Physiological atrophy

pathological atrophy

1. Atrophied cells, tissues and organs reduce in size, weight, and become darker in color. Lipofuscin is commonly found in the cytoplasm. 2. When parenchymal cells atrophy, there is often a certain degree of interstitial fiber and fat hyperplasia, and sometimes the volume is inversely proportional. Normal organs are larger, called pseudohypertrophy

After the cause is removed, cells with mild pathological atrophy may return to normal, but cells with persistent atrophy may eventually die (apoptosis)

physiological hypertrophy

pathological hypertrophy

physiological hyperplasia

Pathological hyperplasia

diffuse hyperplasia

Localized hyperplasia: the formation of single or multiple hyperplastic nodules in tissues and organs

Most pathological (e.g., inflammatory) cell proliferations are usually stopped by removal of the relevant triggering factors. If cell proliferation becomes excessive and out of control, it may evolve into neoplastic hyperplasia.

metaplasia of epithelial tissue

Metaplasia of mesenchymal tissue: Immature fibroblasts in mesenchymal tissue can transform into osteoblasts or chondrocytes after injury, which is called bone or cartilage metaplasia. It is more common in soft tissue injuries such as myositis ossificans and other hand injuries. , also found in the stroma of certain tumors

Metaplasia of epithelial tissue may be reversible after the cause is eliminated, but metaplasia of mesenchymal tissue is mostly irreversible.

It has both advantages and disadvantages. If the factors causing metaplasia persist, it may cause malignant transformation of cells.

For example: metaplasia of respiratory mucosal columnar epithelium into squamous epithelium can strengthen the local ability to resist external stimuli. However, because the surface of squamous epithelium does not have the ciliated structure of columnar epithelium, the self-purification ability of the mucosa is weakened.

Heart failure resulting in insufficient oxygenation of arterial blood

Anemia and carbon monoxide poisoning reduce the oxygen-carrying capacity of the blood

Blocked blood vessels reduce blood supply

Pathogens invade collective growth and reproduction, causing mechanical damage, inducing allergic reactions, releasing internal and external toxins or secreting certain enzymes.

xenobiotics

endogenous substances

Early manifestations include selective loss of membrane permeability, ultimately leading to significant membrane structural damage. Severe disorder of cell membrane function and failure to recover mitochondrial membrane function are characteristics of irreversible cell damage.

Morphologically, damage to the cell membrane phase structure causes swelling of cells, mitochondria, endoplasmic reticulum and other organelles, the disappearance of microvilli on the cell surface, and the formation of vesicles.

Mitochondria are the main site of oxidative phosphorylation and ATP production in cells. After the cessation of mitochondrial oxidative phosphorylation, cells develop acidosis, eventually leading to cell necrosis.

Hypoxia and toxic damage affect the oxidative phosphorylation process of mitochondria, reducing or even stopping ATP production, reducing the synthesis and decomposition functions of cells that require energy maintenance, and causing obstacles to cell life activities.

Ischemia is one of the causes of hypoxia. Ischemia usually causes more rapid and severe tissue damage than hypoxia.

1. Morphological manifestations: deformation or material deposition. When abnormal substances appear in cells or interstitium, the number of abnormal substances exceeds that of normal substances and is accompanied by varying degrees of dysfunction.

watery denaturation

Steatosis

hyaline degeneration

mucoid degeneration

amyloidosis

intracellular glycogen deposition

pathological pigmentation

pathological calcification

Necrosis and apoptosis are the two main forms of cell death. The pathological death of local tissues and cells in vivo is called necrosis

Morphological changes

coagulative necrosis

liquefaction necrosis

Special types of necrosis