L7- Chronic Inflammation Flashcards Preview

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Flashcards in L7- Chronic Inflammation Deck (15):

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...

-prominent signs
-fast onset: mins-hours
-Mild self limiting tissue injury

-Subtle signs
-Slow onset: days
-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


Fibroblasts deposit collagen

Inflammatory cells

Aim is to repair by replacement of injured tissues by fibrous tissues



Formation of excess fibrous connective during repair of damaged tissue


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

Caseous necrosis (blue

Epithelioid macophages
(blue circle)