Primary (essential) hypertension

The cause of this hypertension is unknown. But there are a lot of factors are related to its development. There are as under:

1) genetic factors — the evidences in support are the familial aggregation;

2) racial and environmental factors — surveys in the US have revealed higher incidence of primary hypertension in blacks than in whites.

A number of environmental factors have been implicated in the development of this type of hypertension including salt intake, obesity, skilled occupation, higher living standards and patients in high stress.

There are some factors modifying the course of essential hypertension:

a) age — younger the age at which hypertension is first noted but left untreated, lower the life expectancy;

b) sex—females tolerate hypertension better than males;

c) atherosclerosis — as a rule, accompanies essential hypertension.

The pathogenetic mechanism are:

1) high plasma level of catecholamines;

2) increase in blood volume, i.e. arterial overfilling (volume hypertension) and arteriolar constriction (vasoconstrictor hypertension);

3) increased cardiac output;

4) low-renin essential hypertension found in approximately 20% patients due to decreased responsiveness to renin release;

5) high renin essential hypertension due to decreased adrenal responsiveness to angiotensin 2.

Morphology. The morphological effects of systemic hypertension are manifested as lesions in the heart, peripheral vessels, kidneys and brain.

Accordingly it we distinguish several clinical and morphological types of essential hypertension. There are: 1) cardio-vascular, 2) renal, 3) cerebral.

Hypertensive heart disease is an important and common form of heart disease in all worlds. Macroscopically, the most significant finding is marked hypertrophy of the heart, especially of the left ventricle. The weight of the heart increases to 500— 700 gm (may be 1000 gr) (normal weight is about 300 gr). The weight of the heart is directly related to the severity of hypertension but there is no correlation between the weight of the heart and duration of hypertension. The left ventricular wall is thickened (up to 20 mm or more), the papillary muscles are rounded and prominent, and the cardiac chamber is small (concentric hypertrophy). However, when decompensation and cardiac failure develop, there is eccentric hypertrophy with thinning of the ventricular wall and dilation of the left ventricular and atrial cavities. There may be dilation and hypertrophy of right heart as well.

Changes in the blood vessels involve arterioles and arteries. There are 2 types of these changes:

a) hyaline arteriolosclerosis that results in homogeneous and eosinophilic thickening of the wall of small blood vessels,

b) intimal thickening due to proliferation of smooth muscle cells in the intima.

In the large blood vessels atherosclerosis usually develops.

Renal type of hypertension may be benign and malignant. Benign nephrosclerosis is the term used to describe the kidney of benign phase of hypertension. Macroscopically, both kidneys are affected equally and are reduced in size and weight, often weighing about 100 gm or less. The capsule is often adherent to the cortical surface. The surface of the kidney is finely granular and shows V-shaped areas of scarring («small contracted kidney»). The cut surface shows firm kidney and narrowed cortex. Microscopically there are primarily diffuse vascular changes, which produce parenchymal changes secondarily as a result of ischaemia. Parenchymal changes. There is variable degree of atrophy of parenchyma. These include glomerular shrinkage, deposition of collagen in Bowman's space, periglomerular fibrosis. Clinical features is variable: elevation of the blood pressure with headache, dizziness, palpitation. Renal failure and uremia may occur.

Cerebrovascular diseases (cerebral type).

Hypertension can result in two main types of parenchymal diseases of the brain:

1) ischemic brain damage (hypoxic encephalopathy and cerebral infarction);

2) intracranial hemorrhage (intracerebral and subarachnoid hemorrhage).

The pathologic appearance of the brain in hypoxic encephalopathy varies depending on the duration and severity of hypoxic episode and the length of survival. Macroscopically, there is focal softening. The area supplied by distal branches of the cerebral arteries suffers from the most severe ischemic damage and may develop border zone or watershed infarcts in the adjacent zones between the territories supplied by major arteries. Microscopically, the nerve cells die and disappear and are replaced by reactive fibrillary glia.

Cerebral infarction is a localized area of tissue necrosis caused by local vascular occlusion. Clinically, the signs and symptoms associated with cerebral infarction depend on the region infracted. Cerebral infarcts may be anemic or hemorrhagic.

Macroscopically, an anemic infarct becomes evident 6—12 hours after its occurrence. The affected area is soft and swollen and there is blurry of junction between grey and white matter. Within 2—3 days, the infarct undergoes softening and disintegration. A hemorrhagic infarct is red and superficially resembles a hematoma. It is usually the result of

fragmentation of occlusive arterial emboli or venous thrombosis. Hemorrhage into the brain of patient with hypertension, is intracerebral hemorrhage, which is usually of hypertensive origin.

Most hypertensives over middle age have microaneurism in very small cerebral arteries in the brain tissue. The common sites of hypertensive intracerebral hemorrhage are the region of the basal ganglia, pons and cerebella's cortex. About 40% of patients die during the first 3—4 days of hemorrhage, mostly from hemorrhage into the ventricles. The outcome of intracerebral hemorrhage is cyst formation.

The causes of death among hypertensive patients were the following:

• congestive heart failure;

• coronary artery disease;

• cerebrovascular accidents;

• uremia;

• causes unrelated to hypertension. The cardiac complications therefore account for 36% of the death.

Secondary hypertensionmay be classified as follows:

1. Renal:

a) vascular diseases (atherosclerosis, arteritis, mechanical obstruction attributable to thrombosis, embolism, tumors);

b) parenchymal renal diseases (glomerulonephritis, pyelonephritis, hydronephrosis, amyloidosis, tumors);

c) perinephric diseases (perinephritis, tumors, hematoma).

2. Cerebral:

a) increased intracranial pressure (trauma, inflammation, tumors);

b) anxiety states;

c) lesions of brainstem (poliomyelitis).

3. Cardiovascular: coarctation of aorta (aorta has narrow).

4. Endocrine:

a) pheochromocytoma;

b) adrenocortical adenomas;

c) pituitary adenomas;

d) hyperthyroidism.

5. Preeclampsia and eclampsia.

If these causes of secondary hypertension are eliminated, hypertension disease can cured.