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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

cell enlargementJarosla

va Dušková

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

va Dušková

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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

staining characteristics fibrin - likeJaroslava Duško

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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 formationJaroslava Duško

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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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