Symptomatic arterial hypertension

In the detection of hypertension, a differential-diagnostic search is required to detect symptomatic arterial hypertension. The most common causes of secondary (symptomatic) arterial hypertension are kidney diseases, renal vessel pathologies, diseases of the cortex and medulla, adrenal glands, hemodynamic disorders (coarctation of the aorta), systemic vasculitis (nodular periarteritis, Takayasu disease).

The first place among symptomatic arterial hypertension is renal hypertension associated with congenital or acquired kidney pathology. In this case, both the vasorenal and renal nature of hypertension is possible.

Renal Hypertension

The main causes of renal arterial hypertension: glomerulonephritis, pyelonephritis, polycystic kidney, kidney neoplasms. The pathogenesis of symptomatic arterial hypertension in renal diseases is caused by an increase in the activity of the renin-angiotensin-aldosterone system, a violation of water-salt metabolism with suppression of the activity of the depressor function of the kidneys, a violation of the production of kinins and prostaglandins.

Vasorenal hypertension

The main causes of vasorenal hypertension: malformations of renal vessels, fibromuscular dysplasia of renal vessels; aortoarteriitis, nodular periarteritis. Clinical markers of vasorenal hypertension are the malignant nature of arterial hypertension, systolic noise in the area of the projection of the renal arteries (in the abdominal cavity), asymmetry of arterial pressure on the limbs, widespread arteriospasm and neuroretinopathy. Instrumental research to verify the diagnosis should include excretory urography, kidney scintigraphy, angiography of the kidneys and kidney vessels. Characteristic increase in the level of renin against a background of decreased renal blood flow.

Congenital stenosis of the renal arteries is the most common cause of vaso-renal arterial hypertension in children. Characteristically high, persistent increase in blood pressure. Mainly diastolic, refractory to ongoing antihypertensive therapy. Physically, they often listen to systolic murmur in the navel, as well as in the epigastric region corresponding to the site of the renal artery from the abdominal aorta. Early changes in the target organs: hypertrophy of the left ventricle, marked changes in the fundus.

Fibromuscular dysplasia of the renal arteries is a more rare cause of vasorenal hypertension. More common in women. According to the angiogram, stenosis is localized in the middle part of the renal artery. The artery looks like a rosary, the collateral network is not pronounced. The main type of treatment is surgical correction of stenosis of the renal arteries.

The panarteritis of the aorta and its branches (a disease of lack of pulse, or Takayasu's disease) is a relatively rare pathology in children. Clinical manifestations of the disease are characterized by pronounced polymorphism. At the initial stage of the disease, general inflammatory symptoms predominate - fever, myalgia, arthralgia, erythema nodosum. These changes correspond to the initial stage of vascular inflammation. Further clinical manifestations are associated with the development of stenosis of the arteries, followed by ischemia of the corresponding organ. The clinical picture in Takayasu's disease is characterized by asymmetry or lack of pulse and arterial pressure on the radial arteries, systolic murmur over the affected arteries, aortic (insufficiency) and mitral (insufficiency) valve damage, myocarditis, pulmonary hypertension is possible, and symptoms of circulatory insufficiency.

Arterial hypertension has a malignant character and is associated with stenotic and thrombotic occlusion of the renal arteries, aortic regurgitation with damage to the baroreceptors of the carotid and aortic sinuses, aortic elasticity, stenosis of the carotid arteries leading to cerebral ischemia and irritation of chemoreceptors and vasomotor centers of the medulla oblongata. Therapeutic tactics consists in the appointment of glucocorticoids in combination with antiaggregants and active antihypertensive therapy. The most effective are ACE inhibitors.

Nodular periarteritis is characterized by malignant arterial hypertension, specific skin changes in combination with abdominal and coronary pains, polyneuritis, hyperthermia, marked inflammatory changes in the blood. At the heart of the disease lies vasculitis of small and medium arteries, leading to the defeat of the renal arteries. The diagnosis is verified using a skin biopsy.

Treatment includes a combination of anti-inflammatory, antihypertensive drugs (ACE inhibitors) and disaggregants.

Coarctation of the aorta occurs in 8% of patients with heart defects. The clinical picture depends on the site, degree of narrowing and development of collaterals, which causes the appearance of a specific symptom for coarctation of the aorta - the appearance of pulsating intercostal arteries. When radiography reveals the use of ribs in the areas of collateral intercostal arteries. Often there is a disproportional development of the body: the upper part of the body is well developed, the lower one lags considerably behind. Pink coloring of the skin of the face and chest is combined with pale cold skin on the lower limbs. Arterial pressure is significantly increased on the hands, while on the legs it is normal or decreased. Often determine pulsation in the fossa and in the field of carotid arteries. On the skin of the chest, an extensive network of collaterals is formed. The pulse on the upper limbs is strengthened, on the lower limbs is weakened. A rough systolic murmur over the area of the heart and above the clavicles, which is carried on the back, is heard. The main method of treatment is surgical.

Diseases of the adrenal glands

The increase in blood pressure is detected with the following adrenal gland diseases:

• primary hyperaldosteronism;
• Cushing's syndrome;
• tumors with hyperproduction of glucocorticoids;
• congenital disturbances in the process of biosynthesis of glucocorticoids;
• disease of the adrenal medulla (pheochromocytoma).

The main manifestation of primary hyperaldosteronism (Conn's syndrome) is associated with hyperproduction of aldosterone by the glomerular zone of the adrenal cortex. The pathogenesis of the disease is caused by the following factors:

• a violation of the excretion of sodium and potassium with a change in the intracellular relationships of these ions and the development of hypokalemia and alkalosis;
• increased aldosterone levels;
• a decrease in the level of renin in the blood, followed by activation of the pressor functions of the kidney prostaglandins and an increase in OPSS.

Leading symptoms in the clinical picture - a combination of hypertension and hypokalemia. Arterial hypertension can be both labile and stable, malignant form is rare. Symptoms of hypokalemia are characterized by muscle weakness, transitory paresis, convulsions and tetany. On the ECG, hypokalemia is manifested by the smoothness of the T-wave, ST-segment depression. The appearance of the U wave.

Excessive secretion of aldosterone leads to disruption of the transport of electrolytes in the kidneys with the development of hypokalemic tubulopathy. This causes polyuria, nocturia and hypoisostenuria.

For diagnostics, you must perform the following actions.

• Determine the levels of potassium (reduced) and sodium (elevated) in plasma.
• Determine the content of aldosterone in the blood and urine (increased sharply) and the activity of renin (reduced).
• Eliminate kidney disease and stenosis of the renal artery.
• To carry out a medicinal test with furosemide in conjunction with walking (with aldosterome, a decrease in aldosterone after 4 hours walking against low plasma renin activity is observed).
• To verify the diagnosis, it is advisable to perform adrenal scintigraphy or superimpneoperitoneum with tomography for the purpose of topical diagnosis; conduct adrenal phlebography with a separate determination of renin activity and aldosterone levels in the right and left veins.

Treatment of primary hyperaldosteronism is surgical.

Pheochromocytoma is a benign tumor of the adrenal medulla. It consists of chromaffin cells, which produces a large number of catecholamines. On the share of pheochromocytoma account for 0.2-2% of all arterial hypertension. In 90% of cases, pheochromocytoma is localized in the adrenal medulla. In 10%, there is an intra-adrenal localization of pheochromocytoma - paraganglioma in sympathetic paraganglia along the thoracic and abdominal aorta, in the gates of the kidneys, in the bladder. Catecholamines, produced in the adrenal medulla, enter the blood periodically with pheochromocytoma and are significantly excreted in the urine. The pathogenesis of arterial hypertension in pheochromocytoma is associated with the ejection of catecholamines and subsequent vasoconstriction with an increase in OPSS. In addition to hyperkatecholamineemia, the increase in activity of the renin-angiotesin-aldosterone system is also important in the pathogenesis of hypertension. The increased activity of the latter also determines the severity of the course of the disease. The level of blood pressure fluctuates, reaching 220 mm Hg. For SBP and 120 mmHg. For DBP. At the same time, in some patients outside of crises, blood pressure may be within the limits of normal values. The provoking factors of ejection of catecholamines are physical and emotional overstrain, trauma.

According to the clinical course, three forms of pheochromocytoma are distinguished.

• Asymptomatic (latent) with very rare increases in blood pressure (remember that the patient may die from the first hypertensive crisis).
• With a crisis current against the background of normal arterial pressure during the interictal period.
• With non-severe hypertensive crises against the background of constantly high blood pressure.

In the course of the feohromocytoma, the blood pressure rises instantaneously within a few seconds to a maximum of 250-300 mm Hg. For SBP, and up to 110-130 mm Hg. For DBP. Patients experience a sense of fear, pale, feel a sharp headache of a pulsating nature, dizziness, palpitations, sweating, tremors of hands, nausea, vomiting, abdominal pain. On the ECG, there is a violation of the repolarization process, a violation of the heart rhythm, possibly the development of a stroke, myocardial infarction. Confirmation of the diagnosis - an increase in the level of adrenaline, norepinephrine, vanillmindalic acid against the background of increased blood pressure.

In the presence of clinical signs of pheochromocytoma and the absence of a tumor in the medulla of the adrenal gland, according to ultrasound and CT, it is advisable to carry out thoracic and abdominal aortography. The most difficult to diagnose pheochromocytomas when localized in the bladder, in which case cystoscopy or pelvic phlebography is necessary.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10], [11], [12]