Hypotrophy: Definition, Different Types and Causes of Atrophy in Organs

The term implies that the atrophied part was of a standard size for the individual, considering the age and the circumstances, before the decline.

Hypotrophy or atrophy decreases the size of a part of the body, cell, organ, or other tissue.

In the atrophy of an organ or part of the body, there may be a reduction in the number or size of the component cells.

An example of atrophy is the progressive loss of bone that occurs in osteoporosis.

Specific cells and organs normally atrophy at certain ages or under certain physiological circumstances. For example, in the human embryo, several structures are transitory and have already atrophied at birth.

The adrenal glands become smaller shortly after birth because an inner layer of the cerebral cortex has shrunk. The thymus and other lymphoid tissues atrophy in adolescence.

The pineal gland tends to atrophy around puberty; Calcium deposits or concretions generally form in atrophic tissue.

 

The generalized atrophy of many tissues that accompanies old age, while universal, is influenced by changes in nutrition and blood supply during the active life of maturity.

The average cyclical changes of the female reproductive organs are accompanied by physiological atrophy of portions of these organs.

During the menstrual cycle, the ovary’s corpus luteum atrophies if pregnancy has not occurred.

The muscles of the uterus, which are enlarged during pregnancy, rapidly atrophy after delivery of the child, and after lactation is completed, the acinar milk-producing structures of the breast decrease in size.

After menopause, the ovaries, uterus, and breasts typically undergo atrophic change.

Hypotrophy of the whole body

Hypotrophy, in general, is related to changes in nutrition and the metabolic activity of cells and tissues.

A generalized hypotrophy or generalized atrophy of body tissues occurs under starvation conditions, either because there is no food available or because it cannot be taken and absorbed due to the presence of a disease.

The lack of availability of specific essential protein and vitamin components disrupts metabolic processes and leads to the atrophy of cells and tissues.

Under conditions of protein starvation, the body’s protein is broken down into constituent amino acids, which provide energy and help maintain the structure and cells of the essential organs.

The brain, heart, adrenal glands, thyroid gland, pituitary gland, gonads, and kidneys show less atrophy than the whole body.

This while the body’s fat reserves, liver, spleen, and lymphoid tissues decrease relatively more than the body as a whole.

The brain, heart, and kidneys, organs with abundant blood supply, seem to be the least subject to the effects of hunger.

Associated with generalized atrophy due to lack of protein is the atrophy of certain tissues caused by specific vitamin deficiencies.

Atrophic skin changes increase due to lack of vitamin A and muscle atrophy increases due to lack of vitamin E.

After a period of growth in human metabolism, a gradual decline occurs in slow structural changes other than those due to preventable diseases or accidents.

Aging is eventually characterized by marked atrophy of many tissues and organs, with a decrease in the number of cells and an alteration in their constitution.

This is finally reflected in the modified, diminished, or lost function characteristic of old age and which produces death.

Changes in senescence are affected by both inherited constitution and environmental influences, including illness and accidents.

The atrophic changes of aging affect almost all tissues and organs, but some changes are more evident and essential.

Arteriosclerosis, the thickening and hardening of the arterial walls decreases the vascular supply and, in general, accentuates the aging processes.

Atrophy in old age is especially noticeable on the skin, characteristically flat, shiny or satiny, and wrinkled.

Atrophy is caused by aging changes in the fibers of the actual skin, or dermis, and in the cells and sweat glands of the outer skin.

Muscle wasting accompanied by some loss of muscle strength and agility is expected in the elderly.

In a somewhat irregular pattern, there is a contraction of many individual muscle fibers and a decrease in their number. Other changes have been observed within muscle cells.

High lipofuscin pigment is also characteristic in heart muscle fibers in the elderly, known as brown heart atrophy.

Wear and tear of the heart muscle in old age can be accompanied by an increase in fibrous and fatty tissue on the right-side walls of the heart and an increased replacement of elastic tissue with fibrous tissue in the lining.

Abnormal deposits of the protein substance amyloid also occur more frequently in atrophic heart muscle in old age.

Atrophy of the liver in the elderly is also accompanied by increased lipochrome pigment in atrophied cells.

Bones become progressively lighter and more porous with aging, known as osteoporosis.

The reduction in bone tissue is most marked in cancellous bone, the open-textured tissue at the ends of long bones, and in the inner parts of the cortex of these bones.

In addition to changes and loss of osteocytes or bone cells, there is decreasing mineralization, or calcium deposition, with increased brittleness of the bones.

Atrophy of the brain in old age is shown by narrowing of the ridges, or convolutions, on the brain’s surface and by increased fluid in the space below the arachnoid membrane.

There is a contraction of individual neurons, with an increase in the content of lipochrome pigments, as well as a decrease in their number.

Sometimes nerve fibrils have degenerated, and deposits called senile plaques can be found between neurons, particularly in the frontal cortex and hippocampus.

Similar atrophic changes in the brain are seen in Alzheimer’s disease, a condition of unknown cause that is more likely to occur in older patients.

Mental deterioration (senile dementia) in the elderly is the clinical manifestation of these changes. Senile atrophy can be increased and complicated by the presence of arteriosclerosis.

Reductions in the size of specific brain structures were predictive of mild cognitive impairment and progression to dementia.

Simmonds disease is a chronic deficiency in the function of the pituitary gland, a form of hypopituitarism, which leads to the atrophy of many of the viscera, including the heart, liver, thyroid, and gonads.

The disease causes emaciation and death if it is not treated.

A destructive lesion affecting the pituitary gland with loss of hormones leads to atrophy of the thyroid gland and gonads and, in turn, produces atrophic changes in its target organs and viscera.

The decrease in the size of the endocrine glands can be extreme.

Muscle or muscle and bone hypotrophy

Local hypotrophy of muscle, bone, or other tissues results from disuse or decreased activity or function.

Although the exact mechanisms are not fully understood, decreased blood supply and reduced nutrition occur in inactive tissues.

Muscle disuse resulting from loss of motor nerve supply to the muscle (e.g., polio) leads to extreme inactivity and corresponding atrophy.

The muscles become flabby and paralyzed if there is the destruction of the nerve cells in the spinal cord that generally activate them. The contraction of the paralyzed muscle fibers becomes apparent within a few weeks.

After a few months, the fragmentation and disappearance of muscle fibers occur with a replacement by fat cells and a loose network of connective tissue. It can cause some contracture.

Skeletal muscles forced into inactivity by paralysis (for example, a limb resulting from polio) also suffer disuse atrophy.

If there is a tendency for the bones to become lighter and more porous in a particular area, a condition known as local osteoporosis, this can be recognized by X-rays within a few weeks.

The cortex of long bones becomes considerably thinner or atrophic, with reduced mineral content.

Disuse due to painfully diseased joints produces a similar but lesser degree of atrophy of movement-related muscles.

Local osteoporosis of bone, known as Sudeck’s atrophy, sometimes develops rapidly in the area of ​​a bone lesion.

Severe or prolonged blood sugar deficits deprive the nervous system of necessary energy sources due to degeneration of brain cells and peripheral nerves.

The disuse atrophy of muscle or bone that can occur is fundamentally similar to other disuse atrophy of these tissues.

The persistent pressure will cause atrophy of a compressed cell, organ, or tissue, presumably due to interference with the nutrition and metabolic activity of the affected person.

Cells in a local area (for example, in the liver) are atrophied by the pressure of materials such as amyloid deposited around them.

The pressure of an expanding benign tumor causes atrophy of adjacent typical structures. The stress of a dilatation located in an artery (aneurysm) will cause atrophy of the tissues, including the bones, which it affects.

The growth of an intervertebral disc or the development of a tumor sometimes puts pressure on the nerves near their exit point from the spinal cord.

If the pressure is prolonged, the muscles usually controlled by these nerves can atrophy. Very often, the calf muscles are affected.

The pressure resulting from the involvement of the vertebrae at the neck level or compression of the network of nerves called the brachial plexus produces similar effects in the upper chest and arms.

Simple disuse of muscles and bones, such as immobilization produced when a limb is placed in a cast or sling, results in the atrophy of these tissues.

In the case of muscle, the degree of atrophy is generally less severe than that caused by injury to a nerve, although the nature of the change is similar.

Localized atrophies of the legs and arms muscles can be the result of inherited or familial diseases in which the nerves of the spinal cord that supply them are inactivated or destroyed.

In Charcot-Marie-Tooth disease, the atrophy mainly involves the peroneal muscles on the outer side of the lower legs and sometimes the powers of the hand.

It commonly begins in childhood or adolescence. Peroneal muscular atrophy is also seen in the inherited degenerative disease of the spinal cord known as Friedreich’s ataxia.

Hypotrophy of nervous tissue

Hypotrophy of the brain or spinal cord tissue can be due to injuries that directly affect a localized area or interfere with the blood supply.

When peripheral nerves are cut, degenerative and ultimately atrophic changes occur beyond the injury. This type of atrophy is known as Wallerian degeneration.

Suppose conditions do not allow the regeneration of nerve fibers from the proximal fragment of the severed nerve. In that case, atrophy is the final destination of the nerve tissue distal to the injury.

Retrograde atrophy also occurs due to disuse and affects the ganglion cells of the injured nerve. Prolonged pressure causes atrophy in the central nervous system as elsewhere.

The pressure of an expanding tumor on the membranes that cover the brain produces localized atrophy of the adjacent brain substance it affects.

In hydrocephalus, the most generalized atrophy of brain tissue is due to abnormal amounts of fluid confined within the rigid bony compartment of the skull.

The increased pressure within the skull can force a part of the brain through the foramen magnum; if prolonged, it produces localized atrophy of the cerebellar tissue against the bone wall.

The later stages of chronic infections can be characterized by atrophy of the brain.

A striking example of this is the variety of syphilitic infections of the nervous system known as general paresis, in which the brain shrinks, and we lose weight.

The atrophy mainly affects the cerebral cortex, particularly markedly in the frontal area. Occasionally, the atrophy is local or affects only one side of the brain.

The contraction of brain tissue is mainly due to the loss of many nerve cells in the cortex.

Hypotrophy of fat tissue

Hypotrophy of the body’s fatty tissue occurs as part of the generalized atrophy of prolonged malnutrition.

The localized atrophy of adipose tissue lipodystrophy may result from injury to the local area; for example, repeated insulin injections cause atrophy of fatty tissue at the injection site.

Progressive lipodystrophy is a disease of unknown cause in which adipose tissue atrophies only in some body areas. It occurs mainly in women and often begins in childhood.

The progressive wear of adipose tissue mainly affects the face, arms, and trunk. In the affected areas, the specialized fat-retaining cells of adipose tissue disappear.

Hypotrophy of the skin

A generalized atrophic change in the skin has been an essential part of aging.

Similar atrophic changes in the skin appear to be caused or enhanced by excessive exposure to sunlight.

While several abnormal skin conditions can include localized atrophic changes in the epidermis or dermis, certain generalized skin diseases are mainly characterized by such modifications.

The hardening of the skin, known as scleroderma, can occur in a localized or circumscribed form called morphea or a more severe and diffuse disease.

The advanced stages of scleroderma are characterized by marked atrophy of the tissue and appendages of the actual skin.

Atrophic thinning of the overlying epidermis can also occur, and the underlying fatty tissue and muscle can also atrophy.

The chronic form of lupus erythematosus is also characterized by atrophy. In advanced stages, atrophy occurs mainly in the epidermis in focal areas.

The thinned layer of the epidermis can be a prominent feature of the microscopic appearance of the skin in the aging; skin wrinkles close to age spots and wrinkles on the facial skin of an older adult.

Gland hypotrophy

The glandular endocrine tissues can suffer atrophy when there is an excess of their hormonal product due to the disease.

An example is seen in connection with a hormone-producing tumor of the cortical tissue of an adrenal gland, which may be accompanied by marked atrophy of the cortical tissue of the opposite adrenal gland.

This is probably the result of altering the delicate mechanism of hormonal stimulation through the pituitary gland.

Various endocrine organs (thyroid gland, adrenal glands, gonads) depend on their activity on endocrine stimulation by hormones of the pituitary gland.

A severe general failure of the production of pituitary hormones results in the generalized endocrine atrophy of Simmonds disease.

Minor degrees of functional impairment of the pituitary gland can upset a delicate balance and lead to selective atrophy of the adrenal cortical tissue or the gonads.

Glands that release their secretions through a duct (e.g., salivary glands, pancreas) may become atrophic due to duct obstruction.

In the pancreas, complete obstruction of its duct causes atrophy of the glandular tissue, except for the insulin-producing islets of Langerhans, the secretion of which is absorbed into the bloodstream.

Factors of both disuse and increased pressure may be present in the atrophy that results from obstruction of the outlet channel.

Similarly, rapid and complete obstruction of a ureter is followed by atrophy of the corresponding kidney.

Chemical-induced hypotrophy

Causes of hypotrophy that result from a chemical injury are not expected.

However, in chronic arsenic poisoning, degenerative changes occur in the peripheral nerves, leading to weakness and atrophy in the tissues (usually legs or arms) to which the nerves are distributed.

Similar results may follow chronic lead poisoning peripheral neuropathy.