MindMap Gallery Pathology—Inflammation
The focus of the pathology examination is the defense response of living tissues with vascular systems to damaging factors. Vascular responses are central to the inflammatory process.
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This article discusses the Easter eggs and homages in Zootopia 2 that you may have discovered. The main content includes: character and archetype Easter eggs, cinematic universe crossover Easter eggs, animal ecology and behavior references, symbol and metaphor Easter eggs, social satire and brand allusions, and emotional storylines and sequel foreshadowing.
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Avatar 3 centers on the Sully family, showcasing the internal rift caused by the sacrifice of their eldest son, and their alliance with other tribes on Pandora against the external conflict of the Ashbringers, who adhere to the philosophy of fire and are allied with humans. It explores the grand themes of family, faith, and survival.
This article discusses the Easter eggs and homages in Zootopia 2 that you may have discovered. The main content includes: character and archetype Easter eggs, cinematic universe crossover Easter eggs, animal ecology and behavior references, symbol and metaphor Easter eggs, social satire and brand allusions, and emotional storylines and sequel foreshadowing.
[Zootopia Character Relationship Chart] The idealistic rabbit police officer Judy and the cynical fox conman Nick form a charmingly contrasting duo, rising from street hustlers to become Zootopia police officers!
inflammation
concept
The defense response of living tissues with vascular systems to damaging factors
Vascular responses are central to the inflammatory process
reason
Biological agents (infections)
physical factors
chemical factors
tissue necrosis
allergy
foreign body
Local manifestations and systemic reactions
local manifestation
Red - blood vessels dilate
Swelling—increased blood vessel permeability and leakage
Heat - blood vessels dilate and blood flow accelerates
Pain - inflammatory mediator, local swelling and compression, irritation of peripheral nerves
disfunction
systemic reaction
Fever - inflammatory mediators (exogenous and endogenous pyrogens)
Changes in peripheral blood white blood cell count
Pathological changes of inflammation
spoil
ooze
Vascular response and hemodynamic changes
transient spasmodic contraction of arterioles
Blood vessels dilate and blood flow accelerates
blood flow slows down
Increased vascular permeability
Mainly occurs in the microcirculatory area
mechanism
endothelial cell contraction
endothelial cell damage
Enhanced endothelial cell penetration
High permeability of new capillary walls
Leakage of liquid ingredients
defensive role
dilute toxin
Complement and antibody components eliminate pathogens
Bring nutrients and take away metabolites
Stimulate the body's production of cellular and humoral immunity
The role of cellulose (limiting the spread of pathogens, facilitating phagocytosis by leukocytes, and later repair)
Negative Effects
oppression, obstruction
Mechanization
Extravasation of cellular components
Mainly white blood cells
Red blood cells (passive), harmful to the body
The basic process of leukocyte diapedesis
Edge gathering and rolling of leukocytes (adhesion molecules)
Leukocyte adhesion: endothelial cells and leukocyte surface (adhesion molecules)
adhesion molecules
immunoglobulins, selectins, integrins, myxoid glycoproteins
Endothelial cell surface (ligand)
Immunoglobulin
Intercellular adhesion molecule (ICAM1)
Vascular cell adhesion molecule (VCAM1)
White blood cell surface (receptor)
integrin
Lymphocyte function-associated protein 1 (LFA1)
Macrophage Antigen 1 (MAC1)
VLA4
Collocation relationship during adhesion
ICAM1—LFA1
ICAM1—MAC1
VCAM1—VLA4
swim out
Way
amoebic movements
parts
endothelial cell space
Chemotaxis
The process by which white blood cells move along a concentration gradient toward the site of a chemical stimulus (chemokine).
The local role of white blood cells
Phagocytosis (neutrophils, macrophages)
process
Identify and stick
leukocyte TLRs
G protein coupled receptor
Opsonin receptors (complement)
Cytokine receptor
swallow
Kill and degrade
First: Oxygen-dependent killing mechanism (main)
H2O2-MPO-CL system
Second: Oxygen-independent killing mechanism
BPI protein, lysozyme, bactericide
include
neutrophils
Basic Features
Bleaches out quickly, but has a short lifespan
The main function
Devour
seen in
Early inflammation, acute inflammation, purulent inflammation
monocytes
Basic Features
Slow infiltration and long survival time
Function
phagocytosis, immunity
seen in
Late stage of inflammation, chronic inflammation, bacilli infection
acute inflammatory cells
neutrophils
chronic inflammatory cells
Monocytes, lymphocytes, plasma cells
eosinophils
Kill parasites
anti-allergy
basophils
Secrete inflammatory mediators
Lymphocytes
T cells, B cells
immunity
tissue damage
inflammatory mediators
Source and type
cell release
Vasoactive amines (first released in acute inflammation)
histamine
5-HT (serotonin)
Arachidonic acid metabolites
PG (prostaglandin)
LT (lymphotoxin)
white blood cell products
reactive oxygen metabolites
Lysosomal enzymes
platelet activating factor
Cytokines
IL (interleukin)
TNF (tumor necrosis factor)
IFN (Interferon)
Substance P
Nitric oxide
body fluid production
kinin system
bradykinin
complement system
C3a, C5a
coagulation system
fibrin polypeptide
thrombin
fibrinolytic system
Fibrin degradation products
The role of major inflammatory mediators
Vasodilation (rent a thousand)
prostaglandins, NO, histamine
Increased vascular permeability (renting a house to delay CDEP)
Histamine, Serotonin, C3a and C5a, Bradykinin, LTC4, LTD4, LTE4, PAF, Substance P
Chemotaxis, leukocyte infiltration and activation (pendulum clock supplement B)
TNF, IL-1, C3a and C5a, LTB4
Fever (white money)
IL-1, TNF, prostaglandins
Pain (in exchange for P money)
prostaglandins, bradykinin, substance P
tissue damage
Leukocyte lysosomal enzymes, reactive oxygen species, NO
hyperplasia
defensive significance
Limit the spread of inflammation
repair
ending
get well
full recovery
incomplete recovery
Delayed recovery, becomes chronic
The body’s resistance is low and treatment is incomplete
The condition is sometimes severe and sometimes mild
Spread spread
local spread
Lymphatic spread
Spread of blood
bacteremia
toxaemia
septicemia
sepsis
Classification of various types of inflammation
According to disease course
acute inflammation
Rapid development and short course of disease
The lesions are mainly exudative, exuding acute inflammatory cells (neutrophils)
Inflammatory mediators play a major role
Local clinical manifestations are obvious
chronic inflammation
Slow development and long course of disease
The lesions are mainly hyperplasia, exuding chronic inflammatory cells (mononuclear macrophages)
Inflammatory mediators are not primary
because
Pathogenic factors persist for a long time
immune response
Inflammatory cells cause tissue necrosis
Local clinical manifestations are not obvious
According to the basic pathological changes of inflammation
Degenerative inflammation (Biscuit Medical Center sings)
viral hepatitis
Japanese encephalitis
toxic myocarditis
Intestinal amoebiasis
exudative inflammation
serous inflammation
skin
blisters
II degree burns
subcutaneous
blisters
bees, snake venom
loose connective tissue
inflammatory edema
Mucous membrane
catarrhal inflammation
Early stage of cold
Serosa
pleural effusion
rheumatism, tuberculosis
synovial membrane
joint effusion
rheumatoid arthritis
Fibrinitis
Fibrinitis of mucosa
pseudomembranous inflammation
under the mirror
Cellulose (red stain, intertwined mesh/strips/granules), neutrophils, necrotic debris
naked eye
Fake membrane (off-white)
Common site
Diphtheria (solid membrane inflammation, not easy to fall off)
Trachea (floating membrane inflammation, easy to fall off)
bacillary dysentery
dysbiosis enteritis
fibrinitis of serosa
Cause
rheumatism, tuberculosis
Fluffy heart
Organizing → constrictive pericarditis
Pathological changes are the same as fibrinitis of the mucosa
pulmonary fibrinitis
Lobar pneumonia
Massive fibrin and neutrophil exudation
ending
Dissolve and absorb
Mechanization
suppurative inflammation
pus cells
abscess
Cause
Staphylococcus aureus
Predisposed areas
subcutaneous or visceral
Basic morphological characteristics
Staphylococcus aureus is highly virulent → severe necrosis
Staphylococcus aureus produces thrombin → fibrinogen is converted into cellulose → the lesion is localized
Staphylococcus aureus contains laminin receptors → is prone to produce persistent abscesses in distant locations through the blood vessel wall
cellulitis
Cause
Hemolytic Streptococcus
Predisposed areas
loose tissue (skin, muscle, appendix)
Basic morphological characteristics
Hemolytic Streptococcus has weak virulence → mild necrosis (generally leaves no trace after recovery)
Hemolytic streptococci secrete hyaluronidase to degrade hyaluronic acid, and streptokinase dissolves cellulose → the lesions are diffuse
Superficial suppuration and accumulation of pus
purulent catarrhalitis
Can be discharged
urethra, bronchi
empyema
serosa, gallbladder, fallopian tube
Hemorrhagic inflammation
Features
Not an independent type of inflammation
Example
Epidemic hemorrhagic fever, anthrax, leptospirosis, plague
proliferative inflammation
Acute (mainly mononuclear macrophage proliferation)
acute glomerulonephritis, rapidly progressive glomerulonephritis
Typhoid fever
Chronic
non-specific
Proliferation of chronic inflammatory cells
Inflammatory polyps (mucosa)
Common sites—nose, colon, cervix
Inflammatory pseudotumor (lung)
Common locations—lungs, orbits
Specific (granulomatous inflammation)
Causes and types
infectious granuloma
Bacteria (tuberculosis, leprosy)
Treponema pallidum
Fungi and parasites
foreign body granuloma
surgical sutures
granuloma of unknown cause
sarcoid granuloma
Other granulomas
Traumatic fat necrosis → fat release → macrophage phagocytosis → lipogranuloma
Typhoid fever → macrophages phagocytose typhoid bacilli, lymphocytes, red blood cells, and necrotic debris → typhoid granuloma
Rheumatism
Morphological characteristics (taking tuberculosis nodules as an example)
caseous necrosis
epithelioid cells
langhans giant cells
Lymphocytes
Fibroblasts