Physiological atrophy
Physiological atrophy occurs continuously within the body and acts as a natural mechanism of adaptation to changing living conditions. A clear example is age-related changes (aging). During this period, the number of functionally active cells and the volume of intracellular organelles predictably decrease, leading to a general decline in organ function.
A characteristic sign of aging at the cellular level is the accumulation of the pigment lipofuscin, which leads to the development of so-called "brown atrophy". Microscopically (e.g., in brown atrophy of the liver), hepatocytes appear smaller, and clusters of brown pigment granules are clearly visible in their cytoplasm.
Typical examples of physiological involution include:
- Atrophy of endocrine glands.
- Atrophy of the ovaries, mammary glands, and thymus.
- Atrophy of the spermatogenic epithelium of the testes.
The extreme degree of age-related changes is senile (involutional) cachexia—generalized atrophy of the entire body resulting from a global decrease in metabolic rate and the shutdown of many body functions.
Pathological generalized atrophy
Pathological atrophy develops against the background of various diseases and is always an important link in their pathogenesis. It is traditionally subdivided into generalized and local.
Generalized pathological atrophy manifests as pathological cachexia (wasting). Depending on the primary cause, several types of this condition are distinguished:
- Alimentary cachexia — occurs with prolonged starvation and insufficient nutrient intake.
- Cerebral and pituitary cachexia — develops in severe brain diseases when central regulation is impaired.
- Post-traumatic cachexia — severe wasting accompanying massive bodily injuries.
Pathological local atrophy
Local pathological atrophy is encountered in clinical practice much more frequently than generalized atrophy. Depending on the mechanism of development (pathogenesis), five main types are distinguished:
- Disuse (from inactivity). Occurs when an organ or tissue lacks function. A classic example is the atrophy of skeletal muscles of a limb during bone fracture due to forced immobilization.
- Neurotrophic. Associated with impaired tissue innervation. For example, in poliomyelitis, motor neurons are destroyed, leading to severe atrophy of the corresponding skeletal muscles.
- Pressure atrophy. Develops when tissue is compressed by accumulated fluid or a growing tumor. A characteristic example is brain tissue atrophy in hydrocephalus, when cerebrospinal fluid accumulates in the ventricles and presses on the parenchyma.
- Ischemic (from inadequate blood supply). Caused by the narrowing of the lumen of arteries supplying an organ. Thus, renal artery stenosis (e.g., due to an atherosclerotic plaque) leads to marked renal atrophy.
- Due to damaging factors. Occurs under the influence of physical or chemical agents. An example is bone marrow atrophy developing under the influence of ionizing radiation.
Briefly: answers to topical questions
What types of pathological generalized atrophy (cachexia) exist?
The following types of pathological generalized atrophy (cachexia) exist:
- Alimentary cachexia — develops during starvation (absence or deficiency of food).
- Cerebral and pituitary cachexia — occurs in brain diseases.
- Post-traumatic cachexia — develops as a consequence of sustained injuries.
Senile (involutional) cachexia is also distinguished, but it belongs to the manifestations of physiological atrophy occurring in connection with a decrease in metabolic rate.
Which organs and structures undergo physiological atrophy?
Various organs and structures undergo physiological atrophy in the process of normal life activity and aging:
- Umbilical vessels and ductus arteriosus — atrophy after birth.
- Thymus — undergoes age-related involution.
- Endocrine glands — including gonads (ovaries, spermatogenic epithelium of the testes) in old age.
- Mammary glands — undergo involution.
- Bones and muscles — atrophy in elderly individuals (senile atrophy).
In senile cachexia, physiological atrophy of the entire human body is observed.
How does atrophy differ from hypoplasia and aplasia?
Atrophy differs from hypoplasia in the time of onset and the initial state of the organ.
| Sign | Atrophy | Hypoplasia |
|---|---|---|
| Definition | Decrease in the volume of an organ that had previously reached normal size | Congenital underdevelopment of an organ |
| Initial volume | Was normal before the onset of the process | Initially fails to reach normal volume |
In the provided materials, aplasia is mentioned only as a developmental defect (e.g., of the salivary glands), but its detailed differences from atrophy are not described.
What macroscopic features are characteristic of an atrophied organ?
The following macroscopic features are characteristic of an atrophied organ:
- Size and shape — the organ is usually reduced in size but retains its original shape (with uniform atrophy).
- Consistency — becomes denser due to stromal sclerosis (proliferation of connective tissue) or replacement by proliferating adipose tissue.
- Surface — may become nodular in case of uneven parenchymal cell death (e.g., in granular contracted kidney).
- Color — upon accumulation of the lipofuscin pigment, the organ acquires a brown color (brown atrophy).
What is the mechanism of lipofuscin formation in cells during atrophy?
The mechanism of lipofuscin ("aging pigment") formation is associated with damage to cellular organelles and impairment of their degradation processes.
The pigment accumulates in the cytoplasm due to a lack of intracellular antioxidants, which leads to lipid peroxidation of the membranes. As a result, autolysosomes form, containing undigested cellular debris (fragments of mitochondria and the endoplasmic reticulum). These structures form residual bodies, which are lipofuscin granules—an insoluble pigment consisting of lipid and phospholipid polymers bound to protein.
What ultrastructural changes occur in the cell during atrophy?
Based on the provided materials, using neurotrophic muscle atrophy as an example, the following ultrastructural changes are described:
- Organelle reduction — the number of mitochondria and myofilaments decreases, and the volume of the endoplasmic reticulum is reduced.
- Autophagy — the number of autophagic vacuoles containing fragments of mitochondria and the endoplasmic reticulum increases.
- Lipofuscin accumulation — residual bodies containing undigested cellular debris are formed; lipofuscin granules are an example.
To memorize the five types of local pathological atrophy, use the phrase "Poor Grandad Doesn't Remember Names": Disuse, Pressure, Neurotrophic, Injurious factors, Ischemia.
Class and exam questions
What is brown atrophy and why is it called that?
This is a type of age-related physiological atrophy in which granules of the lipofuscin pigment accumulate in reduced cells (e.g., hepatocytes), giving the tissue a characteristic brown color.
What happens to the organ stroma during atrophy?
The stroma usually retains its original volume, but often undergoes sclerosis—the proliferation of connective tissue that fills the space.
Is atrophy reversible?
Yes, in most cases this is a reversible adaptation process. The function and volume of the tissue can recover if the cause of the pathology is eliminated in time.
What else to study on this topic
- Morphological picture of brown atrophy of the liver
- Pathogenesis of senile (involutional) cachexia
- Types of pathological cachexia (alimentary, cerebral, post-traumatic)
- Mechanisms of stromal sclerosis in parenchymal atrophy
- Differences between atrophy and necrosis at the tissue level
Master the entire topic in the "Pathological Anatomy" course
This is a summary. The course covers everything tested in classes and exams.
- Complete study guide on "Atrophy" and 4,414 other subject pages
- Assignments and quizzes after every topic — just like in a colloquium
- AI tutor answers questions on the topic anytime
- 153 video lessons on the subject
Other topics in the section "Compensatory and Adaptive Processes"
Free video lessons: pathological anatomyShort lessons with study notes — no registration required.
Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.