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2. Adaptation and damage of cells and tissues
The non-damaging response of cells, tissues and organs to continuous stimulation and various harmful factors in the internal and external environment is called adaptation. Adaptation is generally manifested morphologically as atrophy, hypertrophy, hyperplasia, and metaplasia, and these processes involve changes in cell number, cell volume, or cell differentiation.
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2. Adaptation and damage of cells and tissues
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In order to help everyone use DeepSeek more efficiently, a collection of DeepSeek guide mind map was specially compiled! This mind map summarizes the main contents: Yitu related links, DS profile analysis, comparison of DeepSeek and ChatGPT technology routes, DeepSeek and Qwen model deployment guide, how to make more money with DeepSeek, how to play DeepSeek, DeepSeek scientific research Application, how to import text from DeepSeek into MindMaster, the official recommendation of DeepSeek Wait, allowing you to quickly grasp the essence of AI interaction. Whether it is content creation, plan planning, code generation, or learning improvement, DeepSeek can help you achieve twice the result with half the effort!
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- Voice recognition commercial solution
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2. Adaptation and damage of cells and tissues
Adaptation of cells and tissues
shrink
Physiological atrophy
Degenerate
Restore the old
senile atrophy
pathological atrophy
dystrophic atrophy
Chronic starvation Chronic wasting disease Malignant tumors Tuberculosis
neurological atrophy
polio
apraxia of atrophy
Long term inactivity of limbs
compressive atrophy
endocrine atrophy
ischemic atrophy
atherosclerosis
Pathological changes of atrophy
Visual changes: reduction in organ size Loss of quality and darker color
Parenchymal cell atrophy and interstitial reactive hyperplasia (pseudohypertrophy) under light microscope Under the electron microscope, the formation of autophagic vacuoles increased, the number of autophagic lysosomes increased, and the formation of lipofuscin increased.
The ending of shrinking
Eliminating the cause can restore the condition to its original state
Cells that have not eliminated the cause of atrophy pass through Apoptosis and gradually disappear
Fat
physiological hypertrophy
Endocrine Pregnancy Uterus Lactation Breast
Compensatory skeletal muscle hypertrophy of upper limbs in weightlifters
pathological hypertrophy
endocrine
Hyperthyroidism Increased thyroid follicular epithelial cells
compensatory
Myocardial cells thicken in hypertension
One kidney is removed and the other kidney develops compensatory hypertrophy
hyperplasia
physiological hyperplasia
Hormonal hyperplasia (endocrine hyperplasia)
Adolescent female breast pregnancy uterus breast
compensatory hyperplasia
Partial liver resection causes hepatocellular proliferation
Pathological hyperplasia
Endocrine: stimulation by too many hormones Endometrial hyperplasia caused by excess estrogen (dysfunction)
Compensatory: wound healing cell proliferation
Metaplasia
epithelial metaplasia
coated epithelial metaplasia
Squamous metaplasia
glandular metaplasia
intestinal metaplasia
pseudopyloric gland metaplasia
mesenchymal tissue metaplasia
bone or cartilage metaplasia
myositis ossificans
Mature cells cannot be transformed directly
Can only occur between homologous cells
Tissue ectopia caused by developmental abnormalities is not metaplasia
Metaplasia of epithelial tissue may be reversible after the cause is eliminated However, metaplasia of mesenchymal tissue is mostly irreversible.
Nerve fibers cannot metabolize
transdifferentiation
epithelial-mesenchymal transition
Damage to cells and tissues
Cause of injury
hypoxia
physical factors
chemical factors
biological factors
most common
immune response
genetic factors
malnutrition
neuro-endocrine factors
mechanism of injury
membrane damage
mitochondrial damage
Disruption of intracellular calcium homeostasis
Morphological changes of injury
Reversible damage (degeneration)
Watery degeneration (intracellular)
Cellular edema
Hypoxia, poisoning, infection, physical and chemical factors
Damage to cell mitochondria
Sodium-potassium pump dysfunction
Result of not removing the cause: cell lysis and necrosis
Prevalent parts: heart, liver, kidney parenchymal cells
Pathological changes
light microscope
Increased cell size
The cytoplasm is loose and lightly stained, with a large amount of red-stained fine granular material.
nuclear enlargement
electron microscope
Mitochondria are swollen and endoplasmic reticulum is expanded (early stage of disease)
naked eye
swelling, paleness, cloudiness
Steatosis (intracellular)
hepatic steatosis
fatty liver, cirrhosis
myocardial fatty degeneration
Tiger spot heart: Caused by chronic alcoholism or hypoxia, yellow and red stripes appear under the left endocardium and papillary muscles.
Fatty heart: myocardial fat infiltration (non-steatosis) extracellular
renal steatosis
Pathological changes
Light microscope: intracytoplasmic vacuoles
Naked eyes: The organs are enlarged, soft, yellowish, and greasy.
Prevalent sites: liver cells, cardiomyocytes, renal tubular epithelial cells, skeletal muscle cells
hyaline degeneration
connective tissue hyaline degeneration
Aging of collagen fibers > atrophied uterine and breast stroma, scar tissue, atherosclerosis and necrosis
hyaline degeneration of blood vessel wall
Seen in benign hypertension and diabetes
Occurs in arterioles
intracellular hyaline degeneration
Mallory bodies: alcohol>hepatocytes>prokeratin (intermediate filament protein aggregates)
Russell bodies: accumulation of immunoglobulins in the rough endoplasmic reticulum of plasma cells (immunoglobulin aggregation)
Renal proximal tubule epithelial cells: formed by the fusion of reabsorbed protein in the original urine and lysosomes
Definition: Homogeneous red staining, translucent, protein aggregation
Myxoid degeneration (extracellular)
Definition: Myxoid (proteins and mucopolysaccharides) appear in the interstitium
Naked eye: jelly-like
Under the microscope: Myxoid is light blue, starburst-shaped fibroblasts
Found in: Hypothyroidism, rheumatism, atherosclerosis, mesenchymal tumors
Amyloidosis (extracellular)
Light microscope: homogeneous, light red staining
Color reaction: Congo red stains to orange-red, when exposed to iodine, it becomes tan, and when dilute sulfuric acid is added, it becomes blue.
Definition: Amyloid (protein and mucopolysaccharide complex) appears in the intercellular matrix, under the basement membrane of small blood vessels, and in the reticular fibrous scaffold.
intracellular glycogen deposition
pathological pigmentation
Charcoal powder
melanin
lipofuscin
hemosiderin
Normal: Liver, spleen, lymph nodes, bone marrow
Pathology: congestion area, hemorrhage area, hemolysis area (Lobar pneumonia coughs rust-colored sputum)
pathological calcification
dystrophic calcification
Localization, calcium salt deposition in areas of degeneration, necrosis or foreign matter
Normal levels of calcium and phosphorus in the blood
metastatic calcification
Systemic, deposited in normal parts (lung, kidney, gastric interstitium)
Increased levels of calcium or calcium and phosphorus in the blood (occurs in hyperparathyroidism, excessive vitamin D intake, kidney failure, bone tumors, etc.)
irreversible damage
Unexpected cell death (necrosis)
Morphological changes
Nuclear pyknosis, nuclear fragmentation, and nuclear lysis (signs of necrosis)
Enhanced eosinophilic staining
Type of necrosis
coagulative necrosis
Features: The organizational structure outline can be maintained for a long time
Prevalent parts: heart, liver, spleen, kidney
Special type: caseous necrosis (completely disorganized outline of necrosis)
liquefaction necrosis
Example: Encephalomalacia, pus, lysis and necrosis (viral hepatitis > hepatocellular edema)
Special type: fat necrosis
enzymatic fat necrosis
acute necrotizing pancreatitis
Traumatic fat necrosis
Breast trauma
Macrophages>Foreign body giant cells>Foreign body granuloma
fibrinoid necrosis
necrotic tissue fibrous-like material
Site: Connective tissue, blood vessel wall
Found in: Allergic diseases, malignant hypertension Arteriole walls, arterioles at the base of gastric ulcers
gangrene
Concept: Large scope of necrosis (relative to organs) Infection by putrefactive bacteria, showing special color
dry gangrene
Occurs on the body surface (especially at the end of the lower limbs) Arterial obstruction, venous return unblocked
Black, clear boundary, mild poisoning
wet gangrene
Occurs in internal organs connected to the outside world (lungs, intestines, uterus, appendix and gallbladder) Arterial occlusion and venous return disorder (can also occur in limbs with arterial occlusion and venous return obstruction)
Black, dark green, strong odor, heavy poisoning, unclear boundaries
gas gangrene
Severe open trauma deep into the muscle
Rapid development with serious consequences
Necrotic ending
Dissolve and absorb
Separate discharge
Mechanization
Fiber encrustation and calcification (dystrophic calcification)
Regulated cell death (apoptosis)
significance
Morphological changes
Apoptotic cells separate from surrounding normal cells
The cytoplasm is concentrated, deeply stained, and the organelles are densely packed
Nuclear pyknosis, chromatin edge clustering
Apoptotic body formation
mechanism of apoptosis
The difference between necrosis and apoptosis
Apoptotic cell membranes and organelle membranes are intact Necrotic cells autolysis, cell membrane and organelle membrane rupture
Apoptosis does not cause inflammatory response Necrosis causes inflammatory response, repair response
The active process of apoptosis consumes energy and requires the synthesis of new proteins. The passive process of necrosis consumes no energy and no new protein synthesis.
genetically controlled programmed death Death of a single or small number of cells
autophagy
aging
Adipose tissue (triglycerides)
glycerin
fatty acids calcium
calcium soap
Decomposed by pancreatic enzymes
Cardiomyocytes, nerve cells, and skeletal muscle cells can only undergo hypertrophy Hypertrophy and hyperplasia of other cells often occur simultaneously
Lipofuscin: phospholipid-rich membrane-coated organelle residues in cells that have not been completely digested