Chronic Inflammation Flashcards
Chronic criteria
-prolonged duration
-active inflammation
-tissue destruction
-attempts of repair
Causes of chronic inflammation
-persistent/resistant infections
>granulomas
>abscess
-autoimmune diseases
-foreign material reactions
Chronic morphologic features
-mononuclear infiltration (macrophages, lymphocytes, plasma cells)
-tissue destruction (by agent or by inflammation)
-tissue repair (fibrosis, angiogenesis)
-usually absence of hyperemia and edema
Macrophages
-dominant cell players in chronic inflammation
-blood=monocytes, tissue=macrophages
-powerful host defenders that eliminate injurious agents and initiate repair process
Macrophage functions:
-important for chronic inflammation
-host defenders:
>lysosomal oxygen dependent and independent toxic products to microbes and host cells
>secretion of cytokines and chemokines causing influx of inflammatory cells
>secretion of growth factors causing angiogenesis and fibrosis
Lymphocytes
-mobilized in both antibody-mediated and cell-mediated immune reactions in bidirectional way
>macrophages present antigens to T cells and produce cytokines that stimulate T cell response
>Activated T lymphocytes produce cytokines that stimulate macrophages
Plasma cells
-develop from activated B lymphocytes and produce antibody directed against persistent antigen
Lymphoplasmacytic inflammation
-has little diagnostic specificity, many things can cause it
>Rabies, parasitic infections, others
Granulomatous inflammation
-chronic inflammation dominated by epithelioid macrophages
-nodular
>good differential diagnosis for a tumour
-consists of central focus of caseous necrosis, surrounded by epitheloid macrophages with giant cells, and lymphocytes, plasma cells and fibroblasts present
Granulomas macroscopic appearance
-often indistinguishable from neoplasia
Repair routes
1.fibrosis and scarring
2.Regeneration
Stimulus for regeneration
-within hours of tissue injury, the viable parenchymal cells at the periphery of the lesion is aware that the adjacent cells have died. They release growth factors and cytokines (paracrine signalling) allowing for regeneration activity to occur
Requirements for regeneration
-debridement
-tissue scaffold
-available blood supply
-survival of germinal cells
Debridement
-removal of the dead or damaged tissues
Tissue scaffold
-need some sort of scaffold or plan so the body knows where to build off of
Available blood supply
-need blood for energy, removal of waste, and new cells moving in
Mammal tissues
-Labile tissues- able to regenerate
-Stable tissues-able to regenerate
-Permanent tissues
Permanent tissues
-no ability to replicate themselves
-neurons and skeletal and cardiac muscle
Superficial corneal ulceration
1.damage to cornea
2.edema
3.epithelial cells begin to slide, stretch and cover damaged area (epithelial sliding)
4. epithelial proliferation- more cells appear, and less stretch occurring
5.Epithelial maturation and regeneration- does not usually result in scarring because regeneration occurs quickly
Atrophy of small intestinal villi
Coronavirus
1.damage to villi from vacuolar and ballooning degeneration
2. intestinal epithelial regeneration occurs
Foot and mouth disease
- Vesicles rupture
- Result in superficial ulcer
- Complete epithelial regeneration
Compensatory hepatic hyperplasia
-liver has ability to regenerate back to full volume and mass
**more hyperplasia vs regeneration
Repair by scarring and fibrosis
-occurs instead of regeneration when healing does not occur within 48hrs after injury
>fibroblasts and angioblasts proliferate to form granulation tissue
Wound healing
1.inflammatory phase- prepares wound for healing
2.Proliferative phase- building of new tissue to fill wound space
>fibroblasts=angiogenesis and cell proliferation and migration; form granulation tissue
>WBCs leave the site near end
3. Remodeling phase
Fibrin over time
-Fibrin present at wound, fibroblasts come in and add collagen forming the fibrous tissue
Angiogenesis
-new sprouts of vessels from pre-existing vessels
>vasodilation from NO
>increased permeability (VEGF)
>degradation of basement membrane
>migration of endothelium
>proliferation of endothelium
>maturation and remodeling of endothelium
>recruitment of periendothelial cells
New vessels/tissue
-prone to thrombosis
-usually leaky because weaker
Scar formation
-fibroblast migration and proliferation into neovascularized tissue
What occurs due to scars?
-decreased proliferating endothelial cells and fibroblasts
-increased deposition of ECM by fibroblasts
-decreased vascular component of granulation tissue
Granulation tissue
-pale, avascular, contracted scar
-pink-red
-granular appearance
-edema
-pain is from stretching skin around it
-resistant to infection
**more you have, the more of a scar you will have
What influences time it takes to heal?
-blood supply
-depth of wound
-tension that occurs at site of injury
-shape of wound
Tissue remodeling
-balance between extracellular matrix synthesis and degradation (by metalloproteinases)
Healing by first intention
-surgical wounds
>trying to minimize the amount of trauma and tissue damage caused
Healing by second intention
-allowing a wound to heal on its own
>will have larger wound bed and more granulation tissue therefore more scarring
Complications in wound healing
-Wound dehiscence- opening of wound back up due to tissue tension, animal cause, infection
-exuberant granulation- 2 causes: sarcoid tumour, production of excessive granulation tissue production
-fibrous adhesions- connections form between things that you don’t want them to
-constrictive pericarditis- scar tissue formation may inhibit proper function (eg. Hardware disease)
Hepatic cirrhosis
-combination of regeneration and fibrosis (nodules and depressed)
>smaller than normal, lumpy and bumpy
