inflammation ii - Ústav patologie 1.lf uk a...
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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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Inflammation II - table of contents
Healing of Inflammation
Progressive changes – healing of wounds Regeneration (restitution) Repair (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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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 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
Repair – substitution with a less specialised
tissue
Hypertrophy – enlargement of the organ through
cell enlargement
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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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Extracellular Matrix
Intersticial – fbl – amorphous gel
– proteoglycans, hyaluronan, collagens,
elastin, fibronectin
Basement membrane
– type 4 collagen, laminin…
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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 wounds
–by first intention (per primam intentionem) –(wounds without infection, dislocation, foreign bodies)
– by second intention (per secundam intentionem)
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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Granulation Tissue Growth PDGF
from: mph, endoth., platellets
causes: fbl proliferation, proteosynthesis
Transforming GF from: mph, epithelia
causes: fbl proliferation, angiogenesis
IL- 1from: mph, epithelia
causes: fbl proliferation, endogenous pyrogen
TNF αfrom: mph
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 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 fibrinous 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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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
vessels, aneurysms formation
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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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