Body Response To Tissue Damage: Chronic And Granulomatous Inlfammation Flashcards Preview

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Flashcards in Body Response To Tissue Damage: Chronic And Granulomatous Inlfammation Deck (17)


Occurs when there has been minimal damage to the tissue architecture-> cells can re grow
Acute inflammatory exudate eliminates agent
Exudate removed by neutrophils, phagocytosis by macrophages and fluid drainage in to lymph
Damaged cells regenerate
Normal function regained
Regeneration limited to cells that can still divide


Examples of resolution

Lobar pneumonia:
Cells lining alveoli die but stroma and vascular structure remain intact
With antibiotics causative bacteria is removed
Neutrophils make the exudate highly liquid and it is reabsorbed in to lymph
Remnant epithelial stem cells divide to re line the alveoli

Tubular necrosis


Abscess formation

Extensive tissue necrosis
Caused by pyogenic (pus forming) bacteria-> secrete necrotoxins
Mass of necrotic tissue
Dead and viable neutrophils suspended in Purulent exudate
Acute abscess-> surrounded by acute inflammatory exudate
Chronic abscess-> scar tissue starts to form


Organisation and repair

Substantial structural damage to tissue stroma
Healing can't occur by resolution
Remove debris
Grow new vessels and support cells


Stages of organisation and repair 1)

1) Pre existing capillaries from undamaged tissue form new capillaries by budding into the damaged area.
Damaged area infiltrated by macrophages, fibroblasts and myofibroblasts
Macrophages phagocytise exudate and dead tissue
Vascular granulation tissue-> fragile complex of interconnecting capillaries, macrophages and support cells develope
Organisation of exudate


Organisation and repair 2

Progressive growth of fibroblasts and myofibroblasts
More complex capillary network
Few residual macrophages


Organisation and repair 3

Continued proliferation of fibroblasts
Active collagen synthesis begins
Majority of capillaries regress-> some acquire smooth muscle and function as arterioles/venues
Fibrovascular granulation tissue


Organisation and repair 4

Intervening spaces between vessels become progressively filled with fibroblasts synthesising collagen
Fibrous granulation tissue
Fibroblasts aligned so they lay collagen running in a direction that provides maximum strength
Contraction of the area frequently via contractile effects of myofibroblasts to reduce area size.


Organisation and repair 5

Production of dense collagen forms a collagenous scar
Fibroblasts assume a resting status-> fibrocytes
Fibrous repair


Chronic inflammation definition

When a damaging stimulus persists so complete healing can't occur
Organisation with continued inflammation and necrosis
Tissues infiltrated with immune cells
Necrotic debris, acute inflammatory exudate, vascular and fibrous granulation tissue, lymphoid cells, macrophages and collagenous scar
Persists until damaging stimulus removed


Causes of chronic inflammation

Damaging stimuli can't be eradicated
Bacteria persist because they are distanced from neutrophils, antibiotics
Bacteria persist because they are resistant to neutrophils phagocytosis


Examples of chronic inflammation

Chronic peptic ulcer:
Exudate organises into granulation tissue but in meantime more damage is caused on stomach by acid
-> acids removed-> heals with scar
-> acid persists-> damage overwhelms repair-> ulcer perforates


Mechanisms of chronic inflammation

Main effector cell is macrophages
Activated by gamma interferon
Develop voluminous cytoplasm
Fusion of macrophages to produce giant cell
Phagocytotic and secretory roles
Mediators of acute inflammation
Highly reactive O2 metabolites
Proteases and hydrolysis enzymes
Cytokines, IL-1 and TNFa-> fibroblast proliferation and collagen synthesis
Growth factors-> PDGF, EGF, FGF


Granulomatous inflammation definition

Chronic inflammation where neutrophil phagocytosis is inadequate to neutralise the causative agent
Acute inflammation quickly replaced by immune-based cellular reaction-> aggregation of macrophages and lymphocytes
Macrophages often form discrete clusters-> granulomas


Stimuli of granulomatous inflammation

Microorganisms of low inherent pathogenicity but which excite a type IV immune response. Eg mycobacterium
Non living foreign material in tissues, endogenous and exogenous
Unknown factors-> sarcoidosis, collections of granulomas that form nodules in organs such as the lungs


Examples of granulomatous inflammation

Mycobacterium tuberculosis:
lipoprotein coating resistant to neutrophils
Excite a transient but marked immune response-> T cells produce cytokines
Acute inflammation replaced by chronic as neutrophils don't work
Aggregates of macrophages-> tubercle-> centre of caseous necrosis surrounded by macrophages which are surrounded by lymphocytes which are surrounded by fibroblasts


Outcomes of a tubercle

Factors predisposing to extension of infection:
Ingestion of large numbers of highly virulent organisms
Poor immune response
-> necrosis expands and can't be contained by tubercle-> infection spreads via lymph, veins, bronchi
Factors predisposing to containment or eradication:
Ingestion of small numbers of poorly virulent organisms
Administration of appropriate antibiotics
-> fibroblasts around the outside of the tubercle proliferate, make a collagenous shell and contain the infection

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