MindMap Gallery inflammation
Pathology summarizes and organizes knowledge points to help learners understand and remember. Straight to the point, it can be used as study notes and review materials to help you systematically review and consolidate the knowledge you have learned. The knowledge points are systematic and comprehensive. I hope it will be helpful to everyone! Suitable for exam review.
Edited at 2024-10-01 23:36:13這是一篇關於《簡愛》人物關係分析的心智圖,幫助你理解和閱讀這本書,本圖關係梳理清楚,非常實用,值得收藏!
This is a mind map about the analysis of the character relationships in "Jane Eyre" to help you understand and read this book. The relationships in this map are clearly sorted out. It is very practical and worth collecting!
An outline of the knowledge points of air and oxygen in Chemistry, including the production of oxygen, catalysts, and reactions. This mind map will help you become familiar with the key points of knowledge and enhance your memory. Students in need can save it.
這是一篇關於《簡愛》人物關係分析的心智圖,幫助你理解和閱讀這本書,本圖關係梳理清楚,非常實用,值得收藏!
This is a mind map about the analysis of the character relationships in "Jane Eyre" to help you understand and read this book. The relationships in this map are clearly sorted out. It is very practical and worth collecting!
An outline of the knowledge points of air and oxygen in Chemistry, including the production of oxygen, catalysts, and reactions. This mind map will help you become familiar with the key points of knowledge and enhance your memory. Students in need can save it.
inflammationinflammation
Overview
concept
A defense-based response of living tissue with a vascular system to damage caused by inflammatory factors
Vascular reaction refers to the process of appropriate relaxation of blood vessels to increase local blood supply and increase vascular permeability under the stimulation of injury factors, allowing blood components to leak into local tissues.
reason
biological pro-inflammatory factors
most common
causing inflammation called infection
Among them, Salmonella typhi can cause a decrease in the number of white blood cells in peripheral blood.
physical inflammatory factors
chemical inflammatory factors
endogenous gastric acid
immune response
Cause allergic reactions and inflammation
necrotic tissue
Such as fresh infarct edge congestion and hemorrhagic zone
foreign body
Surgical suture, silicon dioxide
Basic pathological changes
metamorphosis
Inflammation refers to degeneration and necrosis of local tissue cells
parenchymal cells
Cellular edema
fatty change
Coagulation and liquefaction necrosis
interstitium
Myxoid change
fibrinoid necrosis
oozingexudation
concept
inflammatory exudation
The process by which body fluid components, cellulose and other proteins and various leukocytes in the blood vessels of local tissues of inflammation enter the tissue space, body cavity, body surface and mucosal surface through the blood vessel wall.
exudateexudate
The fluid and cells that leak out are caused by the increased permeability of the blood vessel wall.
Transudate
Under certain non-inflammatory conditions, increased hydrostatic pressure within the blood vessels causes fluid to move out of the blood vessels, called transudate, with fewer cells and proteins
effusionhydrops
Exudate accumulates in the interstitium of tissues, causing edema, and accumulates in the serosal cavity, causing effusion.
Features
It can phagocytose and kill pathogenic microorganisms locally, dilute and neutralize toxins, phagocytose and remove necrosis and disintegration products, and play an inflammatory defense role. It is the most characteristic pathological change of inflammation.
Exudation of inflammatory cells as a basis for diagnosing inflammation
effect
Dilute bacterial toxins and harmful substances
bring nutrients
Bring antibody complement and eliminate pathogens
Brings fibrinogen, prevents diffusion, and helps phagocytosis
Later fibrin helps repair
Drainage of lymph fluid to lymph nodes, causing immunity
Excessive exudate can affect tissue and organ function
hyperplasiaproliferation
Refers to the reactive proliferation of interstitial and parenchymal cells in the local area of inflammation
It can limit the spread of inflammation and repair damage.
Performance
local manifestation
red
inflammation congestion
swell
Inflammation, congestion, edema or local cell proliferation
hot
Local congestion, enhanced metabolism
pain
Damage factors directly affect
Inflammatory mediators such as prostaglandins, 5-HT, bradykinin
K leads to
Increased pressure such as inflammatory hyperemia compresses nerves
dysfunction
Inflammation causes local tissues and organs to become inoperable due to deterioration and exudation.
systemic reaction
fever
exogenous pyrogen
Bacteria, viruses, etc.
endogenous pyrogen
Inflammatory mediators or cytokines produced by white blood cells
Increased peripheral blood protein
cell type
neutrophils
acute suppurative inflammation
monocytes
chronic granulomatous inflammation
eosinophils
parasitic infection
A leukemia-like reaction when white blood cells reach 40,000
Proliferation of the monocyte-macrophage system
Manifested as liver, spleen, lymph node enlargement
acute inflammation
Vascular reaction
Hemodynamic changes
temporary constriction of arterioles
Appears immediately and lasts for a few seconds
blood flow dilation and blood flow acceleration
Acceleration of local blood flow, increased blood flow and enhanced energy metabolism are the causes of local redness and heat.
blood flow slows down
Increased blood flow permeability leads to plasma leakage and accumulation of red blood cells in small blood vessels, resulting in increased viscosity and slowed blood flow.
Helps white blood cells to approach the blood vessel wall, adhere to the surface of endothelial cells and extravasate
Increased vascular permeability
endothelial cell contraction
Causes gaps in endothelial cells for leukocytes to leak out, which lasts for a short time
The most common mechanisms for increasing permeability
endothelial cell damage
Injured blood vessels have extremely high permeability and continue to leak until thrombosis or endothelial cell regeneration and repair
Enhanced endothelial cell penetration
In the cytoplasm near the junction of endothelial cells, there are interconnected vesicles forming transcellular channels.
High permeability of new capillaries
present during inflammatory repair
leukocyte reaction
Leukocyte extravasation
WBC edge set, scrolling
Slow blood flow causes larger white blood cells to escape from the axis and reach the edges of blood vessels, which is called edge collection of white blood cells.
Selectins mediate leukocyte adhesion to endothelial cells during rolling
leukocyte adhesion
adhesion molecules
selectin
E
endothelial cells
P
endothelial cells and platelets
L
leukocyte
Immunoglobulin superfamily molecules
integrins
adhesion mechanism
Receptor weight distribution
Induces increased synthesis and expression of new adhesion molecules
Increase the direct affinity of adhesion molecules
swim out
concept
The process by which white blood cells pass through blood vessel walls and enter surrounding tissues
process
WBC adhere to endothelial cells
Pseudopodia extend at the junction of endothelial cells and are extruded from the endothelial cells with amoebic movements.
Pass through the basement membrane (secret collagenase to degrade the basement membrane)
Endothelial cell structure returns to normal
Speed (fast to slow)
neutrophils
monocytes/macrophages
Lymphocytes
viral infection
eosinophils
basophils
Chemotaxis
concept
White blood cells move along a concentration gradient toward a chemical stimulus
Chemokines
concept
chemical stimulus that attracts white blood cells to move in a directed manner
divided into
endogenous
C5a, LTB4, Chemokine
exogenous
bacterial products
nature
Let the white blood cell skeleton rebuild and move
White blood cell activation (phagocytosis)
important white blood cells
neutrophils
Acute inflammation, purulent inflammation, early inflammation
Contains abundant lysosomes, which can kill and degrade phagocytosed bacteria
Cationic proteins can promote increased vascular permeability and have chemotactic effects on monocytes
Neutral proteases can cause tissue damage
Lifespan is 1-2 days. It dies quickly after completing phagocytosis. After death, it releases proteolytic enzymes to dissolve necrotic tissue and fibrin.
macrophages
Post-acute inflammation, chronic inflammation, combined with typhoid virus parasitic infection
Derived from monocytes in blood and tissue cells in local tissues
Various forms
Assembled to devour difficult matter
Foreign body giant cells in foreign body granuloma
Lifespan is longer than white blood cells
eosinophils
Parasitic infections and allergic (allergic) reactions
Phagocytosis of antigen-antibody complexes
phagocytosis
concept
It refers to the process in which white blood cells swim out and arrive at the lesion, engulfing pathogens and tissue debris. It is another way to kill pathogens in addition to the release of lysosomes by white blood cells, and is an important process in the inflammatory defense response.
Mainly functions for neutrophils and macrophages
mechanism
Identify and attach
Through opsonization, adding Ig-Fc segment or C3b
swallow
The extension and anastomosis of pseudopods wraps up foreign objects and forms phagosomes
Kill and degrade
Rely on reactive oxygen or reactive nitrogen
Among them, H2O2-MPO-halogen is the most effective sterilization system for neutrophils.
Immunity
Produce lymphokines and antibodies
Leukocyte-mediated tissue damage
Phagolysosomal extravasation
Certain substances that are not easily phagocytosed can trigger hyperactivation of leukocytes and release of lysosomes into the interstitium.
White blood cells engulf the material that melts the lysosomal membrane, causing the lysosome to release
White blood cell function defects
Adhesion defects
Phagolysosome formation disorder
Impairment of bactericidal activity
bone marrow leukopenia
The role of inflammatory mediators
General characteristics
derived from cells or plasma
From plasma, synthesized in liver as precursor form, activated by protease hydrolysis
Acts by binding to target cell surface receptors
Secondary inflammatory mediators can amplify or inhibit the effects of primary inflammatory mediators on target cells.
An inflammatory mediator can act on a variety of cells and produce different effects
Inflammatory mediators have short half-lives
Potentially damaging
type
endogenous
cell
Vasoactive amines
Arachidonic acid metabolites
Cytokines
platelet activating factor
neuropeptides
NO
body fluid
kinin system
Bradykinin causes pain
complement system
coagulation system
exogenous
virus, toxin, product
effect
vasodilation
Histamine, bradykinin, PGF2
Increased vascular permeability
Histamine, bradykinin
Chemotaxis
fever
pain
PGF2, bradykinin
tissue damage
Classification
serous inflammation
feature
Serous exudation is mainly from plasma
parts
Mucosa, serosa, loose connective tissue
Performance
Inflammatory edema, body cavity effusion, serous catarrhal inflammation (serous inflammation of the mucosa)
Catarrhal inflammation generally refers to exudative inflammation of the mucosa
Example
Skin burn → blisters
Shingles, chickenpox
Serous inflammation of the larynx, leading to edema and suffocation
Nasal mucosal catarrhitis (mucosal serous exudative inflammation)
Fibrinitis
Features
Mainly fibrinogen leakage (large change in vascular permeability), followed by the formation of fibrin, that is, cellulose
parts
Mucous membrane, serosa, lung
Performance
pseudomembranous inflammation
pseudomembranous colitis
diphtheria pseudomembrane
When fibrinitis occurs in the mucosa, exuded fibrin, necrotic tissue and neutrophils together form a pseudomembrane
Fluffy heart
Fibrinitis of the cardiac surface
Example
diphtheria
If it occurs in the pharynx, it is not easy to fall off. It is called curative inflammation.
It occurs in the throat and easily falls off, which is called floating membrane inflammation and can cause suffocation.
bacillary dysentery
Mainly occurs in the sigmoid colon and rectum
Epithelial tissue sloughs off repeatedly
Lobar pneumonia (mycoplasma pneumonia)
congestive edema stage
The capillaries are dilated and congested, and the blood flow is accelerated and slowed
Red liver metamorphosis stage
A large amount of cellulose leaks into the alveolar space, and the lungs continue to be congested
Resulting in a liver-like substance
Gray liver metamorphosis
Neutrophils swim out and pulmonary capillaries are no longer congested
Dissolution and dissipation period
Neutrophils kill, degrade and phagocytose, and then decomposed by fibrinolytic enzymes
Fluffy heart
suppurative inflammation
Features
Neutrophil extravasation, accompanied by varying degrees of tissue necrosis and pus formation
suppuration
The process of exudation of neutrophils to dissolve necrotic tissue is called suppuration
Purulent exudate is called pus
Composed of pus cells, bacteria, necrotic tissue and a small amount of serous fluid
Degenerated and necrotic neutrophils are called pus cells
reason
Suppurative bacterial infection, resulting in tissue suppuration
Pyogenic bacteria: Staphylococcus, Streptococcus, Meningitidis, Escherichia coli
divided into
Superficial suppuration and accumulation of pus
Surface suppuration
Occurs in superficial parts of mucosa or serosa
lobular pneumonia
purulent catarrhalitis
meningococcal meningitis
empyema
Pus formed from superficial suppuration accumulates in body cavities or natural lumen
Gallbladder, fallopian tube, tail rot
cellulitis
concept
Diffuse suppurative inflammation of loose connective tissue
parts
appendix
skin
muscle
Features
diffuse inflammation
The degree of necrosis is not as good as that of abscess
reason
Caused by hemolytic streptococci, the toxic substances are streptokinase and hyaluronidase
abscess
feature
Localized suppurative inflammation occurs when local tissue undergoes dissolution and necrosis, forming a cavity filled with pus, and forming a large amount of pus.
reason
Caused by Staphylococcus aureus, the toxic substance is plasma coagulase
Example
boil
Abscesses of hair follicles and sebaceous glands
carbuncle
Multiple boils fuse to form an abscess that communicates with each other
Hemorrhagic inflammation
Features
Severe damage to the blood vessel wall and leakage of a large number of red blood cells
seen in
Epidemic hemorrhagic fever, plague, leptospirosis
ending
get well
completeness
incompleteness
Prolonged to chronic inflammation
Inflammatory factors cannot be completely eliminated
Spread spread
local spread
ulcer
fistula
Hollow
Dou Dao
Lymphatic spread
Causes lymphangitis and lymphadenitis
Spread of blood
bacteremia
No poisoning, blood bacteria positive
toxaemia
Poisoned
septicemia
Poisoning + positive blood bacteria
sepsis
Manifestations of sepsis, multiple embolic abscesses
chronic inflammation
Cause
secondary to acute inflammation
Recurrent episodes of acute inflammation
divided into
General chronic inflammation
Features
lasts longer
major chronic inflammatory cells
Lymphoplasmacytes and macrophages
damage
Tissue damage caused by inflammatory cells
repair
Parenchymal and interstitial hyperplasia is obvious
Appear
inflammatory polyps
Caused by local hyperplasia of mucosal epithelium, glands and granulation tissue, common in nose, cervix, intestines
inflammatory pseudocarcinoma
Formation of lumps of flesh similar to tumors
granulomatous inflammation
concept
Special chronic inflammation characterized by granuloma formation
Granulomas are well-circumscribed nodules composed of local proliferation of macrophages.
reason
infectious granuloma
bacterial infection
Mycobacterium tuberculosis
leprae
Rheumatism
spirochete infection
Treponema pallidum
Fungi and parasites
Histoplasmosis
Schistosomiasis
foreign body granuloma
Surgical sutures, asbestos, etc.
Unknown reason
nodular granuloma
Basic components of granuloma
macrophages
multinucleated giant cells
Macrophage fusion
Classification
infectious granuloma
foreign body granuloma