General Pathology

Inflammation II

Healing processes

Classification

Jaroslava Dušková

Inst. Pathol. ,1st Med. Faculty, Charles Univ. Prague

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 organism or

environment changed conditions

Progressive Changes Regeneration (restitution) Reparation (substitution) Hypertrophy Hyperplasia Metaplasia Adaptation

Progressive changes 1.

Regeneration - restitution of former status

Reparation – substitution with a less specialised

tissue

Hypertrophy – enlargement of the organ through

cell enlargement

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

Angiogenesis Endogenous Inhibitors Angiostatin Brain Angiogenesis Inhibitor 1 BAI1 Endostatin Interferons Platelet factor-4 cleavage products Prolactin fragment (16kd) Thrombospondin-1 VEGI 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 1.

wounds– per primam intentionen (wounds without infection, dislocation, foreign

bodies)

– per secundam intentionen

hematoma organisation thrombus organisation

(possible recanalisation)

Proliferation - steps dissolution of exsudate &

necrotic tissue granulation tissue

fibronectin formation, fibroblasts & endothelia organisation

collagen production scar maturation scar contraction myofibroblasts

Wound Healing - steps

Day 0: fibrin – fibronectin gel

Day 1: neutrophils

Day 1-2: macrophages

Day 2-4: fibroblasts, myofibroblasts,

capillaries

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

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 necrosisforeign bodispatient´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

Interstitial fibrinose 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

Significance of Fibrinoid Change diminished quality of the collagen

( firmness, permeability) tendency to thrombosis in the

vessels, aneurysms formation

Inflammation - Classification:

Type of exsudate: serous nonpurulent –

lymphoplasmocellular purulent fibrinous gangrenous

Gangrenous Inflammation

tends to be interstitial putrefactive bacteria severe alteration