MindMap Gallery Chapter 1 Adaptation and Injury of Cells and Tissue
This is a mind map about the adaptation and damage of cells and tissues in Chapter 1. The main contents include: Section 4 Cell Death, Section 3 Cell Reversible Injury, Section 2 Causes and Mechanisms of Cell and Tissue Injury, Section 1 Adaptation.
Edited at 2025-01-05 20:53:43Rumi: 10 dimensions of spiritual awakening. When you stop looking for yourself, you will find the entire universe because what you are looking for is also looking for you. Anything you do persevere every day can open a door to the depths of your spirit. In silence, I slipped into the secret realm, and I enjoyed everything to observe the magic around me, and didn't make any noise. Why do you like to crawl when you are born with wings? The soul has its own ears and can hear things that the mind cannot understand. Seek inward for the answer to everything, everything in the universe is in you. Lovers do not end up meeting somewhere, and there is no parting in this world. A wound is where light enters your heart.
Chronic heart failure is not just a problem of the speed of heart rate! It is caused by the decrease in myocardial contraction and diastolic function, which leads to insufficient cardiac output, which in turn causes congestion in the pulmonary circulation and congestion in the systemic circulation. From causes, inducement to compensation mechanisms, the pathophysiological processes of heart failure are complex and diverse. By controlling edema, reducing the heart's front and afterload, improving cardiac comfort function, and preventing and treating basic causes, we can effectively respond to this challenge. Only by understanding the mechanisms and clinical manifestations of heart failure and mastering prevention and treatment strategies can we better protect heart health.
Ischemia-reperfusion injury is a phenomenon that cellular function and metabolic disorders and structural damage will worsen after organs or tissues restore blood supply. Its main mechanisms include increased free radical generation, calcium overload, and the role of microvascular and leukocytes. The heart and brain are common damaged organs, manifested as changes in myocardial metabolism and ultrastructural changes, decreased cardiac function, etc. Prevention and control measures include removing free radicals, reducing calcium overload, improving metabolism and controlling reperfusion conditions, such as low sodium, low temperature, low pressure, etc. Understanding these mechanisms can help develop effective treatment options and alleviate ischemic injury.
Rumi: 10 dimensions of spiritual awakening. When you stop looking for yourself, you will find the entire universe because what you are looking for is also looking for you. Anything you do persevere every day can open a door to the depths of your spirit. In silence, I slipped into the secret realm, and I enjoyed everything to observe the magic around me, and didn't make any noise. Why do you like to crawl when you are born with wings? The soul has its own ears and can hear things that the mind cannot understand. Seek inward for the answer to everything, everything in the universe is in you. Lovers do not end up meeting somewhere, and there is no parting in this world. A wound is where light enters your heart.
Chronic heart failure is not just a problem of the speed of heart rate! It is caused by the decrease in myocardial contraction and diastolic function, which leads to insufficient cardiac output, which in turn causes congestion in the pulmonary circulation and congestion in the systemic circulation. From causes, inducement to compensation mechanisms, the pathophysiological processes of heart failure are complex and diverse. By controlling edema, reducing the heart's front and afterload, improving cardiac comfort function, and preventing and treating basic causes, we can effectively respond to this challenge. Only by understanding the mechanisms and clinical manifestations of heart failure and mastering prevention and treatment strategies can we better protect heart health.
Ischemia-reperfusion injury is a phenomenon that cellular function and metabolic disorders and structural damage will worsen after organs or tissues restore blood supply. Its main mechanisms include increased free radical generation, calcium overload, and the role of microvascular and leukocytes. The heart and brain are common damaged organs, manifested as changes in myocardial metabolism and ultrastructural changes, decreased cardiac function, etc. Prevention and control measures include removing free radicals, reducing calcium overload, improving metabolism and controlling reperfusion conditions, such as low sodium, low temperature, low pressure, etc. Understanding these mechanisms can help develop effective treatment options and alleviate ischemic injury.
Chapter 1 Adaptation and Injury of Cells and Tissue
Section 1 Adaptation
No damage Injury answer answer opposite answer
一、 Shrinkage
Concept: A decrease in the volume of a normally developed cell tissue or organ may be accompanied by a decrease in the number of parenchymal cells
type
Physiological
Thymus atrophy during puberty and reproductive system after menopause
Pathological
Malnutrition, compression, disabling, denervative, endocrine, aging and damaging
Pathological changes
naked eyes
Reduced volume, weight loss, darker color → reduced metabolic function
Electron microscope
Light Mirror
二、 Hypertrophy
The essence of pseudo-hypertrophy is "atrophy"
Myocardium, skeletal muscle, nerve cells, only hypertrophy but not hyperplasia
concept
Parenchymal cell volume enlargement
type
Physiological
Compensatory
Fitness, muscle hypertrophy
Endocrine
During pregnancy, uterine smooth muscle hypertrophy
Pathological
Compensatory
Hypertension, left ventricular myocardial hypertrophy
One side of nephrectomy, the opposite side of kidney hypertrophy
Endocrine
Hyperthyroidism, hypertrophy of thyroid follicular epithelial cells
Pituitary basophil adenoma, adrenocortical hypertrophy
Pathological changes
Enlarged cell size, large nucleus and deep staining
三、 Hyperplasia
concept
Increased number of parenchymal cells
type
Physiological
Compensatory
High altitude hypoxia, increasing number of red blood cells
Endocrine
Menstrual cycle, endometrial gland hyperplasia
Pathological
Compensatory
Tissue damage, chronic inflammation
Endocrine
Estrogen↑, endometrial gland hyperplasia, functional uterine bleeding
四、 Transformation
concept
The process in which one differentiated mature cell type is replaced by another differentiated mature cell type
type
Metagenesis of epithelial tissue (reversible)
Metagenesis of scaly epithelium
Metagenesis of columnar epithelium
Metagenesis of mesenchymal tissue (irreversible)
Mesenchymal cells → cartilage or bone tissue (cartilage or ossicogenesis)
Section 2 Causes and mechanisms of cell and tissue damage
Causes of cell and tissue damage
Biological factors—the most common cause
Mechanisms of cell and tissue damage
1. Damage to the cell membrane
Characteristics of irreversible cell damage—serious disorder of membrane function and inability to recover mitochondrial membrane function
Myelin-like structure—the cell membrane and organelle membrane are spiral or concentric circle-like curled
2. Mitochondria damage—an important early marker of irreversible cell damage
Amorphous dense body containing calcium
3. Damage to reactive oxygen species
4. Damage to free calcium in the cytoplasm
Intracellular calcium overload
5. Ischemia and hypoxia damage
6. Chemical damage
7. Genetic Variation
Section 3 Cell reversible damage
Cell edema (hydrodenosis)
First appeared
Good hair parts
Liver, kidney, heart
mechanism
Hypoxia, infection, poisoning → mitochondria damage, ATP↓→ sodium and potassium pump dysfunction → Na accumulation, a large amount of water enters the cells
Pathological changes
naked eyes
Swelling, pale, turbid (turbid and swelling)
Under the mirror
Swelling of mitochondria, endoplasmic reticulum, etc. → red-stained fine particles
Cavoid, balloon-like
Fat transformation
concept
Triglycerides accumulate in the cytoplasm of non-adipocytes
Good hair parts
Hepatocytes, cardiomyocytes, skeletal muscle cells, and tubular epithelial cells
Pathological changes
naked eyes
Increased volume, light yellow, round edges, greasy sections
Light Mirror
The nucleus is squeezed to one side, and the vacuoles of varying sizes in the cell Sudan III and IV→Orange red Osmium acid→Black
type
Hepatocytes (most commonly occur) - fatty liver - cirrhosis, liver necrosis
Myocardium (left subventricular and papillary muscles) - yellow-red markings - tabby heart
Myocardial fat infiltration-fat heart (non-steat degeneration)
Glass-like change (transparent change)
Pathological changes
1. Intracellular glass-like transformation
a. Reabsorption of renal tubular epithelial cells → glass-like droplets
b. The crude endoplasmic reticulum of plasma cells → immunoglobulin accumulation, Rusell body
c. Alcohol → Hepatocytes → Prokeratin → Mallory body
2. Connective tissue glass-like
The manifestation of collagen fiber aging
Collagen cross-linking, denature, fusion
Common in
The organizing of scar tissue and necrotic tissue
3. Glassy-like transformation of fine artery walls (fine arteriosclerosis)
Common in
Slow-prone hypertension, diabetic arteries of kidney, brain, and spleen
Amyloidosis
Pathological changes
Light red homogeneous
Color reaction
Congo red dye - orange red, iodine-orange brown, dilute sulfuric acid-blue
Mucus-like change
Pathological changes
Multiprotruding astral fibroblasts scattered in gray-blue mucus matrix
Pathological pigmentation
Exogenous pigments
Carbon dust inhaled in the lungs and pigments injected into the tattoo
Endogenous pigment
Contains hemosiderin (Prussian blue → blue), lipofuscin, melanin, bilirubin, etc.
Pathological calcification
type
Malnutrition – normal calcium and phosphorus metabolism in the body
Metastatic calcification—systemic calcium and phosphorus metabolism disorder
Good hair: lungs, kidneys and stomach (with carbonic anhydrase)
Section 4 Cell Death
Necrosis
Basic lesions
Nucleus: nuclear consolidation, nuclear fragmentation, nuclear lysis
type
Coagulant necrosis – the most common necrosis
Good hair: heart, liver, spleen and kidney
Gray yellow, dry, solid
Clear boundaries with healthy organizations
Liquefied necrosis
Example: Bacterial and fungal infection cause abscess, brain softening
There are few proteins that can coagulate; neutrophils infiltrate, releasing a large number of lyses enzymes
Cellulose-like necrosis
Frequently developed areas: connective tissue and small blood vessel walls Commonly found in: some allergic diseases, acute hypertension
Special types
Coffeelike necrosis – coagulated necrosis
Tuberculosis, many lipids, yellow
No residual image of the original organizational structure
Fat necrosis – liquefied necrosis
Fatty acid Ca2 → Off-white calcium soap
type
Enzymatic fat necrosis-acute pancreatitis
Traumatic fat necrosis – breast trauma
gangrene
Large necrosis range, spoilage bacteria infection, special color
Dry gangrene - coagulated necrosis
Artery occlusion and venous parenchyma
Black, clear boundaries
Corruption changes lightly
Wet gangrene - liquefied necrosis, coagulated necrosis
Internal organs that are connected to the outside world - lungs, gallbladder, intestine, appendix, uterus
Much moisture, blue-green, unclear boundaries with surrounding tissues
Gas gangrene - Wet gangrene
Open trauma, Bacillus perfringens, produces a large amount of gas
ending
1. Dissolution and absorption
2. Separation and discharge
Erosion (shallower), ulcer (deeper), sinus tract (opening in the skin), fistula (connecting two internal organs), holes
3. Mechanization and parcel
4. Calcification
Apoptosis
Morphological characteristics
Apoptotic bodies
Viral hepatitis-hepatocytes-eosinophils
mechanism
Genes that promote apoptosis—Bad, Bax, p53
Apoptosis inhibition gene—Bcl-2
The difference between apoptosis and necrosis
Floating theme