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