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Inflammaione. (Subject 4) презентация
Содержание
- 1. Inflammaione. (Subject 4)
- 2. Causes of inflammation Exogenous Infectious factors
- 3. Inflammation – local manifestation of the organism
- 4. Signs of inflammation Local: Calor - heat
- 5. Alteration Primary alteration - direct action
- 6. Metabolism changes Prevalence of catabolic processes in
- 7. Inflammatory mediators
- 8. Arachidonic acid metabolites Cell membrane phospholipids Phospholipases
- 9. Arachidonic acids metabolites Thromboxane A2 - platelet
- 10. Cellular mediators Active oxygen radicals: endothelial
- 11. Cellular mediators Lysosomal enzymes: mediate tissue injury
- 12. Plasma mediators Clotting system mobilization of molecules
- 13. The summary of inflammatory mediators’ activity
- 14. Changes in vascular flow Arterioles constriction
- 15. Changes in vascular flow Venous hyperemia and
- 16. Venous hyperemia and stasis prevent the spreading
- 17. Mechanisms of exudation ↑ vascular permeability
- 18. Increase of vascular permeability Endothelial cells contraction
- 19. Mechanisms of exudation ↑ hydrostatic pressure -
- 20. The role of exudation Negative
- 21. Extravasation of leukocytes
- 22. Leukocytes migration Move pseudopods into the junctions
- 23. Chemotaxis Chemotactic agents: bacterial membrane lipopolysaccharides
- 24. Leukocytes role in inflammation Protective function
- 25. Stages of phagocytosis Chemotaxis 2. Adherence
- 26. Two mechanisms of bacterial killing Oxygen-dependent mechanism
- 27. Proliferation in inflammation Regeneration - replacement of
- 28. The steps of repair Phagocytosis
- 29. Factors influencing proliferation Local: Persisting
- 30. Classification of inflammation Classification based on
- 31. Classification of inflammation Classification based on the
- 32. Types of exudative inflammation Serous inflammation -
- 33. Types of exudative inflammation Purulent (suppurative) inflammation
- 34. Neural and hormonal control of inflammation Pro-inflammatory
- 35. Inflammation outcomes Complete resolution - the injury
- 36. Chronic inflammation follow acute inflammation chronic from
Causes of inflammation Exogenous Infectious factors Exogenous Non-infectious factors: physical chemical biological Endogenous products of tissue decay Endogenous chemical agents
Слайд 2Causes of inflammation
Exogenous Infectious factors
Exogenous Non-infectious factors:
physical
chemical
biological
Endogenous products
of tissue decay
Endogenous chemical agents
Endogenous chemical agents
Слайд 3Inflammation – local manifestation of the organism general reaction to the
tissue injury
Inflammation events
Alteration (injury)
primary and secondary
Exudation
vascular reactions
vascular leakage
leukocyte exudation
phagocytosis
Proliferation
Inflammation events
Alteration (injury)
primary and secondary
Exudation
vascular reactions
vascular leakage
leukocyte exudation
phagocytosis
Proliferation
Слайд 4Signs of inflammation
Local:
Calor - heat
Rubor - redness
Dolor - pain
Tumor - swelling
Functio laesa -loss of function
Systemic:
peripheral blood leukocytosis
fever
↑ globulins blood level
↑ erythrocytes sedimentation rate
↑ cateholamines and corticosteroids
Слайд 5Alteration
Primary alteration - direct action of pathogenic factor (functional and
structural injury of the cells)
Secondary alteration mechanisms:
disturbances of local nervous regulation and blood circulation;
influence of inflammatory mediators;
alteration of T 0 , pH, oncotic, osmotic pressure;
lysosomal effect.
Secondary alteration mechanisms:
disturbances of local nervous regulation and blood circulation;
influence of inflammatory mediators;
alteration of T 0 , pH, oncotic, osmotic pressure;
lysosomal effect.
Слайд 6Metabolism changes
Prevalence of catabolic processes in the early stages
High speed
of metabolic reaction (heat)
Metabolic acidosis
↑ osmotic and oncotic pressure
Intracellular and extracellular hyperhydration (swelling)
Prevalence of anabolism – final stages
Metabolic acidosis
↑ osmotic and oncotic pressure
Intracellular and extracellular hyperhydration (swelling)
Prevalence of anabolism – final stages
Слайд 8Arachidonic acid metabolites
Cell membrane phospholipids
Phospholipases
Arachidonic Acid
Lipooxygenase
Cyclooxygenase
Leukotrienes
Thromboxane
Prostacycline
Prostoglandins
- Inflammation
- Activation of
the complement
Слайд 9Arachidonic acids metabolites
Thromboxane A2 - platelet aggregator and vasoconstrictor
Prostacyclin -
↓ platelet aggregation and vasodilator.
Prostaglandins:
dilation of vessels , ↑ vessels permeability
aggregation and adhesion of blood cells
fever, pain
Leukotrienes :
↑ smooth muscles tone (GIT, bronchi, blood vessels)
↑ vessels permeability
chemotaxins for neutrophiles
Prostaglandins:
dilation of vessels , ↑ vessels permeability
aggregation and adhesion of blood cells
fever, pain
Leukotrienes :
↑ smooth muscles tone (GIT, bronchi, blood vessels)
↑ vessels permeability
chemotaxins for neutrophiles
Слайд 10Cellular mediators
Active oxygen radicals:
endothelial cells damage (↑ vessels permeability)
other cells
injury
Platelet activating factor (PAF):
Platelet aggregation and release
↑ smooth muscles tone (bronchi, vessels)
↑ leukocyte adhesion to endothelium
↑ leukocyte chemotaxis, degranulation and oxidative burst
Platelet activating factor (PAF):
Platelet aggregation and release
↑ smooth muscles tone (bronchi, vessels)
↑ leukocyte adhesion to endothelium
↑ leukocyte chemotaxis, degranulation and oxidative burst
Слайд 11Cellular mediators
Lysosomal enzymes:
mediate tissue injury
activate bradykinine synthesis
mast cells degranulation
chemotaxis
Nitric oxide:
vasodilation
cytotoxic
effect
Cytokines:
interleukins
TNF
interpherone
Cytokines:
interleukins
TNF
interpherone
Слайд 12Plasma mediators
Clotting system
mobilization of molecules of adherence
activation of cyclooxygenase
production of
NO and PAF
Слайд 13The summary of inflammatory mediators’ activity
Vasodilation
↑ of blood vessels permeability
Leukocyte
adhesion
Chemotaxis
Fever
Tissue damage
Pain
Chemotaxis
Fever
Tissue damage
Pain
Слайд 14Changes in vascular flow
Arterioles constriction (activation of sympathetic nerves, mediators
influence) -localization of injuring agent
Arterial hyperemia (dilatation of arterioles due to BAS) - increase the general rate of metabolism
Arterial hyperemia (dilatation of arterioles due to BAS) - increase the general rate of metabolism
Слайд 15Changes in vascular flow
Venous hyperemia and pre-stasis (dilation of venules and
post-capillaries):
increased blood viscosity
swollen vessel walls
squeezing with inflammatory exudates
leukocytes margination along the vessels walls
Stasis - complete stop of blood flow.
increased blood viscosity
swollen vessel walls
squeezing with inflammatory exudates
leukocytes margination along the vessels walls
Stasis - complete stop of blood flow.
Слайд 16Venous hyperemia and stasis prevent the spreading of the damage to
surrounding tissues.
Arterial and venous hyperemia result in the increase of vessels permeability and promote exudate formation.
Arterial and venous hyperemia result in the increase of vessels permeability and promote exudate formation.
Слайд 17Mechanisms of exudation
↑ vascular permeability (vascular leakage).
↑ intravascular hydrostatic pressure
↑
osmotic and oncotic pressure of interstitial fluid
Слайд 18Increase of vascular permeability
Endothelial cells contraction
histamine, bradykinin
occurs rapidly after exposure
to mediator
reversible
reversible
Direct endothelial injury
severe non-specific injuries (burns or bacterial infection)
leakage lasts until vessels are thrombosed or repaired
Leukocyte-dependent endothelial injury
toxic oxygen radicals and proteolytic enzymes
Слайд 19Mechanisms of exudation
↑ hydrostatic pressure - ↑ filtration of fluid from
capillaries.
Ultrafiltrate of blood plasma with protein less then 2 % - transudate.
Inflammatory - more then 2 % protein.
↑ osmotic and oncotic pressure
Inflow of protein rich fluid from plasma to the site of inflammation.
Destruction of molecules by the enzymes
Ultrafiltrate of blood plasma with protein less then 2 % - transudate.
Inflammatory - more then 2 % protein.
↑ osmotic and oncotic pressure
Inflow of protein rich fluid from plasma to the site of inflammation.
Destruction of molecules by the enzymes
Слайд 20The role of exudation
Negative
squeezing of tissues and organs
exudate outflow
to body cavities and big vessels
abscess and phlegmon formation
abscess and phlegmon formation
Positive
transport of antibodies, inflammatory mediators
elimination of toxins and metabolites from inflammatory site
localization of the inflammatory agents
Слайд 22Leukocytes migration
Move pseudopods into the junctions between the endothelial cells
Squeeze through
interendothelial junctions
Release proteolytic lysosomal enzymes making gaps in vessels walls
Order of migration: neutrophiles, monocytes, lymphocytes
Release proteolytic lysosomal enzymes making gaps in vessels walls
Order of migration: neutrophiles, monocytes, lymphocytes
Слайд 23Chemotaxis
Chemotactic agents:
bacterial membrane lipopolysaccharides
components of the complement (3b, 5a,5b,6,7
leukotrienes
products of
tissue decay
Mechanism
Binding to receptors→
calcium mobilisation→
contraction of microfilaments→
movement
Mechanism
Binding to receptors→
calcium mobilisation→
contraction of microfilaments→
movement
Слайд 24Leukocytes role in inflammation
Protective function – phagocytosis.
Synthesis and secretion of
inflammatory mediators.
Processing and presentation of foreign agents for the immune systems.
Tissue damage with :
Lysosomal enzymes
Active oxygen radicals
Products of AA metabolism (prostaglandins and leukotrienes)
Processing and presentation of foreign agents for the immune systems.
Tissue damage with :
Lysosomal enzymes
Active oxygen radicals
Products of AA metabolism (prostaglandins and leukotrienes)
Слайд 25Stages of phagocytosis
Chemotaxis
2. Adherence (opsonins - IgM, IgG, C3b)
3. Phagosome
formation
4. Killing or degradation of the ingested material
4. Killing or degradation of the ingested material
Слайд 26Two mechanisms of bacterial killing
Oxygen-dependent mechanism reactive oxygen species – superoxide
anion, hydroxyl ion, hydroperoxide
Oxygen Independent Mechanisms – using the content of granules (lysozyme, proteins influencing bacterial cell wall)
Oxygen Independent Mechanisms – using the content of granules (lysozyme, proteins influencing bacterial cell wall)
Слайд 27Proliferation in inflammation
Regeneration - replacement of dead cells with new ones;
the function is restored.
Repair - replacement with fibrous connective tissue cells and fibers; the functions is not restored.
Repair - replacement with fibrous connective tissue cells and fibers; the functions is not restored.
Слайд 28The steps of repair
Phagocytosis
Proliferation of endothelial cells and fibroblasts
in the damaged area.
The growth of new vessels to establish blood circulation in the healing area
Fibroblasts produce collagen.
Mature scar is produced.
The growth of new vessels to establish blood circulation in the healing area
Fibroblasts produce collagen.
Mature scar is produced.
Слайд 29Factors influencing proliferation
Local:
Persisting infection, foreign material
Inadequate blood supply
Excessive movement
Irradiation
Systemic:
Age
Nutritional deficiencies
Metabolic diseases
Catabolic state associated with malignancies
Substances:
Growth factors, TNF – activation
Chalones, glucocorticoids - inhibition
Слайд 30Classification of inflammation
Classification based on the cause of inflammation:
Infectious: non-specific
(cocci) and specific (tuberculosis, syphilis)
Non-infectious (aseptic) – caused by infarctions, hemorrhages, salt deposition
Non-infectious (aseptic) – caused by infarctions, hemorrhages, salt deposition
Слайд 31Classification of inflammation
Classification based on the prevailing mechanism:
Alterative –prevailing alteration develops
in parenchymal organs (myocardium, liver, kidneys).
Exudative - prevailing exudate formation.
Proliferative (productive) - prevalence of reparative process; proceeds chronically
Exudative - prevailing exudate formation.
Proliferative (productive) - prevalence of reparative process; proceeds chronically
Слайд 32Types of exudative inflammation
Serous inflammation - 3-8% of protein, single neutrophiles
in exudate.
Catarrhal inflammation presence of mucus in exudates.
Fibrinous inflammation presence of fibrin in exudate
Croupous inflammation - fibrinous pericarditis (hairy heart), croupous pneumonia.
Diphtheritic – throat, pharynx, tonsils
Catarrhal inflammation presence of mucus in exudates.
Fibrinous inflammation presence of fibrin in exudate
Croupous inflammation - fibrinous pericarditis (hairy heart), croupous pneumonia.
Diphtheritic – throat, pharynx, tonsils
Слайд 33Types of exudative inflammation
Purulent (suppurative) inflammation production of pus - pyogenic
bacteria (staphylococci).
Abscesses are localized collections of pus.
Phlegmon and empyema are diffuse pus infiltrations.
Putrefactive inflammation - a result of putrefactive bacteria injury.
Haemorrhagic inflammation - presence of erythrocytes in exudates. (anthrax, plague, influenza).
Abscesses are localized collections of pus.
Phlegmon and empyema are diffuse pus infiltrations.
Putrefactive inflammation - a result of putrefactive bacteria injury.
Haemorrhagic inflammation - presence of erythrocytes in exudates. (anthrax, plague, influenza).
Слайд 34Neural and hormonal control of inflammation
Pro-inflammatory hormones - growth hormone, mineralocorticoids
Glucocorticoids, catecholamines - anti-inflammatory effect
Violation of peripheral innervation leads to chronic inflammation development
Слайд 35Inflammation outcomes
Complete resolution - the injury is limited
Healing by scarring –
impossibility of regeneration or s abundant fibrin exudation.
Abscess formation - pyogenic microorganisms.
Progression to chronic inflammation
Abscess formation - pyogenic microorganisms.
Progression to chronic inflammation
Слайд 36Chronic inflammation
follow acute inflammation
chronic from the onset due to:
disturbances of phagocytosis
high
level of glucocorticoids and catecholamines
persistent infections or intoxications.
prolonged exposure to nondegradable material (silica particles – silicosis)
autoimmune diseases.
persistent infections or intoxications.
prolonged exposure to nondegradable material (silica particles – silicosis)
autoimmune diseases.
