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General Pathology
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General Pathology
Inflammation II
Healing processes
Classification
Jaroslava Dušková
Inst. Pathol. ,1st Med. Faculty, Charles Univ. Prague
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InflammationDefinition:
complex reaction of organism to damage
(aim: homeostasis maintenance)
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InflammationSense
defensive – agent elimination
reparative – damage reparation
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Inflammation Celsus´ features:
rubor tumor calor dolor functio laesa
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Inflammation - Classification:
Time view acute (days)
subacute (weeks)
chronic (months-years)
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Phases of Inflammatory Response
Alteration
Exsudation
Proliferation
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Healing of Inflammation
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Progressive Changes
Def.:processes leading to
lost or damaged tissue substitution
or adaptation to the organism or
environment changed conditions
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Progressive Changes Regeneration (restitution) Reparation (substitution) Hypertrophy Hyperplasia Metaplasia Adaptation
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Progressive changes 1.
Regeneration - restitution of former status
Reparation – substitution with a less specialised
tissue
Hypertrophy – enlargement of the organ through
cell enlargement
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Angiogenesis Endogenous Promotors VEGF - A,B,C,D Angiopoietins Angiogenin basic FGF bFGF Hepatocyte Growth Factor HGF Interleukin-8 PDGF Transformation Growth Factor ß TGF ß TNF
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Angiogenesis Endogenous Inhibitors Angiostatin Brain Angiogenesis Inhibitor 1 BAI1 Endostatin Interferons Platelet factor-4 cleavage products Prolactin fragment (16kd) Thrombospondin-1 VEGI Vasostatin
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Progressive changes 2.
Hyperplasia – enlargement of the organ through cell multiplication
Metaplasia – transformation of one differentiated tissue into another differentiated tissue
Adaptation - functional adjustment
It is done by means of metaplasia, hypertrophy, hyperplasia, metalaxia, (rebuilding).
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Healing Processes 1.
wounds– per primam intentionen (wounds without infection, dislocation, foreign
bodies)
– per secundam intentionen
hematoma organisation thrombus organisation
(possible recanalisation)
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Proliferation - steps dissolution of exsudate &
necrotic tissue granulation tissue
fibronectin formation, fibroblasts & endothelia organisation
collagen production scar maturation scar contraction myofibroblasts
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Wound Healing - steps
Day 0: fibrin – fibronectin gel
Day 1: neutrophils
Day 1-2: macrophages
Day 2-4: fibroblasts, myofibroblasts,
capillaries
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Granulation Tissue Growth PDGF
from: mf, endoth., platelletscauses: fbl proliferation, proteosynthesis
Transforming GF from: mf, epithelia causes: fbl proliferation, angiogenesis
IL- 1 from: mf, epithelia causes: fbl proliferation, endogenous pyrogen
TNF α from: mf
causes: endothelial growth, killing bacteria, cachexia
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Healing Processes 2.
ischemic and traumatic
necroses foreign bodies healing bone fractures
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Factors Influencing Wound Healing age nutrition status – protein deficit vitamins A,C – collagen, epithelisation Zinc – enzyme function steroids local factors
infection necrosisforeign bodispatient´s motilityarterial perfusionvenous drainage
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Inflammation - Classification:
According to the dominant phase:
alterative EXSUDATIVE proliferative
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Inflammation - localisation
superficial mucous membranes
serous membranes
skin
interstitial
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Inflammation - Classification:
Type of exsudate: serous nonpurulent –
lymphoplasmocellular purulent fibrinous gangrenous
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Interstitial fibrinose inflammation
fibrin exsudation & fibrinoid change of the collagen containing connective tissue
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Fibrinoid Change of Collagen
vessels and connective tissue damage plasmorrhagia (leakage of plasma) deposits of Ag-AB complexes staining characteristics fibrin - like
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Significance of Fibrinoid Change diminished quality of the collagen
( firmness, permeability) tendency to thrombosis in the
vessels, aneurysms formation
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Inflammation - Classification:
Type of exsudate: serous nonpurulent –
lymphoplasmocellular purulent fibrinous gangrenous
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Gangrenous Inflammation
tends to be interstitial putrefactive bacteria severe alteration