Wondershare EdrawMind
MindMap Gallery of cells and tissues
- 56
of cells and tissues
Mind map of adaptation, damage and repair of cells and tissues. Repair of damage: It is accomplished through cell regeneration or proliferation of granulation tissue, including regeneration and fibrous repair.
Edited at 2023-07-27 19:45:11
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of cells and tissues
- 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.
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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, injury and repair
adapt
Hypertrophy: An increase in the size of normally developing cells, tissues, or organs
physiological hypertrophy
Compensatory hypertrophy: The most common cause is high demand and increased load. Such as the thickening and hypertrophy of the skeletal muscles of the upper limbs of weightlifters
Endocrine hypertrophy: hypertrophy caused by endocrine hormones acting on effectors eg: During pregnancy, due to estrogen, progesterone and their effects on receptors, uterine smooth muscle cells increase, accompanied by an increase in cell number; Breast acinar epithelial cell hypertrophy during lactation
pathological hypertrophy
Compensation...the increased workload of tissues and organs causes functional compensatory effects eg: Myocardial hypertrophy caused by increased cardiac afterload in patients with hypertension or valve closure in patients with heart valve disease; Removal of one kidney causes hypertrophy of the other side
Endocrine...eg: acromegaly caused by excessive secretion of growth hormone in pituitary oncocytoma
Note: ① Hypertrophy of tissues or organs is usually caused by an increase in the size of parenchymal cells, and also an increase in the number of parenchymal cells. ② Uterus and breast cells can both hypertrophy and proliferate, but cardiomyocytes can only hypertrophy but not proliferate, because cardiomyocytes cannot divide.
Atrophy: A normally developing tissue or organ with reduced size of its parenchymal cells
Physiological eg: thymus atrophy in adolescence, ovary, uterus and testicle atrophy in menopause
pathological
Dystrophic atrophy: first is fat atrophy, followed by muscle and visceral atrophy, and finally brain and heart atrophy. For example, atherosclerosis narrows arterial tubes and reduces blood supply, causing atrophy.
Compressive atrophy such as urinary tract stones causing hydronephrosis, resulting in compressive atrophy of the renal parenchyma. Hydrocephalus compresses brain tissue, causing brain atrophy and organ enlargement
Disuse atrophy, such as long-term bed rest, long-term immobilization of limbs after fracture, etc., causing muscle atrophy of the affected limb
In patients with denervation atrophy, such as in patients with poliomyelitis, damage to the motor neurons in the anterior horn of the spinal cord leads to atrophy of the muscles they control.
endocrine atrophy
Pathological changes: The original cell morphology is still maintained, but the cytoplasm is reduced and the nuclear staining becomes darker. To the naked eye, the atrophied organs are reduced in size, weight, and texture.
Note: ① Undevelopment or underdevelopment of tissues and organs does not constitute atrophy. ②Organ volume may also increase after atrophy. For example, after hydronephrosis, the kidney volume increases and the renal cortex becomes thinner. ③Atrophy refers to the reduction in the size of parenchymal cells, which can be accompanied by a reduction in the number of parenchymal cells. ④ Plasma cells may proliferate during atrophy
Hyperplasia: An increase in the number of parenchymal cells in a normally developing tissue or organ is called hyperplasia, which often leads to an increase in the size and active function of the tissue or organ.
Physiological
Compensatory eg: residual liver cell proliferation after partial liver resection; The air content in high altitude areas is low, and the body's bone marrow red blood cell precursor cells and peripheral blood red blood cells increase in compensation.
Endocrine eg: hyperplasia of the lobular gland epithelium of normal female adolescent breasts and endometrial glands during the menstrual cycle
pathological
Compensatory eg: proliferation of renal tubular epithelial cells during renal metabolism
Endocrine eg: irregular menstruation, hyperthyroidism, hyperplasia of thyroid follicular epithelial cells, Prostatic hyperplasia in elderly men is endocrine hyperplasia. Reason: The androgen metabolite dihydrotestosterone causes prostatic body and interstitial fibrous tissue hyperplasia.
Note: There is an essential difference between adaptive hyperplasia and neoplastic hyperplasia. Adaptive hyperplasia stops when the stimulus is eliminated, while neoplastic hyperplasia does not stop normally.
Metaplasia: The process by which one mature cell type is replaced by another differentiated cell type Metaplasia is the result of stem cell transdifferentiation. Some metaplasia is a precancerous lesion related to multi-step tumor cell evolution.
metaplasia of epithelial tissue
Squamous metaplasia: most common, often found in the trachea and bronchi
Intestinal metaplasia: gastric mucosal epithelium transforms into intestinal epithelium in chronic atrophic gastritis Can become the basis for the occurrence of gastric adenocarcinoma
Metaplasia of mesenchymal tissue
Note: ① Reduced volume - atrophy; increased volume - hypertrophy + hyperplasia; ② Decrease in number - shrinkage; increase in number - hyperplasia; ③Uterus during pregnancy and breast during lactation - hyperplasia + hypertrophy; breast during adolescence - hyperplasia
damage
Degeneration (reversible damage to cells)
Cellular edema: Excessive accumulation of water and sodium in cells is called cell edema, also known as water degeneration. It is the most common and mild degeneration, and is more likely to occur in organs with strong metabolism and abundant mitochondria. Especially the parenchymal cells of the heart, liver, kidney and other organs.
Cause: Mainly hypoxia, ischemia, infection and poisoning
Pathological changes: It is called turbidity and swelling. Severe liver cell edema, abnormally loose and translucent liver cell cytoplasm, and highly swollen cell bodies like balloons, called ballooning, which is common in viral hepatitis
Note: The cause of accumulation is that normal or abnormal substances are produced too much or too fast, and cell tissues lack corresponding metabolism, clearance or transport mechanisms, causing them to accumulate in the cytoplasm, nucleus, and intercellular substance. After the cause is removed, such injuries as cell edema and fatty degeneration can return to normal, so they are non-fatal and reversible injuries.
Steatosis: Triglycerides accumulate in the cytoplasm of non-adipocytes, which is called steatosis. Under a light microscope, the fat components fuse into lipid droplets. In paraffin sections, lipid droplets appear vacuolated. In frozen sections, fatty components can be stained orange-red by Sudan III. Fatty degeneration occurs mostly in organs with strong metabolism and high oxygen consumption. Such as liver, kidney, heart, etc. Fatty degeneration of liver cells is the most common. Because the liver is the main place of fat metabolism.
Hepatic steatosis: In chronic liver congestion, steatosis occurs first in the central area of the liver lobules, while in poisoning, steatosis occurs first in the peripheral areas of the liver lobules.
Myocardial fatty degeneration: Chronic alcoholism can cause myocardial fatty degeneration, often involving the left ventricular subendometrium and papillary muscles. Fatty degeneration is yellow, arranged alternately with the dark red of normal myocardium, and looks like tiger skin stripes, so it is called "tiger spot heart". Sometimes the extracardiac hyperplasia of fat tissue can extend into the myocardial cells along the interstitium, which is called myocardial fat infiltration. Severe myocardial fatty degeneration infiltration can cause heart rupture and sudden death.
renal steatosis
Hyalinous degeneration, also known as hyaline degeneration, refers to the accumulation of translucent proteins within cells or in the interstitium. HE staining is eosinophilic and homogeneous.
Connective tissue hyaline degeneration: common in hyperplasia of fibrous connective tissue and a manifestation of aging of collagen fibers
Hyalinous degeneration of small arterial walls: common in the walls of small arteries in kidneys, brain, spleen and other organs with slowly progressive hypertension and diabetes
intracellular hyalinization
Myxoid degeneration: common in mesenchymal tumors, rheumatic lesions, and atherosclerotic plaques
pathological pigmentation
Hemosiderin: When left heart failure causes pulmonary congestion, red blood cells emerge from the alveolar space and are engulfed by macrophages to form hemosiderin in the cytoplasm. Macrophages with hemosiderin in their cytoplasm are called heart failure cells.
Bilirubin: When there is too much bilirubin in the blood, the tissue will be stained yellow, which is called jaundice.
melanin
lipofuscin
Pathological calcification: Normally, only bones and teeth contain solid calcium salts. In addition, there are deposits of solid calcium salts, which are called pathological calcium salts. The deposited calcium salt is mainly calcium carbonate of calcium phosphate.
dystrophic calcification
metastatic calcification
Note: ① Atherosclerosis is hyaline degeneration of connective tissue; ② Slowly progressive hypertension is hyaline degeneration of arterial walls; ③Glomerulonephritis is intracellular hyaline degeneration
cell death
Necrosis
Pathological changes: changes in cell nuclei are the main morphological signs of cell necrosis After necrosis, the cytoplasm appears dark red and granular due to coagulation or dissolution. The stroma appears as red-stained granular structureless material.
Nuclear pyknosis: dehydration of the nucleus condenses the chromatin, darkens the staining, and reduces the size of the nucleus.
Nuclear fragmentation: The nuclear chromatin is disintegrated into small fragments, the nuclear membrane is fragmented, and the chromatin fragments are dispersed in the cytoplasm.
Nucleolysis: chromatin DNA is decomposed, and the cell nucleus loses its affinity for basic dyes, so the chromatin becomes pale and only the outline of the nucleus can be seen. Finally, the remaining proteins in the chromatin are dissolved by proteases
type
Coagulative necrosis: necrotic tissue dries out due to water loss and protein coagulation, turning into a gray-white or gray-yellow relatively dry solid. It is more common in ischemic necrosis of solid organs such as the heart, liver, spleen, and kidneys. Hepatocytes often undergo coagulation necrosis, liquefaction necrosis may also occur, and eosinophilic bodies may appear (essentially apoptosis).
Caseous necrosis: It is a special type of coagulative necrosis, mainly seen in tuberculosis. The necrotic tissue completely disintegrates and appears as red-stained particles without structure under the microscope. The tissue outline disappears and the boundary with healthy tissue is unclear. Because the necrotic tissue has more lipids, it is yellow and cheese-like when it dies, hence its name.
Liquefactive necrosis: Necrotic tissue decomposes and liquefies into a liquid form, which is liquefaction necrosis, which often occurs in the brain and spinal cord. Brain tissue is prone to liquefaction necrosis, mainly because the brain tissue has high lipid content and low protein content, also known as encephalomalacia.
Gangrene: When a large area of tissue necrosis is accompanied by varying degrees of putrefactive bacterial infection, causing the necrotic tissue to turn dark brown, dirty green and other special morphological changes, it is called gangrene.
Dry gangrene: mostly occurs at the ends of the limbs. At this time, the arteries are blocked but the veins are still open, and there is a clear dividing line with the surrounding healthy tissue.
Wet gangrene: mostly occurs in internal organs connected to the outside world (such as lungs, intestines, appendix, uterus, gallbladder). It can be seen in limbs and animals with occlusion and venous return blocked. When accompanied by blood stasis and edema. The dividing line between necrotic tissue and healthy tissue is not obvious
Gas gangrene: Mainly seen in open wounds that reach deep into the muscles. When combined with infection by anaerobic bacteria such as Clostridium perfringens, a large amount of gas is produced when the bacteria decompose necrotic tissue, causing the necrotic tissue to contain bubbles in a honeycomb shape with crepitus. .
Note: The liver is prone to ballooning and fatty degeneration; the brain is prone to liquefaction necrosis; the limbs are prone to dry gangrene, and wet gangrene can also occur. Gangrene is less likely to occur in the brain and wet gangrene is less likely to occur in the hands. The most common sites for wet gangrene are the non-(lungs), often (intestines), the uterus, the appendix and the gallbladder.
Fibrinoid necrosis: A type of necrosis that often occurs in connective tissue and small blood vessel walls. Mainly seen in rheumatism, nodular periarteritis, crescentic glomerulonephritis and other allergic diseases, as well as rapidly progressive hypertension and gastric ulcer
Note: hyaline degeneration occurs in slowly progressive hypertension, and fibrinoid necrosis occurs in rapidly progressive hypertension.
ending
Dissolve and absorb
Separation and exclusion: If the necrotic tissue is located in the skin or mucous membrane, the local defect left after the necrotic tissue falls off is called erosion (shallower) or ulcer (deeper) Deep blind tubes formed after tissue necrosis that only open on the surface of the skin and mucosa are called sinus tracts; A channel-like defect with openings at both ends that connects two internal organs or leads from an internal organ to the body surface is called a fistula; Necrotic tissues in internal organs such as kidneys and lungs can be discharged through corresponding natural channels after liquefaction, leaving a cavity called a cavity.
Organization and encapsulation: The process of new granulation tissue growing into and replacing necrotic tissue, thrombus, pus, foreign matter, etc. is called organization.
Calcification
Apoptosis: refers to programmed cell death that occurs during the development process of body cells or under the influence of certain factors, through the regulation of specific genes and their products. It manifests as necrosis of single cells or small focal necrosis, shrinkage of apoptotic cells, no rupture or autolysis of cell membranes and organelle membranes, no acute inflammatory response, and no induction of proliferation and repair of surrounding cells, so it is different from damaging necrosis of cells. . The occurrence of apoptosis is related to gene regulation
Note: necrosis - nuclear pyknosis, apoptosis - nuclear condensation
Damage repair: completed through cell regeneration or granulation tissue proliferation Including regeneration and fibrous repair
Regeneration: After tissue and cell damage, the surrounding healthy cells of the same type divide and proliferate to achieve repair.
type
physiological regeneration
pathological regeneration
Note: ① The formation of false lobules in liver cirrhosis is regeneration ② Complete regeneration can be seen in punctate necrosis of liver cells, recovery of fractures, skin recovery of first-degree burns and shallow second-degree burns
The mechanism and ability of tissue cell regeneration
Unstable cells are also called cells that continue to divide, such as epidermal cells, respiratory and digestive tract epithelial cells, urogenital organ covering epithelium, lymphatic and hematopoietic cells
Stable cells, also known as resting cells, include parenchymal cells of various glands or gland-like organs Such as liver, pancreas, endocrine glands, sweat glands, sebaceous glands, renal tubular epithelial cells and primitive mesenchymal cells
Permanent cells, also known as non-dividing cells, include nerve cells, skeletal muscle cells and cardiomyocytes but do not include nerve fibers.
Note: ① Regenerative ability: Connective tissue cells > Smooth muscle cells > Cardiomyocytes > Nerve cells ②Nerve cells cannot regenerate, but glial cells and nerve fibers can regenerate ③Smooth muscle cells are stable cells, while skeletal muscle cells are permanent cells. ④ Bone tissue has a strong regeneration ability and can be completely regenerated (completely repaired) after a fracture; however, cartilage regeneration ability is poor.
Mechanisms and processes of tissue regeneration
epithelial tissue regeneration
regeneration of coated epithelium
glandular epithelial regeneration
Fibrous tissue regeneration
blood vessel regeneration
Regeneration of nervous tissue: Nerve cells in the brain and spinal cord cannot regenerate after damage. They are repaired by glial cells and their fibers, forming glial scars. If the two severed ends are too far apart (more than 2.0cm), or there is a scar or other tissue barrier between the two ends, or the distal end is lost due to amputation, the regenerated axons will not be able to reach the distal end and will be separated from the proliferated connective tissue. Mixed together, curled into a ball, becoming a traumatic neuroma, clinically intractable pain
NOTE: There are gliomas but not neuronal tumors. Because nerve cells cannot regenerate but glial cells and neurofibrillary cells can regenerate
Fibrous repair: When the surrounding cells regenerate and repair tissue damage caused by various diseases, except that the defect is small and the damaged tissue has strong regeneration ability and can be completely regenerated, most of them are incomplete regeneration, that is, they are filled by granulation tissue. After the defect, the granulation tissue gradually transforms into scar tissue mainly composed of collagen fibers. This repair process is called fibrous repair, also called scar repair.
Granulation tissue: composed of new thin-walled capillaries and proliferated fibroblasts, accompanied by inflammatory cell infiltration. It appears to the naked eye as bright red, granular, soft and moist, and looks like fresh granulation, hence its name.
Function
Anti-infection and wound protection
Organize or encapsulate necrotic tissue, thrombi, inflammatory exudates and other foreign bodies
Fill wounds and other tissue defects
Outcome: The water in the interstitium gradually decreases; inflammatory cells decrease and gradually disappear; some capillary lumens are occluded and the number is reduced, and a few capillary walls are thickened and transformed into arterioles and venules according to normal function requirements; fibroblasts More and more collagen fibers are produced, while the number of fibroblasts gradually decreases, and the nuclei become elongated and deeply stained, turning into fibroblasts. As time goes by, the amount of collagen fibers increases and hyaline degeneration occurs, with fewer cellular components.
Note: ① The formation of granulation tissue is like building a house, which requires water pipes (capillaries), beams (fibroblasts) and security guards (inflammatory cells) ②The main inflammatory cells in granulation tissue are macrophages; ③The cells with contractile function are myofibroblasts; ④The characteristic cells when necrosis becomes organized are fibroblasts ⑤ When granulation tissue transforms into scar tissue, it has the characteristics of “three few” (inflammatory cells, capillaries, and fibroblasts) and “one many” (collagen fibers). ⑥The tensile strength of granulation tissue is limited and it is difficult to maintain the firmness of tissues and organs; scar tissue can maintain the firmness of tissues and organs. ⑦If collagen formation is insufficient or the endurance is large and long-lasting, and the scar lacks elasticity, it can cause scar bulging. Hernias can form in the abdominal wall, and ventricular aneurysms can form in the heart wall.
scar tissue
favorable
Fill and connect damaged wounds or other defects to maintain the integrity of tissues and organs
Maintain organ robustness
unfavorable
scar shrinkage
scarring adhesions
hardening of organs
Excessive scar tissue proliferation
wound healing
skin healing
healing process
Early changes in the wound: The early leukocyte infiltration is mainly neutrophils, and after 3 days, it becomes mainly macrophages.
Wound shrinkage
Granulation tissue proliferation and scarring
Regeneration of epidermis and other tissues
healing type
Primary healing: In 5-7 days, collagen fiber connections appear on both sides of the wound and sufficient tensile strength has been reached (the sutures can be removed at this time); The primary healing time is short and the scar formed is small.
secondary healing
Healing under the scab: Dry scab skin is not conducive to bacterial growth, so it has a certain protective effect on the wound. However, if there is a lot of exudate under the scab, especially if there is a bacterial infection, the scab will become an obstacle to the drainage of the exudate, aggravating the infection and not conducive to healing. At this time, the scab should be peeled off.
fracture healing
Hematoma formation
fibrous callus formation
bony callus formation
Callus reconstruction or reshaping
Factors affecting wound healing
systemic factors
age
Nutrition: Among vitamins, vitamin C is the most important for healing.
Drugs and Hormones
local factors
Infection and foreign bodies: Infected wounds cannot be sutured, and drainage and anti-infective measures should be taken as soon as possible. Only when the infection is controlled can the repair proceed smoothly.
local blood circulation
innervation
ionizing radiation
Factors affecting fracture healing
Timely and correct reduction of the broken end of the fracture: Timely and correct reduction is a necessary condition for complete fracture healing.
The broken end of the fracture is fixed promptly and firmly
Carry out systemic and local functional exercises as soon as possible to maintain good local blood supply