Atrophy is defined as a reduction in the size of an organ or tissue due to a decrease in cell size and number. Atrophy can be physiologic or pathologic. Physiologic atrophy is common during normal development. Some embryonic structures, such as the notochord and thyroglossal duct, undergo atrophy during fetal development. The decrease in the size of the uterus that occurs shortly after parturition is another form of physiologic atrophy.

Pathologic atrophy has several causes and it can be local or generalized. The common causes of atrophy are the following:

• Decreased workload (atrophy of disuse). When a fractured bone is immobilized in a plaster cast or when a patient is restricted to complete bed rest, skeletal muscle atrophy rapidly ensues. The initial decrease in cell size is reversible once activity is resumed. With more prolonged disuse, skeletal muscle fibers decrease in number (due to apoptosis) as well as in size; muscle atrophy can be accompanied by increased bone resorption, leading to osteoporosis of disuse.

• Loss of innervation (denervation atrophy). The normal metabolism and function of skeletal muscle are dependent on its nerve supply. Damage to the nerves leads to atrophy of the muscle fibers supplied by those nerves (Chapter 27).

• Diminished blood supply. A gradual decrease in blood supply (ischemia) to a tissue as a result of slowly developing arterial occlusive disease results in atrophy of the tissue. In late adult life, the brain may undergo progressive atrophy, mainly because of reduced blood supply as a result of atherosclerosis (Fig. 1). This is called senile atrophy, which also affects the heart.

• Inadequate nutrition. Profound protein-calorie malnutrition (marasmus) is associated with the utilization of skeletal muscle proteins as a source of energy after other reserves such as adipose stores have been depleted. This results in marked muscle wasting (cachexia; Chapter 9). Cachexia is also seen in patients with chronic inflammatory diseases and cancer. In the former, chronic overproduction of the inflammatory cytokine tumor necrosis factor (TNF) is thought to be responsible for appetite suppression and lipid depletion, culminating in muscle atrophy.

• Loss of endocrine stimulation. Many hormone-responsive tissues, such as the breast and reproductive organs, are dependent on endocrine stimulation for normal metabolism and function. The loss of estrogen stimulation after menopause results in physiologic atrophy of the endometrium, vaginal epithelium, and breast.

• Pressure. Tissue compression for any length of time can cause atrophy. An enlarging benign tumor can cause atrophy in the surrounding uninvolved tissues. Atrophy in this setting is probably the result of ischemic changes caused by compromise of the blood supply by the pressure exerted by the expanding mass.

Fig1. Atrophy. A, Normal brain of a young adult. B, Atrophy of the brain in an 82-year-old man with atherosclerotic cerebrovascular disease, resulting in reduced blood supply. Note that loss of brain substance narrows the gyri and widens the sulci. The meninges have been stripped from the right half of each specimen to reveal the surface of the brain.

The fundamental cellular changes associated with atrophy are identical in all of these settings. The initial response is a decrease in cell size and organelles, which may reduce the metabolic needs of the cell sufficiently to permit its survival. In atrophic muscle, the cells contain fewer mitochondria and myofilaments and a reduced amount of rough endoplasmic reticulum (RER). By bringing into balance the cell’s metabolic demands and the lower levels of blood supply, nutrition, or trophic stimulation, a new equilibrium is achieved. Early in the process atrophic cells and tissues have diminished function, but cell death is minimal. However, atrophy caused by gradually reduced blood supply may progress to the point at which cells are irreversibly injured and die, often by apoptosis. Cell death by apoptosis also contributes to the atrophy of endocrine organs after hormone withdrawal.

Mechanisms of Atrophy

Atrophy results from decreased protein synthesis and increased protein degradation in cells. Protein synthesis decreases because of reduced metabolic activity.

The degradation of cellular proteins occurs mainly by the ubiquitin-proteasome pathway. Nutrient deficiency and disuse may activate ubiquitin ligases, which attach the small peptide ubiquitin to cellular proteins and target these proteins for degradation in proteasomes. This pathway is also thought to be responsible for the accelerated proteolysis seen in a variety of catabolic conditions, including cancer cachexia. In many situations, atrophy is also accompanied by increased autophagy, marked by the appearance of increased numbers of autophagic vacuoles. Autophagy (“self-eating”) is the process in which the starved cell eats its own components in an attempt to reduce nutrient demand to match the supply. Some of the cell debris within the autophagic vacuoles may resist digestion and persist in the cytoplasm as membrane-bound residual bodies. An example of residual bodies is lipofuscin granules, discussed later in the chapter. When present in sufficient amounts, they impart a brown discoloration to the tissue (brown atrophy). Autophagy is associated with various types of cell injury, and we will discuss it in more detail later.

اخر الاخبار

اخبار العتبة العباسية المقدسة

وزارة التعليم العالي تكرم جامعة العميد لحصولها على جائزة المكتبة الأكاديمية المتميزة

جمعية العميد تناقش استعداداتها لانطلاق فعاليات المؤتمر العلمي الرابع لإحياء تراث أمير المؤمنين (عليه السلام)

أكاديمية التطوير الإداري تواصل برنامج الخطة الخمسينية لعدد من ملاكات العتبة العباسية المقدسة

المجمع العلمي يواصل تقديم دورته التطويرية لعدد من الملاكات التربوية في الديوانية

المزيد

الآخبار الصحية

الرياضة وحدها لا تكفي.. كيف يؤثر الجلوس الطويل على الصحة؟

دراسة: بدائل السكر ليست آمنة على الكبد

تفاحة قبل النوم.. عادة بسيطة مفيدة أم خطر على الصحة؟

احذر مشاركتها مع الآخرين.. 3 أدوات شائعة قد تنقل أمراض خطيرة

المزيد

الآخبار التكنلوجية

الهنغاري لاسلو كراسناهوركاي يفوز بجائزة نوبل للآداب 2025

رسميا.. إعلان الفائز بجائزة نوبل للسلام لعام 2025

باحثون: تشات جي بي تي ونماذج الذكاء الاصطناعي يمكن "تسميمها"

عالمان في الأعصاب يرفعان دعوى قضائية ضد شركة آبل

المزيد

مواضيع ذات صلة

Endocrine Disorders of the Ovary

Mitochondrial Damage

Morphologic Alterations in Cell Injury

Metaplasia

Risk factors for type 2 diabetes

Hyperplasia

Hypertrophy

Occurrence of type 1 diabetes by age

Classification of diabetes types

Peritonitis in Patients Undergoing Continuous Ambulatory Peritoneal Dialysis

Secondary Peritonitis

Primary (Spontaneous) Bacterial Peritonitis