Pathology - Inflammation and repair 1 Flashcards
(51 cards)
what is inflammation?
a responsive process to perceived aggression: infection, tissue damage, non-self recognition
What happens to the concentration of cells and molecules during inflammation?
Concentration of cells and molecules of immunity increase to the sites where the trigger of inflammation happens
Why is inflammation is important?
Inflammation is important to fight infection, to heal wounds, to repair injury
What are the changes in vascular flow during inflammation?
- Arteriolar dilatations (vascular ectasia/dilation) and opening of capillary bed
- Localized increased blood flow: increased pressure (heat and redness)
What happens to vascular permeability during inflammation ?
Increased vascular permeability (vascular leakage) (leakage of palsma proteins that creates edema)
- Endothelial gaps
- Endothelial injury (endothelial cell death)
Describe a normal vascular environment
hydrostatic pressure = colloid osmotic pressur, plasma protein stays in the lumen. No net fluid or protein leakage
Describe the formation of exudate
Increased interendothelial space, along with vasodilation and stasis leads to fluid and protein leakage
describe the formation or transudate
Increased (++) pressure (venous outflow obstruction, like in congestive heart failure)
+
Decreased colloid osmotic pressure (decresed protein synthesis; increased protein loss; protein malnutrition) leads to fluid leakage
What is exudate
High protein content and may contain some white and red cells
What is transudate
Low protein content, few cells.
Consequences of the vascular leakage
- Outpouring of protein-rich fluid in the extravascular tissues: exsudative edema (tumor)
- Localized increased viscosity: blood stasis
- Leukocyte migration
Process of leukocyte migration
- Rolling along the endothelium
- Adhesion to the endothelium
- Transmigration across the endothelium (diapedesis)
- Piercement of the basement membrane
- Migration and cell-matrix interactions
Caracteristics of a neutrophil (4)
- Innate immune system
- Nucleus divided in 2-5 lobes
Type of phagocytes - Migrate through interstitial tissue
- Predominate during the first 6-24 hrs
Caracteristics of a monocyte (5)
- Innate immune system
- Bean-shaped nucleus, unilobar
- Change into macrophages after entering the tissue spaces
- Phagocytosis
- Replace neutrophils in 24-48 hrs
Phases of phagocytosis
- Recognition and attachement of the particle to be ingested by the leukocyte: mannose receptors
- Engulfment: phagocyte membrane zips up around particle
- Killing and degradation within neutrophils and macrophage.
Process of killing and degradation within neutrophils and macrophages
- Fusion of phagosome with lysosomes
- Killing by lysosomial enzymes
- Killing by ROIs and NO (oxygen compounds)
What happens after phagocytosis
Neutrophils undergo apoptosis and are ingested by macrophages
Why are toll-like receptors (TLRs) are important players in leukocyte activation
They recognize pathogen-associated signatures and initiate the inflammatory response of the innate immune system
What are TLRs
receptors expressed at the surface of leukocytes involved in their activation (i.e., TLR3, ligand: viral double-strand RNA)
Name some chemical mediators of inflammation
- Vasoactive amines (i.e., histamine, serotonine)
- Complement and kinin systems
- Clotting system (i.e., FXII, FX, fibrin, plasmin)
- Arachidonic acid metabolites.
- IFN-gamma by NK cells and T lymphocytes
- Reactive Oxygen Intermediates (ROIs), Nitric Oxyde (NO), Lysozymes, O2 free radicles
How is the acute inflammatory response is terminated
- Many chemical mediators have a short half-life: rapid decline
- Stop signals:
Switch in the production of pro-inflammatory to anti-inflammatory products from arachidonic acid
Secretion of TGF beta
Inhibition of TNF - Tissue macrophages half-life is prolonged (months or years)
What is the outcome of acute inflammation?
- Resolution
- Fibrosis after healing (i.e., hypertrophic scar)
- Progression to chronic inflammation:
Angiogenesis
Mononuclear cell infiltrate
Fibrosis
Example of a serous inflammation
Skin blister
Example of fibrinous inflammation
fibrin (large molecule) extravasation needs severe vascular modification; more often associated with secondary fibrosis
