L7- Chronic Inflammation Flashcards
What is Inflammation?
A protective response involving host cells, blood vessels and proteins
Purpose is:
- Remove the cause of injury
- Remove necrosis
- Initiate repair
Can be inappropriate – chronic inflammatory diseases
Can damage nearby tissues and be destructive
Acute vs Chronic…
Acute:
- prominent signs
- fast onset: mins-hours
- Neutrophils
- Mild self limiting tissue injury
Chronic:
- Subtle signs
- Slow onset: days
- Macrophages/Lymphocytes
- Severe progressive
Chronic Inflammation
Chronic is applied to anything that persists over a long period of time
In inflammation, chronic has a different cellular response to acute:
Lymphocytes, plasma cells and macrophages
Granulation and scar tissue
Usually primary but can be sequential from acute.
Acute vs Chronic processes
Acute inflammation is initial reaction to tissue injury – vessels dilate and become leaky – leaking a protein rich exudate. Outcome is either resolution, supporation (abscess formation), organisation or going on to become chronic inflammation
Chronic inflammation is an inflamatory process in which the dominant cells are lymphcytes, plasma cells and macrophages.
How does it go from acute to chronic?
Most common in supporative (pus forming) acute inflammation
Pus can form an abscess
If deep enough the walls thicken
Granulation and fibrous tissue
Recurrent acute can lead to chronic e.g cholecystitis = gall bladder inflammation usually due to stones
Morphological Features of chronic inflammation
Infiltration with mononuclear cells (macrophages, lymphocytes, plasma cells)
Tissue destruction
Healing by fibrosis
What does chronic inflammation look like Macroscopically ?
Fibrosis – prominent once Inflammatory infiltrate has stopped
Granulomatous- E.g in crohns
Chronic abscess cavity
Chronic peptic ulcer- Mucosal breach, granulation tissue
Base, fibrous tissue extends through wall
Importance of Macrophages
Very important in chronic inflammation
Increase inflammation, stimulate immune system
Macrophages already at sight of damage release cytokines which signal to monocytes
Monocytes enter damaged tissue from endothelium of blood vessel (leukocyte extravasion/diapedesis) = RECRUITMENT
Macrophages PROLIFERATE locally in damaged tissue
Process of macrophage action
Cause tissue injury –Proteases are released after they debride damaged tissue –> Stimulated by low oxygen content to produce factors that induce angiogenesis
They also induce cells to re-epithelialise the wound and create granulation tissue. Also induce angiogensis factors for blood vessel formation in granulation tissue.
They can also hold and contain viable organisms if they cannot kill them – examples include M. tuberculosis and M. leprae.
Wound healing - what occurs
Angiogenesis
Fibroblasts deposit collagen
Inflammatory cells
Aim is to repair by replacement of injured tissues by fibrous tissues
Fibrosis
Formation of excess fibrous connective during repair of damaged tissue
Scarring
Called fibroma if arises from 1 cell line
Macrophage induced laying down of connective tissue inc collagen
Granulomatous Inflammation
A granuloma = aggregate (nodule) of epithelioid histiocytes and other cells; lymphocytes and histiocytic giant cells
Granulomatous disease includes TB and leprosy.
Histiocytic giant cells can form where material is indigestible to macrophages e.g tubercle bacilli which have cell walls resistant to macrophages
Histiocytic giant cells
Histiocytic giant cells can form where material is indigestible to macrophages e.g tubercle bacilli which have cell walls resistant to macrophages
They’re multinucleate giant cells. May have >100 nuclei.
Develop when 2+ macrophages try to engulf the same particle.
No known function. Not phagocytic
Granulomatous Disease examples
Bacterial = TB, leprosy
Parasitic = schistosomiasis
Fungal = cryptococcus
Synthetic materials = silicosis
Unknown = Sarcoidosis, crohn’s disease
Histology of Granuloma
Langhans giant cell (blue
heart)
Caseous necrosis (blue Sun)
Epithelioid macophages
(blue circle)
