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MindMap Gallery Chapter 2 Adaptation and Damage of Cells and Tissues Mind Map

Chapter 2 Adaptation and Damage of Cells and Tissues Mind Map

Regarding the mind map of Chapter 2: Adaptation and Damage of Cells and Tissues, when an organism is stimulated by the outside world, cells and tissues will undergo corresponding changes to adapt to the new environment. If the stimulation exceeds the tolerance of the organism, it will cause damage to cells and tissues.

Edited at 2023-11-08 16:43:18

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Chapter 2 Adaptation and Damage of Cells and Tissues Mind Map

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Adaptation and damage of cells and tissues

Overview

Adaptation and damage of cells and tissues is a response of organisms to environmental changes or stimuli. When an organism is stimulated by the outside world, cells and tissues will undergo corresponding changes to adapt to the new environment. If the stimulation exceeds the tolerance of the organism, it will cause damage to cells and tissues.

Adaptation of cells and tissues

Overview: When the environment changes, the body's cells, tissues or organs make corresponding changes in their own metabolism, function and structure to avoid damage caused by environmental changes.

shrink

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

(1) Physiological atrophy

When many cells, tissues and organs develop to a certain stage, they gradually Atrophy, this phenomenon is called degeneration eg. Senile atrophy

(2) Pathological atrophy

dystrophic atrophy

eg. cachexia → general muscle atrophy Long-term systemic malnutrition → atrophy of body fat and muscles → atrophy of organs such as heart, brain, liver and kidneys

Ischemic atrophy (localized dystrophic atrophy) : Decreased arterial blood supply causes tissue atrophy in the blood supply area → cerebral atherosclerosis

neurological atrophy

eg. Poliomyelitis: muscle paralysis

apraxia of atrophy

eg. Long-term bed rest → muscle atrophy

compressive atrophy

eg. Hydronephrosis → hydronephrosis, renal cortex thinning

endocrine atrophy

eg. Atrophy of adrenal glands, thyroid, gonads and other organs caused by hypopituitarism

(3) Pathological changes

naked eye observation

The volume becomes smaller, the weight becomes lighter, and the color becomes darker.

Observe under the microscope

The size/number of parenchymal cells decreases; lipofuscin granules may appear in the atrophic cytoplasm of cardiomyocytes and liver cells.

(4) Ending

Reversible disease, which can gradually return to its original state by eliminating the cause

The cause of the disease cannot be eliminated, leading to the disappearance of atrophic cells through apoptosis, resulting in smaller organ size, harder texture, and reduced function.

Shrunken tissue or reduced organ function

Fat

An increase in the size of a cell, tissue, or organ (increased organelles, increased metabolism)

(1) Physiological hypertrophy

(2) Pathological hypertrophy

endocrine hypertrophy

eg. Pituitary tumors cause gigantism

compensatory hypertrophy

eg. Hypertensive heart disease

≠Pseudohypertrophy→parenchymal cell atrophy, interstitial tissue fibrosis, and adipose tissue hyperplasia

hyperplasia

An increase in the number of parenchymal cells causes an increase in the size of tissues and organs

(1) Physiological hypertrophy

hormonal hyperplasia

Pathological hyperplasia

Commonly caused by increased hormones

(2) Pathological hyperplasia

Hyperplasia: the cause is eliminated → returns to normal Neoplasia: Growth that persists and develops

Metaplasia

The process of transforming one differentiated organization into another differentiated organization in order to adapt to changes in the environment

transformation process

The differentiation results of undifferentiated cells or stem cells with the ability to divide, proliferate and differentiate into multiple directions

Cell types with more active ability to divide and proliferate

in homologous cells

Certain irritants have long-term effects

(1) Epithelial tissue metaplasia

squamous metaplasia

Benefits: Can enhance local resistance

Disadvantages: Loss of original epithelial function, which may lead to malignant transformation of cells

Intestinal metaplasia

Commonly found in the body or antrum of the stomach

small intestinal metaplasia

large intestinal metaplasia

(2) Mesenchymal tissue metaplasia

Commonly metamorphoses from fibrous connective tissue into bone, cartilage or adipose tissue

Damage to cells and tissues

Overview: After cells and tissues are stimulated by harmful factors that exceed their compensatory capacity, abnormal changes in cell and interstitial material metabolism, histochemistry, ultrastructure, light microscopy and naked eye visible

Cause of injury

Hypoxia (systemic, local), physical factors, chemical factors, biological factors, immune response, genetic factors, nutritional disorders

damage mechanism

Mainly reflected in ATP depletion, increase in free radicals, increase in intracellular free calcium, destruction of cell membrane integrity and irreversible mitochondrial damage.

Injury morphological changes

(1) Reversible damage

transsexual

watery denaturation

(1) Concept: refers to the excessive accumulation of water and sodium ions in cells, also known as water degeneration, which is the most common early degeneration of cell damage.

(2) Mainly occurs in cells with strong metabolism and abundant mitochondria, and is more common in cells of the heart, liver, kidney and other organs.

(3) Pathological changes

Under a light microscope → the cell volume becomes larger, the moisture in the cytoplasm increases, the cells become transparent and lightly stained, and even vacuoles appear.

ballooning degeneration

(4) Summary: Cell edema (turbid swelling) is a reversible injury, but severe cell edema can develop into cell death.

eg. Liver edema

Steatosis/fat deposition

(1) Main ingredients: Neutral fat

(2) Common causes: infection, alcoholism, poisoning, hypoxia, diabetes, obesity, etc.

(3) Prevalent parts: organs with strong metabolism and high oxygen consumption, such as liver, kidney, heart, etc.

hepatic steatosis

Pathological changes: Lipid droplets are dissolved by organic solvents and appear vacuolated. Sudan III staining turns orange-red, and the cell nuclei are squeezed aside.

myocardial fatty degeneration

Most commonly occur in papillary muscles, left ventricle and subendocardial myocardium

"Tabby Heart"

renal steatosis

hyaline degeneration

(1) Homogeneous, translucent glass-like protein accumulation appears in cells or interstitium, which appears as homogeneous red staining in HE-stained sections.

(2) Prevalent sites: connective tissue, blood vessel wall, intracellular

connective tissue hyaline degeneration

Aging of collagen fibers

hyaline degeneration of blood vessel wall

Small arteries that mostly occur in the kidneys, brain, spleen and retina during hypertension

eg. Hyalinous degeneration of splenic arterioles

intracellular hyaline degeneration

Under light microscopy, it appears as round, eosinophilic bodies or masses.

myxoid degeneration

eg. Acute rheumatism, hypothyroidism (hypothyroidism), atherosclerosis

amyloidosis

locality

eg. chronic inflammation

Systemic

intracellular glycogen deposition

pathological pigmentation

pigment

exogenous

Charcoal powder

endogenous

lipofuscin

Yellow-brown particles formed by cells autophagocytosis of organelle fragments in lysosomes that cannot be digested by lysosomal enzymes

Common in the elderly and some chronic wasting diseases

hemosiderin

Golden or brown

pathological significance

Chronic pulmonary congestion → RBCs leaking into the alveolar space are phagocytosed by macrophages and are called heart failure cells.

In the case of old bleeding and hemolytic diseases → hemosiderin accumulation can be seen in tissues such as liver, spleen, lymph nodes and bone marrow.

melanin

pathological calcification

eg. Silicosis

(2) Irreversible damage

cell death

unexpected cell death

(1) Morphological changes of necrosis

nuclear changes

Nuclear pyknosis, nuclear fragmentation, nuclear dissolution

Cytoplasmic changes

interstitial changes

Matrix disintegration, collagen fibers swell, disintegrate, break or liquefy, and finally melt into flaky red-stained structureless material

(2) Type of necrosis

coagulative necrosis

Site of disease: Avascular necrosis commonly seen in the heart, kidneys, spleen and other organs

eg. Renal coagulative necrosis

To the naked eye: there are many and obvious boundaries

View under the microscope: The outline of the organizational structure still exists

liquefied necrosis

eg. Encephalomalacia forming cystic cavity

special type of necrosis

caseous necrosis

More complete coagulative necrosis (no tissue outline visible under the microscope, only some red-stained structureless granular material)

Mainly seen in tuberculosis

gangrene

dry gangrene

It is more common in the distal extremities of diseases such as atherosclerosis, vasculitis obliterans, ischemia, and frostbite.

Arteries are blocked, but venous return remains unobstructed

The lesion is dry and concentrated, dark brown in color

wet gangrene

Frequently occurs in the intestines and lungs

Blockage of arteries and veins (severe infection) → wetness and swelling

gas gangrene

special wet gangrene

Anaerobic infection

There is a "twirling" sound and a "holding snow" feeling when pressed.

fat necrosis

Enzymatic

Common in eg. acute pancreatitis and breast trauma

Traumatic

fibrinoid necrosis

Commonly seen in eg. acute rheumatism, systemic lupus erythematosus, glomerulonephritis, and malignant hypertension.

(3) Necrosis ending

Dissolve and absorb

separate exclusion

Erosion, ulcer, cavity, sinus tract, fistula

Mechanization

encapsulation, calcification

regulated cell death

apoptosis

Features: Does not rupture the plasma membrane, does not cause cell autolysis, and does not cause acute inflammatory reactions.

apoptotic body

Ageing