Symptomatic arterial hypertension

When arterial hypertension is detected, differential diagnostic search is required to detect symptomatic arterial hypertension. The most common causes of secondary (symptomatic) arterial hypertension are kidney diseases, renal vascular pathology, diseases of the cortex and medulla, adrenal glands, hemodynamic disorders (coarctation of the aorta), systemic vasculitis (nodular periarteritis, Takayasu's disease).

The first place among symptomatic arterial hypertensions is occupied by renal hypertension associated with congenital or acquired kidney pathology. In this case, both vasorenal and renal hypertension are possible.

Renal hypertension

The main causes of renal arterial hypertension are: glomerulonephritis, pyelonephritis, polycystic kidney disease, and renal neoplasms. The pathogenesis of symptomatic arterial hypertension in kidney diseases is due to increased activity of the renin-angiotensin-aldosterone system, impaired water-salt metabolism with suppression of the activity of the renal depressor function, and impaired production of kinins and prostaglandins.

Vasorenal hypertension

The main causes of renovascular hypertension are: malformations of the renal vessels, fibromuscular dysplasia of the renal vessels; aortoarteritis, periarteritis nodosa. Clinical markers of renovascular hypertension include the malignant nature of arterial hypertension, systolic murmur in the projection area of the renal arteries (in the abdominal cavity), asymmetry of arterial pressure in the extremities, widespread arteriospasm and neuroretinopathy. Instrumental examination to verify the diagnosis should include excretory urography, renal scintigraphy, angiography of the kidneys and renal vessels. An increase in the renin level against the background of a decrease in renal blood flow is characteristic.

Congenital renal artery stenosis is the most common cause of vaso-renal arterial hypertension in children. Characterized by high, persistent increase in blood pressure, mainly diastolic in nature, refractory to hypotensive therapy. Physically, systolic noise is often heard in the umbilical region, as well as in the epigastric region, corresponding to the site of origin of the renal artery from the abdominal aorta. Changes in target organs develop early: left ventricular hypertrophy, pronounced changes in the fundus.

Fibromuscular dysplasia of the renal arteries is a rarer cause of renovascular hypertension. It is more common in women. According to angiograms, stenosis is localized in the middle part of the renal artery. The artery has a rosary-like appearance, and the collateral network is not expressed. The main type of treatment is surgical correction of renal artery stenosis.

Panarteritis of the aorta and its branches (pulseless disease, 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 of Takayasu's disease is characterized by asymmetry or absence of pulse and arterial pressure in the radial arteries, systolic murmur over the affected arteries, damage to the aortic (insufficiency) and mitral (insufficiency) valves, myocarditis, pulmonary hypertension is possible, symptoms of circulatory failure are characteristic.

Arterial hypertension is malignant 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, decreased elasticity of the aorta, stenosis of the carotid arteries, leading to cerebral ischemia and irritation of the chemoreceptors and vasomotor centers of the medulla oblongata. Treatment tactics include the administration of glucocorticoids in combination with antiplatelet agents and active hypotensive therapy. ACE inhibitors are the most effective.

Nodular periarteritis is characterized by malignant arterial hypertension, specific skin changes in combination with abdominal and coronary pain, polyneuritis, hyperthermia, pronounced inflammatory changes in the blood. The disease is based on vasculitis of small and medium arteries, leading to damage to the renal arteries. The diagnosis is verified by skin biopsy.

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

Coarctation of the aorta occurs in 8% of patients with heart defects. The clinical picture depends on the location, degree of narrowing and development of collaterals, which causes the occurrence of a specific symptom for coarctation of the aorta - the appearance of pulsating intercostal arteries. Radiography reveals rib usurpations in the places of collaterals of the intercostal arteries. Disproportionate development of the body is often encountered: the upper part of the body is well developed, the lower part lags significantly behind. Pink coloring of the skin of the face and chest is combined with pale cold skin on the lower limbs. Blood pressure is significantly increased in the arms, while on the legs it is normal or decreased. Pulsation is often determined in the jugular fossa and in the area of the carotid arteries. An extensive network of collaterals is formed on the skin of the chest. The pulse on the upper limbs is increased, on the lower ones - weakened. A rough systolic murmur is heard over the heart area and over the collarbones, which is transmitted to the back. The main method of treatment is surgery.

Adrenal diseases

Increased blood pressure is detected in the following adrenal diseases:

• primary hyperaldosteronism;
• Cushing's syndrome;
• tumors with hyperproduction of glucocorticoids;
• congenital disorders of the process of glucocorticoid biosynthesis;
• diseases of the adrenal medulla (pheochromocytoma).

The main manifestation of primary hyperaldosteronism (Conn's syndrome) is associated with hyperproduction of aldosterone by the zona glomerulosa of the adrenal cortex. The pathogenesis of the disease is due to the following factors:

• disruption of the excretion of sodium and potassium with changes in the intracellular ratios of these ions and the development of hypokalemia and alkalosis;
• increased aldosterone levels;
• a decrease in the level of renin in the blood with subsequent activation of the pressor functions of renal prostaglandins and an increase in total peripheral vascular resistance.

The leading symptoms in the clinical picture are a combination of arterial hypertension and hypokalemia. Arterial hypertension can be either labile or stable, the malignant form is rare. Symptoms of hypokalemia are characterized by muscle weakness, transient paresis, convulsions and tetany. On the ECG, hypokalemia is manifested by smoothing of the T waves, depression of the ST segment, and the appearance of the U wave.

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

To diagnose, you need to do the following:

• Determine the levels of potassium (decreased) and sodium (increased) in plasma.
• Determine the aldosterone content in the blood and urine (sharply increased) and renin activity (decreased).
• Rule out kidney disease and renal artery stenosis.
• Conduct a drug test with furosemide in combination with walking (with aldosterone, a decrease in aldosterone is observed after a 4-hour walk against the background of low plasma renin activity).
• To verify the diagnosis, it is advisable to perform adrenal scintigraphy or apply retropneumoperitoneum with tomography for the purpose of topical diagnostics; phlebography of the adrenal glands is performed with 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 and produces a large amount of catecholamines. Pheochromocytoma accounts for 0.2-2% of all arterial hypertensions. In 90% of cases, pheochromocytoma is localized in the adrenal medulla. In 10%, extra-adrenal localization of pheochromocytoma is noted - paraganglioma in the sympathetic paraganglia along the thoracic and abdominal aorta, in the renal hilum, in the urinary bladder. Catecholamines produced in the adrenal medulla enter the blood periodically in pheochromocytoma and are significantly excreted in the urine. The pathogenesis of arterial hypertension in pheochromocytoma is associated with the release of catecholamines and subsequent vasoconstriction with an increase in OPSS. In addition to hypercatecholaminemia, increased activity of the renin-angiotensin-aldosterone system is also important in the pathogenesis of arterial hypertension. Increased activity of the latter determines the severity of the disease. The level of arterial pressure fluctuates, reaching 220 mm Hg for SBP and 120 mm Hg for DBP. At the same time, in some patients outside of crises, arterial pressure may be within normal values. Physical and emotional stress, trauma are provoking factors for the release of catecholamines.

Based on the clinical course, three forms of pheochromocytoma are distinguished.

• Asymptomatic (latent) with very rare increases in blood pressure (it should be remembered that the patient may die from the first hypertensive crisis).
• With a crisis course against the background of normal blood pressure in the interictal period.
• With mild hypertensive crises against the background of constantly elevated blood pressure.

In the case of a pheochromocytoma crisis, blood pressure increases instantly within a few seconds to a maximum of 250-300 mm Hg for SBP and to 110-130 mm Hg for DBP. Patients experience fear, are pale, have a sharp pulsating headache, dizziness, palpitations, sweating, hand tremors, nausea, vomiting, and abdominal pain. The ECG shows a violation of the repolarization process, heart rhythm disturbances, and the development of a stroke or myocardial infarction is possible. Confirmation of the diagnosis is an increase in the level of adrenaline, noradrenaline, and vanillylmandelic acid against the background of increased blood pressure.

In the presence of clinical signs of pheochromocytoma and the absence of a tumor in the adrenal medulla, according to ultrasound and CT data, it is advisable to perform thoracic and abdominal aortography. Pheochromocytomas are most difficult to diagnose when localized in the bladder; in this case, cystoscopy or pelvic phlebography is necessary.

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