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MindMap Gallery Pathology Chapter 1 Adaptation and Damage of Cells and Tissues Mind Map
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Pathology Chapter 1 Adaptation and Damage of Cells and Tissues Mind Map
Pathology Chapter 1: Adaptation and Damage of Cells and Tissues Mind Map, with a detailed introduction and comprehensive description. I hope it can help interested friends learn.
Edited at 2023-11-25 17:09:47
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Pathology Chapter 1 Adaptation and Damage of Cells and Tissues Mind Map
- bacteria
This is a mind map about bacteria, and its main contents include: overview, morphology, types, structure, reproduction, distribution, application, and expansion. The summary is comprehensive and meticulous, suitable as review materials.
- Plant asexual reproduction
This is a mind map about plant asexual reproduction, and its main contents include: concept, spore reproduction, vegetative reproduction, tissue culture, and buds. The summary is comprehensive and meticulous, suitable as review materials.
- Reproductive development of animals
This is a mind map about the reproductive development of animals, and its main contents include: insects, frogs, birds, sexual reproduction, and asexual reproduction. The summary is comprehensive and meticulous, suitable as review materials.
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- Outline
Cell and tissue adaptation and damage
adapt
shrink
concept
Reduced size of parenchymal cells, tissues, or organs that have developed normally
type
Physiological atrophy
Thymic atrophy during puberty
Postmenopausal atrophy of ovaries, uterus, and testicles
pathological atrophy
dystrophic atrophy
systemic dystrophic atrophy
Cachexia
localized dystrophic atrophy
Brain atrophy
compressive atrophy
hydrocephalus
apraxia of atrophy
Lying still for a long time causes muscle atrophy in the affected limb, which can be restored by returning to normal activities.
denervation atrophy
polio
endocrine atrophy
Ischemic necrosis of the hypothalamus-adenopituitary gland, resulting in reduced release of adrenocorticosteroids and adrenal cortex atrophy
Anterior pituitary hypofunction, thyroid, adrenal gland, gonad atrophy
Estrogen therapy shrinks prostate cancer cells
aging and damage atrophy
Gastric mucosal atrophy in chronic gastritis
Atrophy of small intestinal mucosal villi in chronic enteritis
atrophy caused by chronic inflammation
Massive nerve cell apoptosis causes brain shrinkage, Alzheimer's disease
atrophy due to apoptosis
Pathological changes
Reduced volume, lighter weight, darker color
Lipofuscin granules appear
cardiomyocytes, liver cells
Protein synthesis is reduced, decomposition is increased, and cell organelles are massively degraded
Decreased functionality
Pseudohypertrophy: When parenchymal cells atrophy, interstitial fibrous tissue and adipose tissue proliferate.
ending
recover
apoptosis
Fat
concept
Due to increased functions and strong anabolism, the size of cells, tissues, and organs increases
type
physiological hypertrophy
compensatory hypertrophy
Organ or tissue function complex is overweight
Upper limb skeletal muscle hypertrophy in weightlifters
endocrine hypertrophy
Too many endocrine hormones acting on effectors
Uterine smooth muscle hypertrophy during pregnancy
pathological hypertrophy
compensatory hypertrophy
Hypertension or partial left ventricular myocardial necrosis occurs when healthy myocardial function compensates, causing left ventricular myocardial hypertrophy.
Removal of one kidney or occlusion of one renal artery, loss of renal function, and hypertrophy of the contralateral kidney
endocrine hypertrophy
Hyperthyroidism causes thyroid follicular epithelial hypertrophy
Pituitary basophiloma increases adrenotropic hormone secretion, leading to adrenocortical cell hypertrophy
Pathological changes
Increased size, enlarged and darkly stained nuclei
DNA content and the number of organelles increase, structural protein synthesis is active, and cell functions are enhanced.
ending
Loss of compensation
hyperplasia
concept
The phenomenon of active cell mitosis leading to an increase in the number of cells in a tissue or organ
type
physiological hyperplasia
compensatory hyperplasia
Residual hepatocyte proliferation after liver resection
Compensatory increase in bone marrow red blood cell precursor cells and peripheral blood red blood cells when oxygen content is low
endocrine hyperplasia
Breast lobular gland epithelial hyperplasia in adolescent girls
Endometrial gland hyperplasia during menstrual cycle
Pathological hyperplasia
compensatory hyperplasia
During wound healing, fibroblasts and capillary endothelial cells proliferate
In chronic inflammation, the cells covering the skin and certain organs proliferate.
endocrine hyperplasia
Increased estrogen causes functional uterine bleeding
Pathological changes
The number of cells increased, and the morphology of cells and nuclei was normal or slightly enlarged.
Diffuse enlargement or formation of hyperplastic nodules
Evolves into neoplastic growth when out of control
Metaplasia
concept
One mature cell type is replaced by another mature cell type
Not caused by direct transformation of original mature cells
type
metaplasia of epithelial tissue
metaplasia of squamous epithelium
Smokers' bronchial pseudostratified ciliated columnar epithelium is prone to squamous metaplasia
columnar metaplasia
In chronic gastritis, gastric mucosal epithelial cells transform into small intestinal or large intestinal mucosal epithelial tissue containing Panette cells or goblet cells.
intestinal metaplasia
The glands in the gastric antrum and body of the stomach are replaced by pyloric glands, which is pseudopyloric gland metaplasia.
In chronic reflux esophagitis, the squamous epithelium of the lower esophagus metaplasates into gastric or intestinal columnar epithelium.
Chronic cervicitis, cervical squamous epithelial metaplasia into cervical mucosal columnar epithelium, resulting in cervical erosion
Metaplasia of mesenchymal tissue
Fibroblasts transform into bone or cartilage cells after injury
bone or cartilage metaplasia
significance
Strengthen local ability to resist external stimulation
lose original function
Cause malignant transformation of cells
Causes and mechanisms of injury
reason
hypoxia
cardiorespiratory failure
anemia
CO poisoning
biological factors
Pathogens
physical factors
chemical factors
nutritional imbalance
endocrine factors
immune factors
genetic defect
social psychological factors
mechanism
cell membrane damage
The key link in early irreversible damage of cells
mitochondrial damage
An important early sign of irreversible cell damage
Reactive oxygen species (AOS) damage
Basic steps of cell damage
Intracellular free calcium damage
Many factors damage the terminal links of cells
Potential mediators of cell death
Ischemia and hypoxic injury
Ischemia: Insufficient arterial blood supply to local cells and tissues (more severe damage)
Hypoxia: Cells cannot get enough oxygen or oxygen utilization is impaired
Mild transient hypoxia, cell edema, and fatty degeneration
Mild sustained hypoxia, cell apoptosis
Severe and persistent hypoxia, cell necrosis
ischemia reperfusion injury
The most common and important central link in cell damage
chemical damage
Genetic Variation
Irreversible damage (death)
Necrosis
concept
Cell death in local tissues in vivo characterized by changes in enzyme solubility
The basic manifestations are cell swelling, organelle disintegration, and protein denaturation.
Involves multiple cells
Basic lesions
changes in cell nuclei
nuclear pyknosis
nuclear fragmentation
nuclear lysis
cytoplasmic changes
Increased eosinophilia
Mitochondrial endoplasmic reticulum swells to form vacuoles
Amorphous calcium dense accumulation in mitochondrial matrix
Lysosomes release acid hydrolase
interstitial changes
Injury occurs later than parenchymal cells
The extracellular matrix disintegrates and liquefies, and finally fuses into a sheet-like fuzzy structureless material
type
coagulative necrosis
The protein is denatured and coagulated, the action of lysosomal hydrolase is weak, and the necrotic area appears gray-yellow, dry, and solid.
Commonly found in the heart, liver, kidney, and spleen, caused by ischemia and hypoxia, bacterial toxins, and chemical corrosives
There is a clear boundary with healthy tissue, forming a zone of congestion, hemorrhage and inflammatory reaction.
liquefaction necrosis
There is little protein that can be coagulated, or it may be digested and decomposed by hydrolase.
Common in brain (encephalomalacia), pancreas
fibrinoid necrosis
Is a common form of necrosis of connective tissue and small blood vessel walls
Structureless material in the form of filaments, granules or small strips
Commonly seen in rheumatism, polyarteritis nodosa, crescentic glomerulonephritis, rapidly progressive hypertension, and small blood vessels at the base of gastric ulcers
caseous necrosis
It is a special type of coagulative necrosis with more complete necrosis.
More common in tuberculosis
The necrotic area is yellow and looks like cheese
fat necrosis
Is a special type of liquefaction necrosis
gangrene
concept
Massive necrosis of local tissue and secondary infection by putrefactive bacteria
type
dry gangrene
Ends of limbs with blocked arterial blood but smooth venous return
Necrotic tissue appears black
Clear boundary with normal tissue, mild systemic poisoning reaction
Mostly coagulative necrosis
wet gangrene
Limbs with blocked internal organs or arteries and blocked venous return to the outside world
Necrotic tissue is blue-gray
unclear boundaries with normal tissue
gas gangrene
Is a special type of wet gangrene
Open wounds that reach deep into the muscle, combined with infection by anaerobic bacteria such as Clostridium perfringens
A large amount of gas is produced, and there is a twirling sensation in the necrotic area
Symptoms of systemic poisoning are severe, mostly a mixture of coagulative necrosis and liquefaction necrosis
ending
Dissolve and absorb
Separate discharge
erosion, ulcer
Fistula, sinus tract
Hollow
Mechanization and packaging
Organization: the process in which new granulation tissue grows into and replaces necrotic tissue, thrombus, pus and foreign bodies, etc.
Encapsulation: When the necrotic tissue is too large, it is difficult for the granulation tissue to completely grow or absorb into the center, and it is surrounded by the surrounding hyperplasia of granulation tissue.
fibrous scar formation
Calcification
can cause dystrophic calcification
apoptosis
Programmed death of single cells, active
feature
Morphological characteristics
cell shrinkage
chromatin condensation
shrinkage
Bianji
shatter
Apoptotic body formation
hallmarks of apoptosis
Plasma membrane intact
biochemical characteristics
apoptotic protease
Endonuclease
The main executor of apoptosis
Calpain required
mechanism
Signaling
Central control
Initial stage
structural change
Execution phase
disease
Eosinophilic bodies in liver cells during viral hepatitis
Insufficient apoptosis
tumor
autoimmune disease
Excessive apoptosis
neurodegenerative diseases
Alzheimer's disease
Parkinson's Disease
Huntington's disease
ischemic injury
infected cells
Reversible damage (degeneration)
Cellular edema (water degeneration)
The earliest changes in cell damage
mechanism
Mitochondria are damaged, ATP production is reduced, sodium-potassium pump dysfunction occurs, sodium ions accumulate, and water molecules enter the cell. Metabolites accumulate, the osmotic load increases, and edema worsens.
Commonly found in parenchymal cells of liver, kidney, heart and other organs during ischemia, hypoxia, infection, and poisoning
Pathological changes
Naked eyes: Increased volume, tight capsule, and lighter color
under the mirror
Light: cytoplasmic red-stained granules
Middle: loosening of cytoplasm
Heavy: balloon-like change
Electron microscope: mitochondria and endoplasmic reticulum swelling
fatty change
mechanism
Triglycerides accumulate in the cytoplasm of non-adipocytes
Occurs mostly in liver cells, cardiomyocytes, renal tubular epithelial cells, and skeletal muscle cells
The mechanism of hepatocellular steatosis
Increased intracellular fatty acids
Too much triglyceride synthesis
Decreased lipoprotein M apolipoprotein
Pathological changes
fatty liver
Tabby heart
Myocardial fatty infiltration
hyalinization
mechanism
Protein accumulation, HE staining showed eosinophilic homogeneity
Pathological changes
intracellular hyalinization
Hyaline bodies (reabsorptive proteins) in renal tubular epithelial cells
Russell bodies (immunoglobulins) in plasma cells
Mallory bodies (intermediate filament prokeratin) in alcoholic liver disease
Inclusion bodies (microtubule-associated proteins) in Alzheimer's disease
Hyalinization of fibrous connective tissue
scar
Hyalinization of small arterial walls
Arteriosclerosis, common in the kidneys, brain, and spleen of high blood pressure
Thickening and hardening of blood vessel walls, narrowing of the lumen, or nasal congestion
The elasticity of the blood vessel wall decreases, the fragility increases, and it is easy to rupture and bleed.
slowly progressive hypertension
amyloidosis
concept
Accumulation of amyloid protein and mucopolysaccharide complexes in the cytoplasm
amyloid color reaction
Congo red stains orange
It turns brown when exposed to iodine, and turns blue when dilute sulfuric acid is added.
Myxoid change
Mucopolysaccharide and protein accumulation
pathological pigmentation
hemosiderin
Ferritin particle aggregates formed after red blood cell hemoglobin is phagocytized and degraded by macrophages
Under the microscope, it looks like golden yellow or brown particles, which can be dyed blue by Prussian blue.
Indicates red blood cell destruction and systemic or localized iron-containing excess
lipofuscin
Autophagy of undigested organelle fragments in lysosomes
Phospholipids and proteins
Normally, epididymal duct epithelial cells, testicular interstitial cells and ganglion cytoplasm may contain
In the elderly and patients with nutritional depletion, atrophic myocardial cells and liver cell nuclei appear
When most cells contain, more pronounced organ failure accompanies
melanin
Bilirubin
The product of aging and destruction of red blood cells
From hemoglobin, does not contain iron
Bilirubin in the blood increases, and the patient develops yellow staining of the skin and mucous membranes
pathological calcification
concept
Deposition of solid calcium salts in tissues other than bone and teeth
It is an accompanying disease of many diseases
type
dystrophic calcification
Calcium salts are deposited in necrotic or imminent necrosis tissue or foreign matter
Normal calcium and phosphorus metabolism
Commonly seen in tuberculosis, blood clots, atherosclerotic plaques, heart valve disease, and scar tissue
metastatic calcification
Systemic calcium and phosphorus metabolism disorders (hypercalcemia)
Calcium salts are deposited in normal tissues
Mainly seen in hyperparathyroidism, excessive vitamin D intake, renal failure and certain tumors
Commonly occurs in blood vessels and interstitial tissues of kidneys, lungs and stomach