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MindMap Gallery Pathology Chapter 1 Adaptation and Damage of Cells and Tissues

Pathology Chapter 1 Adaptation and Damage of Cells and Tissues

Pathology Chapter 1: Adaptation and damage of cells and tissues are important concepts in the fields of biology and medicine, involving the response of cells, tissues, organs, and the entire body to changes in the internal and external environment.

Edited at 2024-03-12 20:22:46

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Pathology Chapter 1 Adaptation and Damage of Cells and Tissues

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Outline

Cell and tissue adaptation and damage

adapt

The non-damaging response of cells and the tissues and organs they constitute to continuous stimulation and various harmful factors in the internal and external environment

shrink

A reduction in the size of normally developed cells, tissues, or organs

type

Physiological atrophy

apoptosis

pathological atrophy

dystrophic atrophy

compressive atrophy

apraxia of atrophy

denervation atrophy

endocrine atrophy

aging and damage atrophy

Pathological changes of atrophy

The volume is reduced, the weight is reduced, and the color becomes darker (visible to the naked eye)

Lipofuscin granules, reduced protein synthesis, increased decomposition, and massive degradation of cell organelles

Fat

Increased function and strong anabolism

type

physiological hypertrophy

Compensatory hypertrophy: strong demand, increased load

endocrine hypertrophy

pathological hypertrophy

compensatory hypertrophy

endocrine hypertrophy

Pathological changes of hypertrophy

Increased size

The cell nuclei are hypertrophied and deeply stained, and the volume of hypertrophic tissues and organs increases uniformly.

Enhanced cell function and relative lack of blood supply

hyperplasia

Active cell mitosis, increased number of cells in tissues or organs

type

physiological hyperplasia

compensatory hyperplasia

endocrine hyperplasia

Pathological hyperplasia

compensatory hyperplasia

Wound healing process after tissue damage

endocrine hyperplasia

Pathological changes of proliferation

The number of cells increased, and the morphology of cells and nuclei was normal or slightly enlarged.

Uniform and diffuse enlargement of tissues and organs

Solitary or multiple hyperplastic nodules

Metaplasia

One mature cell type is replaced by another mature cell type

The result of transformation of stem cells or undifferentiated mesenchymal cells in connective tissue with the ability to divide, proliferate and multi-lineage differentiation

Usually occurs between homologous cells

Strengthen the local ability to resist external stimuli: some metaplasias are precancerous lesions related to multi-step tumor cell evolution.

Causes and mechanisms of cell and tissue damage

Mechanisms of Cell and Tissue Damage

cell membrane damage

Mitochondrial damage: an important early criterion for irreversible cell damage

Damage from reactive oxygen species

Damage to intracytoplasmic free calcium

Ischemic and hypoxic injury

chemical damage

Genetic Variation

reversible cell damage

Morphological changes are called degeneration. After the cells or intercellular substance are damaged, abnormal substances or abnormal accumulation of normal substances appear in the cells or intercellular substance.

Cellular edema

The earliest changes in cell damage

Pathological changes: under light microscope, the cytoplasm is red-stained and fine granular, and the cytoplasm is vacuolated. The organ size increases, the cut surface is everted, the color becomes lighter, and the myelin-like structure Ballooning: viral hepatitis

fatty change

Triglycerides accumulate in the cytoplasm of non-adipocytes

Pathological changes: lipid droplets are vacuolated, and the main component is triglyceride

Where fatty changes occur

Hepatocytes: Mild hepatic steatosis does not cause significant morphological changes and dysfunction of the liver Chronic liver congestion: central area of liver lobules Phosphorus poisoning: perilobular areas Significant diffuse hepatic steatosis is called fatty liver, and severe hepatic steatosis develops into liver necrosis and cirrhosis.

Myocardium: Chronic alcoholism or hypoxia causes myocardial fatty degeneration, tiger spot heart, and adipose tissue hyperplasia leads to myocardial fat infiltration.

Renal tubular epithelial cells: excess reabsorbed prourinary lipoproteins

mechanism

Increased fatty acids in liver cytoplasm

Too much triglyceride synthesis

Decreased lipoproteins and apolipoproteins

hyalinization

Translucent protein accumulation appears in the cells or interstitium and is eosinophilic and homogeneous.

Pathological changes:

Intracellular hyalinization: homogeneous red-stained round bodies in the cytoplasm Renal tubular epithelial cells, plasma cells, hepatocytes

Hyalinization of fibrous connective tissue: aging of fibrous tissue

Hyalinization of small arterial walls: small arterial walls of kidneys, brain, spleen, etc. in slowly progressive hypertension and diabetes

amyloidosis

Accumulation of amyloid protein and mucopolysaccharide complexes in the intercellular substance

Pathological changes: light red homogeneous substance local or systemic

Myxoid change

Accumulation of mucopolysaccharides and proteins in the intercellular substance

pathological pigmentation

Pigment increases and accumulates inside and outside cells

Hemosiderin: Aggregation of ferritin particles, formed by combining ferric iron with protein

Lipofuscin: undigested organelle fragments in autophagic lysosomes

melanin

Bilirubin: a product of aging and destruction of red blood cells in the blood

pathological calcification

Deposition of solid calcium salts in tissues other than bone and teeth

Pathological calcification type

Dystrophic calcification: Abnormal calcium and phosphorus metabolism in the body in necrotic or imminent necrotic tissue or foreign matter

Metastatic calcification: systemic calcium and phosphorus metabolism is disordered, calcium salts are deposited in normal tissues

Pathological changes: blue granular to flaky, fine granules or clumps

cell death

Necrosis

changes in cell nuclei

Main morphological signs of cell necrosis

nuclear pyknosis

nuclear fragmentation

nuclear lysis

Increased cytoplasmic eosinophilia

type

After tissue necrosis, the color becomes pale, elasticity is lost, and normal sensory and motor functions are lost.

coagulative necrosis

Protein denaturation and coagulation, weak hydrolysis by lysosomal enzymes

The most common, mostly seen in solid organs (heart, liver, kidney, spleen)

The fine cell structure disappears, the outline of the tissue structure can still be preserved, and a zone of congestion, hemorrhage and inflammatory reaction forms around the necrotic area.

liquefaction necrosis

A large amount of hydrolytic enzymes can easily cause dissolution and liquefaction (encephalomalacia) of cells and tissues after necrosis.

Dead cells are completely digested and local tissues are quickly dissolved

caseous necrosis

Tuberculosis, the necrotic area is yellow and looks like cheese

No structure granular red stain, the original tissue outline disappears

A special type of coagulative necrosis with more complete necrosis

fibrinoid necrosis

Common in connective tissue and small blood vessel walls

Rapidly progressive hypertension

fat necrosis

Belonging to the category of liquefaction necrosis, gray-white calcium soap can be seen

gangrene

dry gangrene

Arterial obstruction and venous return at the ends of limbs (ends of lower limbs)

Dry and shriveled

Clear boundaries with normal tissue

wet gangrene

Internal organs connected to the outside world, limbs with blocked arteries and veins at the same time

unclear boundaries with surrounding tissues

gas gangrene

Wet gangrene

Open wounds of muscles, combined with infections such as Clostridium perfringens

Often accompanied by systemic poisoning

ending

Dissolve and absorb

Separate discharge

Mechanization and packaging

Organization: New granulation tissue grows and replaces necrotic tissue, thrombus, pus, foreign matter, etc.

Encapsulation: The necrotic tissue is too large and is surrounded by new granulation tissue

Calcification

apoptosis

single cell programmed death

Morphological characteristics

Cell shrinkage

Chromatin condensation and edge cell nuclear fragmentation

Apoptotic body formation (an important morphological sign of apoptosis)

Plasma membrane intact