanied by high blood pressure. In the case of primary hyperaldosteronism (in the presence of a tumor or bilateral hyperplasia of the adrenal cortex), high blood pressure is caused by sodium retention. With sodium retention, aldosterone in the renal tubules enables its exchange for potassium: that’s why hypokalemia is characteristic for primary hyperaldosteronism. The examination of those patients should begin with the determination of blood potassium.
Diagnosis is largely based on the fact that constantly increased blood volume and sodium retention inhibit renin secretion. In normal conditions, plasma renin activity is at the level defined by aldosterone in plasma and urine, but with primary hyperaldosteronism, levels of aldosterone are high due to uncontrolled secretion, and renin activity is reduced, increasing as sodium in blood decreases.
Sodium retention with excessive glucocorticoids leads to an increase in blood pressure with severe Cushing's syndrome. In this disease, mineralocorticoid hyperproduction is also possible. Many scientists believe that it’s based on angiotensinogen hyperproduction secondary to glucocorticoids. At the same time, hyporenin arterial hypertension occurs.
In the presence of pheochromocytoma, adrenaline and noradrenaline secretion in a tumor located in the medulla of the adrenal glands leads to excessive stimulation of adrenoreceptors, increasing total peripheral vascular resistance, myocardial contractility, higher heart rate, and a sharp increase in blood pressure.
Hypertension occurs in almost a third of patients diagnosed as suffering from hyperparathyroidism. This is caused by a lesion of renal parenchyma due to the formation of stones in it. In this case, hypercalcemia can have a direct vasoconstrictive effect. After its surgical removal, blood pressure returns to normal and does not require additional treatment. Thus, hypercalcemia secondary to hyperparathyroidism causes arterial hypertension and a strong hypotensive effect from calcium antagonists.
Some 20 years ago, estrogens as ingredients of oral contraceptives were the common cause of endocrine hypertension. Recent studies have shown that the risk of developing hypertension when taking modern oral contraceptives is not that high, because their estrogen content is significantly lower than it was 20-30 years ago.
If blood pressure rises, it is definitely caused by activation of renin-angiotensin system (RAS). Estrogens stimulate the synthesis of angiotensinogen (renin substrate) in the liver and enable the hyperproduction of angiotensin II and secondary hyperaldosteronism.
Some women taking oral contraceptives have increased levels of angiotensin II and aldosterone and slightly increased blood pressure, but only in some cases it’s more than 140/90 mmHg, and in half the cases it returns to normal within 6 months after discontinuing the use of contraceptives. It remains completely unknown, however, why some women’s blood pressure rises, while others don’t. Many researchers believe that contraceptives only affect (increasing) blood pressure, but that they’re not its cause.
Increased blood pressure can be caused by coarctation itself, or by concomitant renal ischemia with progression of an unusual form of renovascular hypertension. Diagnosis is made by a physical examination and a chest X-ray.
Damage on target organs
The most common cause of death in the presence of hypertension is heart damage, followed by stroke and renal failure.
Effects on the heart
At the very beginning of the disease, the left ventricle handles high loads due to the uniform thickening (hypertrophy) of its walls. Over time, its contractility begins to decrease, it expands, and signs of heart failure appear. Angina attacks begin to appear as coronary atherosclerosis progresses, and hypertrophied myocardium has increased oxygen demand.
Signs of left ventricular hypertrophy can be seen on the ECG. In later stages of the disease, myocardial infarction is common, which finally leads to the death of most patients. Some of them die from progressive heart failure which is not responsive to medical treatment.
Effect on fundus
Arteries and arterioles can be examined only in the area of the fundus. For monitoring their condition, patients with hypertension need regular ophthalmoscopies. Signs of disease progression include an increase in total arteriole contraction, local narrowing, hemorrhage, exudates, and swelling of the optic nerve head. These changes often lead to blurred vision and sometimes blindness, especially with swelling of the optic nerve head and hemorrhage in the area of the macula.
Hypertensive retinopathy occurs acutely and resolves quickly if blood pressure is lowered with drugs. Arteriosclerotic retinopathy develops more slowly but is almost impossible to treat. It’s caused by proliferation of the endothelium and smooth muscle cells.
The same as in the fundus occurs in all vessels. At the point of intersection with them, sclerotic arteries with thickened walls bend and squeeze the veins.
Effect on the CNS
Hypertension often leads to damage of central nervous system (CNS). One of the early symptoms of high blood pressure is a headache in the back of the head, usually in the morning. Dizziness, nausea, tinnitus, feeling sick are possible. Blurred vision and fainting have been reported, and in more severe cases, stroke and hypertensive encephalopathy.
There are 2 types of stroke: ischemic – caused by atherosclerosis progression, and hemorrhagic – caused by high blood pressure and microaneurysms of the cerebral vessels. The process of microaneurysm formation in the brain depends only on age and blood pressure, that’s why the higher these are, the higher the risk is of hemorrhagic stroke. Ischemic stroke and myocardial infarction have no clear connection with blood pressure.
Hypertensive encephalopathy is characterized by high blood pressure with impaired consciousness, swelling of the optic nerve head, and seizures. Focal neurological symptoms are not characteristic.
Effect on the kidneys
Among the causes of death from arterial hypertension, renal failure accounts for about 10%. For such patients, sclerosis of the afferent and efferent arterioles and glomerular capillaries is characteristic which leads to a reduction of glomerular filtration rate and impaired tubular transport. Glomerular damage causes proteinuria and microhematuria.
The cause of increased pressure is rarely determined (only in 5% of cases), but it must be found out. First of all, ruling out the cause can sometimes help to cure the disease. Secondly, research of symptomatic hypertension gives new information on its etiology. In the vast majority of cases, the determined cause is associated with either endocrine or renal pathologies.
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