Chronic Tissue Injury And Inflammation Flashcards
Granulation tissue
Growth of non specific new connective tissue which was not there before and has little purposed
Surrounds dead tissue, pus or irritants and allows circulatory system to continue to deliver exudate
Macrophages infiltrate in chronic inflammation
Enhanced emigration and activation of monocytes via activated interstitial monocytes
Some monocytes become activated interstitial macrophages which have pro-inflammatory behaviours
Macrophages during chronic inflammation
Have enhanced killing capabilities via IFN gamma
Modulate the immune response via cytokines, chemokine and antigen presentation
Can clear cells
Can create new and remodel connective tissue
NET during chronic disease
Cause; autoimmunity, auto inflammation, and allergy
Autoimmunity in NET
e.g. systemic lupus erythematosis (t-cells react against own self)
NET is a source of antigens - DNA is usually immune hidden but is exposed in NETS, immune system can recognise these as foreign and attack
Immune system therefore triggered more NET release injuring the endothelium
Auto inflammation in NET
e.g. gout (urate crystal arthritis)
Immune reaction to crystal formation -> very inflammatory
Allergy
E.g asthma
Common colds can exacerbate NETosis which exacerbated asthma/other injuries as pro inlammatory
Inflammasomes
Caspase rich multi protein complexes - assembled by pattern recognition receptor signals in myeloid cells
Inflammasomes are important in
Antimicrobials defence and chronic disease as caspase enzymes produce inflammatory cytokines ands induce pyroptosis
Pyroptosis
Programmed lyric cell death
Liberates the cytokines and inflammasomes, traps bacteria in cell corpse and is resistant bro anti inflammatories as glucocorticoid cleaves receptors
Granulomas
Organised clusters of mature macrophages in response to persistent stimuli
Low turnover of caused by foreign body
High turnover if caused by toxin incited agent -> Tuberculosis
Cellulitis
Uncontrolled, unlocalised subcutaneous spreading of infection
Bacteria proliferates as exudate combats is -> resulting in build up of pressure in fascial compartments
Sinus
A blind ending pit surrounded by granulation tissue that tracks to the epithelial surface
E.g. a hair follicle becoming infected under the skin and appearing as inflamed abscess at skin surface
Abscess
Controlled, localised pus in newly formed cavity
Surrounded by granulation tissue delivering new exudate
Need to be drained or else they persist and scar
Fistula
Abnormal anatomical link between two epithelial cells
E.g. in Crohn’s disease; intestine attaching to abdominal wall creating abnormal hole
Interfering surgically can worsen symptoms
Ulcer
Localised defect in epithelial surface caused by sluffing of inflammatory necrotic tissue
Exposes tissue under the epithelium as lost full thickness of epithelium
Regeneration is slow as no basement membrane so no tissue has to regenerate from the side
Erosion
When defect occurs but the whole epithelial layer is not lost
If injury is resolved then regeneration will occur in a matter of days
Tuberculosis
Mimics the complement system -> when inhaled the bacteria is taken up by macrophages so can’t be killed -> survives in the cytoplasm -> promotes macrophage chemotaxis and phagocytosis to increase its spread in the body -> adaptive immune system is lowered so takes longer to activate -> finally causes granulomas which kill bacteria -> some bacteria lay dormant and reinfect when the host is immunosuppressed
Amyloid
Extracellular accumulation of insoluble fibrils made from a misfolded polypeptide (either aggregation prone mutant or overproduction of normal protein)
Caused by different disease proteins - either local or multi organ
Beta pleated sheets which are hard to digest
Outcomes of chronic inflammation
Focal scarring can protect -> widespread scarring is destructive
Persistence causes cancer -> cells are encouraged to proliferate so increased chance of mutations