Inflammation II - pau.lf1.cuni.cz · Meningitis purulenta CSF Jaroslava Du ková ... Jaroslava Du...
Transcript of Inflammation II - pau.lf1.cuni.cz · Meningitis purulenta CSF Jaroslava Du ková ... Jaroslava Du...
General Pathology
Inflammation II
Healing processes
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Classification
Jaroslava Dušková
Inst. Pathol. ,1st Med. Faculty, Charles Univ. Prague
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Inflammation II - table of contents
Healing of Inflammation
Progressive changes - definition Regeneration (restitution) Reparation (substitution) Hypertrophy Hyperplasia Metaplasia Adaptation
Classification of inflammationsuperficial
skin serous membranes mucous membranes
intersticialaccording to the type of exudate
serous non purulent purulent fibrinous gangrenous
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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 changed conditions in the organism or environment
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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
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Cell Proliferation in
the Gastrointestinal
Tract
a Oesophagus
b Stomach
c Sm Bowel
d L Bowel
e Anus
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Angiogenesis
Endogenous Promotors
VEGF - A,B,C,D
Angiopoietins
Angiogenin
Basic fibroblast growth factor 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
VEG I
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 intentionem – primary union
(wounds without infection, dislocation, foreign bodies)
– per secundam intentionem- secondary union
hematoma organisation
thrombus organisation (possible recanalisation)
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Proliferation - steps
dissolution of exsudate & necrotic tissue
granulation tissuefibronectin formation, fibroblasts &
endothelia organisation
collagen production
scar maturation
scar contraction myofibroblasts
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Wound Healing – Steps-
Timing
Day 0: fibrin –
fibronectin gel
Day 1: neutrophils
Day 1-2: macrophages
Day 2-4: fibroblasts,
myofibroblasts,
capillaries
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Deposition and Remodeling of Connective
Tissue
PDGF from: mf, endoth., platellets
causes: fbl proliferation, proteosynthesis
Transforming GF from: mf, epithelia
causes: fbl proliferation, angiogenesis
IL- 1from: mf, epithelia
causes: fbl proliferation, endogenous pyrogen
TNF αfrom: mf
causes: endothelial growth, killing bacteria, cachexia
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Deposition and Remodeling of Connective
Tissue
Extracellular matrix proteins – matrix metaloproteinases MMPs dependent on Zinc ions
MMPs are deactivated by tissue inhibitors of metaloproteinases - TIMPs
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Wound Healing - I.
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Wound Healing - II.
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Healing Processes 2.
ischemic and traumatic
necroses
foreign bodies healing
bone fracturesJarosla
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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 necrosis foreign bodiespatient´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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Inflammation - Classification:
Type of exsudate: serous
nonpurulent –lymphoplasmocellular
purulent
fibrinous
gangrenous
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Herpes zoster
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H. zoster
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Epidermolysis bullosa staphylococcica
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Pericarditis serosa (CMV)
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Inflammation - Classification:
Type of exsudate: serous
nonpurulent –lymphoplasmocellular
purulent
fibrinous
gangrenous
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Sinusitis chronica
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Metaplasia intestinalis mucosae ventriculi
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Urocystitis chronica
metaplasia squamocellularis
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Inflammation - Classification:
Type of exsudate: serous
nonpurulent –lymphoplasmocellular
purulent
fibrinous
gangrenous
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Impetigo
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Acne conglobata
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Meningitis purulenta
CSF
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CSFMeningitis
purulenta
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Cholelithiasis. Empyema vesicae felleae chronicum.
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Osteomyelitis purulenta
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Sepsis puerperalis
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Diverticulitis
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Inflammation - Classification:
Type of exsudate: serous
nonpurulent –lymphoplasmocellular
purulent
fibrinous
gangrenous
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Fe
Pericarditis serofibrinosohaemorrhagica
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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
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Granulomatosis Wegeneri
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Polyarteritis nodosa
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Significance of Fibrinoid
Change
diminished quality of the collagen ( firmness, permeability)
tendency to thrombosis in the
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Rheumatic Heart Disease
acute myocarditis –Aschoff nodules/bodies
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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
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Appendicitis
gangraenosa
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