Hypertrophy

Mechanisms and morphological basis

The increase in the volume of any organ is always based on hyperplasia, an increase in the number of structural elements. Depending on the anatomical characteristics of the tissue, this process can occur primarily through the reproduction of the cells themselves or through an increase in the number of intracellular structures (or a combination thereof).

Pronounced biochemical shifts occur at the subcellular level:

• Proteins are intensively synthesized, which increases the number of fibrous structures.
• The concentration of RNA increases in the cytoplasm, and DNA in the nuclei.
• The activity of enzymes in the oxidation-reduction cycle increases.

Organelles are forced to adapt to high energy demands. For example, mitochondria can fuse with each other, forming giant shapes with an increased number of cristae.

Physiological and compensatory hypertrophy

Depending on the conditions of development, the process is divided into two large groups: adaptive (under healthy conditions) and compensatory (in diseases).

• Physiological (working) hypertrophy occurs in completely healthy individuals as an adequate response to increased function. A classic example is the increase in skeletal muscle and myocardial mass in professional athletes. The function of the organ remains within the limits of homeostasis.
• Compensatory hypertrophy develops in pathologies. Its main goal is to compensate for the lost functions of a damaged organ. It is important to note that the expanding tissue itself is not affected by the pathological process. A typical example is myocardial thickening in arterial hypertension.

Types of hypertrophy in diseases

If an organ or its part is damaged, the body tries to compensate for the loss of function. Depending on the nature of the damage, several types of compensation are distinguished:

1. Regenerational. Triggered in the surviving areas of a damaged organ. For example, the muscular tissue of the heart increases around the scar after myocardial infarction (large-focal cardiosclerosis), and the healthy kidney tissue proliferates in nephrosclerosis.
2. Vicarious (replacement). Characteristic exclusively for paired organs. If one organ dies or is surgically removed, the remaining one takes on a double load and increases in size.
3. Idiopathic. Occurs for unclear reasons and is often hereditary and familial in nature (e.g., hypertrophic cardiomyopathy).

Pathological hypertrophy

Unlike compensatory hypertrophy, true pathological hypertrophy has no adaptive meaning. It does not restore lost function, but often distorts it, serving as a direct symptom of disease that requires treatment.

Pathological forms include:

• Neurohumoral. Associated with impaired neuroendocrine gland function. A striking example is acromegaly, in which pituitary and hypothalamic damage leads to enlargement of facial bones, hands, feet, and internal organs (splanchnomegaly).
• Hormonal. Occurs during endocrine disruptions. This includes glandular endometrial hyperplasia in ovarian dysfunction, gynecomastia in men, and prostatic hypertrophy in elderly individuals.
• Hypertrophic growths. Formed in zones of prolonged chronic inflammation or lymphatic circulation disorders (e.g., elephantiasis of the lower extremities).
• False (Pseudohypertrophia). The organ visually increases in size, but not at the expense of working cells. This occurs when adipose tissue and connective tissue proliferate in place of the atrophying functional parenchyma.

Class and exam questions

What else to study on this topic

• Microscopic picture of hypertrophied myocardium
• Pathomorphology of glandular-cystic endometrial hyperplasia
• Mechanisms of giant mitochondria formation
• Clinical manifestations of splanchnomegaly in acromegaly
• Differences between true hypertrophy and false hypertrophy (Pseudohypertrophia)

Other topics in the section "Compensatory and Adaptive Processes"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.