Post on 26-May-2018
General Pathology
Inflammation II
Healing processes
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Classification
Jaroslava Dušková
Inst. Pathol. ,1st Med. Faculty, Charles Univ. Prague
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
InflammationDefinition:
complex reaction of organism to damage
(aim: homeostasis maintenance)
InflammationSense
defensive – agent elimination
reparative – damage reparation
Inflammation Celsus´ features:
rubor
tumor
calor
dolor
functio laesa
Inflammation - Classification:
Time view
acute (days)
subacute (weeks)
chronic (months-years)
Phases of Inflammatory Response
Alteration
Exsudation
Proliferation
Healing of Inflammation
Progressive Changes
Def.:
processes leading to
lost or damaged tissue substitution
or
adaptation to the changed conditions in the organism or environment
Progressive Changes
Regeneration (restitution)
Reparation (substitution)
Hypertrophy
Hyperplasia
Metaplasia
Adaptation
Progressive changes 1.
Regeneration - restitution of former status
Repair – substitution with a less specialised
tissue
Hypertrophy – enlargement of the organ through
cell enlargement
Cell Proliferation in
the Gastrointestinal
Tract
a Oesophagus
b Stomach
c Sm Bowel
d L Bowel
e Anus
Extracellular Matrix
Intersticial – fbl – amorphous gel
– proteoglycans, hyaluronan, collagens,
elastin, fibronectin
Basement membrane
– type 4 collagen, laminin…
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
Angiogenesis
Endogenous Inhibitors
Angiostatin
Brain Angiogenesis Inhibitor 1 BAI1
Endostatin
Interferons
Platelet factor-4 cleavage products
Prolactin fragment (16kd)
Thrombospondin-1
VEG I
Vasostatin
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)
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)
Proliferation - steps
dissolution of exsudate & necrotic tissue
granulation tissuefibronectin formation, fibroblasts &
endothelia organisation
collagen production
scar maturation
scar contraction myofibroblasts
Wound Healing – Steps-Timing
Day 0: fibrin – fibronectin gel
Day 1: neutrophils
Day 1-2: macrophages
Day 2-4: fibroblasts, myofibroblasts,
capillaries
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
Healing Processes 2.
ischemic and traumatic
necroses
foreign bodies healing
bone fractures
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
Inflammation - Classification:
According to the dominant
phase:
alterative
EXSUDATIVE
proliferative
Inflammation - localisation
superficial
mucous
membranes
serous
membranes
skin
interstitial
Inflammation - Classification:
Type of exsudate: serous
nonpurulent –lymphoplasmocellular
purulent
fibrinous
gangrenous
Inflammation - Classification:
Type of exsudate: serous
nonpurulent –lymphoplasmocellular
purulent
fibrinous
gangrenous
Herpes zoster
H. zoster
Epidermolysis bullosa staphylococcica
Pericarditis serosa (CMV)
Inflammation - Classification:
Type of exsudate: serous
nonpurulent –lymphoplasmocellular
purulent
fibrinous
gangrenous
Sinusitis chronica
Metaplasia intestinalis mucosae ventriculi
Urocystitis chronica
metaplasia squamocellularis
Inflammation - Classification:
Type of exsudate: serous
nonpurulent –lymphoplasmocellular
purulent
fibrinous
gangrenous
Impetigo
Acne conglobata
Meningitis purulenta
CSF
CSFMeningitis
purulenta
Cholelithiasis. Empyema vesicae felleae chronicum.
Osteomyelitis purulenta
Sepsis puerperalis
Diverticulitis
Inflammation - Classification:
Type of exsudate: serous
nonpurulent –lymphoplasmocellular
purulent
fibrinous
gangrenous
Fe
Pericarditis serofibrinosohaemorrhagica
Inflammation - Classification:
Type of exsudate: serous
nonpurulent –lymphoplasmocellular
purulent
fibrinous
gangrenous
Interstitial fibrinous inflammation
fibrin exsudation & fibrinoid change of
the collagen containing connective
tissue
Fibrinoid Change of
Collagen vessels and connective tissue damage
plasmorrhagia (leakage of plasma)
deposits of Ag-AB complexes
staining characteristics fibrin - like
Granulomatosis Wegeneri
Polyarteritis nodosa
Significance of Fibrinoid
Change
diminished quality of the collagen ( firmness, permeability)
tendency to thrombosis in the
vessels, aneurysms formation
Rheumatic Heart Disease
acute myocarditis –Aschoff nodules/bodies
Inflammation - Classification:
Type of exsudate: serous
nonpurulent –lymphoplasmocellular
purulent
fibrinous
gangrenous
Gangrenous Inflammation
tends to be interstitial
putrefactive bacteria
severe alteration
Appendicitis
gangraenosa