Pathogenetic factors and vascular wall lesion
The development of the disease is determined by a triad of factors: chronic psychoemotional overstrain, a genetic defect in cell membranes (with impaired transport of $Ca^{2+}$ and $Na^{+}$ ions), and hereditary alterations in the renal-volemic mechanism. Lipid metabolism imbalance (elevated LDL and VLDL with decreased HDL) additionally accelerates atherosclerotic processes.
The morphogenesis of hypertensive macroangiopathy in the aorta, large, and medium-sized arteries includes successive phases:
- Hyperelastosis — initial thickening of the elastic framework;
- Elastofibrosis — proliferation of connective tissue;
- Endothelial injury with the development of arteriosclerosis.
Circular fibrous plaques severely narrow the lumen of the aorta, coronary, carotid, renal, and cerebral arteries. The stiffening of the walls leads to the destruction of baroreceptors, which closes the "vicious circle" of blood pressure stabilization at a high level.
Stages of morphogenesis of the benign form
The benign course of the disease is divided into three clinico-morphological stages:
- Transitory (preclinical) — characterized by functional vascular spasm without marked organic changes.
- Vascular — accompanied by progressive arteriolosclerosis (hyalinosis) and atherosclerosis of muscular-elastic and elastic type arteries.
- Organ — leads to secondary organ remodeling due to impaired intraorgan blood flow.
Cardiac changes
In response to the load, left ventricular myocardial hypertrophy develops along with a sharp increase in organ weight up to 900–1000 g (the term cor bovinum — "bovine heart"). The wall thickness reaches 2–3 cm. Subsequently, hypoxia and cardiomyocyte dystrophy cause diffuse finely focal cardiosclerosis, culminating in myogenic dilation of the cavities (eccentric hypertrophy).
Organ pathology and acute complications
Chronic blood flow disturbances cause atrophic and sclerotic changes in target organs:
- Arteriolosclerotic nephrosclerosis: Hyalinosis of afferent arterioles and glomeruli develops, along with tubular atrophy and renal stromal sclerosis. The organ shrinks, and its surface becomes finely granular. The process is always bilateral and results in a primary contracted kidney (arteriolosclerotic nephrocirrhosis) with progression to chronic renal failure.
- Hypertensive retinopathy: Characterized by hyalinosis of retinal vessels, optic disc edema ("choked disc"), focal detachment, and hemorrhages.
Acute lesions occur during hypertensive crises against the background of spasm, thrombosis, or vascular wall necrosis. The most frequent causes of death are acute myocardial infarction, stroke, acute renal failure, and aortic dissection.
Features of malignant hypertension
The malignant variant of the course is not a separate nosology, but represents an extremely aggressive form of the disease. It most commonly affects men aged 30–50 years and is accompanied by a sharp rise in blood pressure (up to 220/140 mmHg).
- Main morphological criterion: Fibrinoid necrosis of arterioles.
- Vascular changes: Development of microaneurysms and their subsequent ruptures.
- Dynamics: Rapid progression with frequent hypertensive crises and rapidly progressive organ failure.
Briefly: answers to topical questions
What clinico-morphological forms are distinguished in the organ stage of hypertension?
Depending on the predominant target organ involvement, three clinico-morphological forms of hypertension are distinguished.
- Cardiac form — constitutes the essence of ischemic heart disease (left ventricular hypertrophy, cardiosclerosis, myocardial infarction).
- Cerebral form — forms the basis of cerebrovascular diseases (hemorrhages, cerebral infarctions, hypertensive encephalopathy).
- Renal form — characterized by acute changes (infarctions) and chronic changes (arteriolosclerotic nephrosclerosis progressing to chronic renal failure).
What microscopic changes in cardiomyocytes are observed in compensatory myocardial hypertrophy?
In compensatory myocardial hypertrophy, an increase in cardiomyocyte size is observed due to the hyperplasia of intracellular ultrastructures. Microscopic examination reveals the following changes:
- Cardiomyocyte nuclei — enlarged, hyperchromatic (intensely stained), with an increase in their area and polyploidization.
- Cytoplasm — increases in volume due to the accumulation of myofibrils and mitochondria.
- Organelles — hyperplasia of mitochondria and myofilaments occurs, along with an increased number of ribosomes.
An increased mass of the organ's stroma is also determined microscopically.
Which cerebral arteries most commonly serve as the source of massive hemorrhage during a hypertensive crisis?
The source of intracerebral hemorrhage in hypertension is most frequently small perforating arteries.
- Lenticulostriate artery — ruptures most frequently (usually in the region of its bend).
- Cortico-medullary arteries — supplying the deep regions of the brain.
The mechanism of rupture is related to the fact that elevated blood pressure damages the walls of small arteries, leading to the formation of microaneurysms (Charcot-Bouchard aneurysms), which spontaneously rupture.
Remember the triad of renal involvement in hypertension: Arteriolosclerosis (hyalinosis) $\rightarrow$ Finely granular surface $\rightarrow$ Primary contracted kidney (cor bovinum develops in the heart instead!).
Class and exam questions
What does the term "cor bovinum" mean in pathological anatomy?
This is marked myocardial hypertrophy in hypertension, where the heart mass reaches 900–1000 g and the left ventricular wall thickness reaches 2–3 cm (cor bovinum).
What are the macroscopic signs of a primary contracted kidney?
The kidneys are symmetrically reduced in size, firm, and their surface acquires a finely granular appearance due to depressed areas of sclerosis and nephron atrophy.
How does the malignant form differ morphologically from the benign form?
The main morphological sign of the malignant form is fibrinoid necrosis of arteriole walls and the formation of microaneurysms, whereas the benign form is characterized by hyalinosis.
What three stages are distinguished in the morphogenesis of benign hypertension?
The disease sequentially passes through transitory (preclinical), vascular, and organ stages.
What else to study on this topic
- Fibrinoid necrosis of arterioles and its consequences in malignant hypertension
- Microscopic changes in renal glomeruli and tubules in hyalinosis
- The role of ion pump dysfunction ($Ca^{2+}, Na^{+}$) in cell membrane injury
- Pathomorphology of fundus changes and optic disc edema
- Mechanisms of transition from concentric to eccentric myocardial hypertrophy
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