Infalmmation Flashcards
Inflammation
This is the stereotype response of living vascularized cell to a sub lethal injury
Exudation
Is an inflammatory response at site of injury due to increase permeability of small blood vessels.
•movement of fluid, proteins, and blood cells from the vascular system into the interstitium or body cavities.
•Are extravascular fluid having high protein concentration, contains cellular debris, and has a high specific gravity >1.020
Transudate
An extra vascular fluid with low specific gravity <1.012, low protein, low cellular component.
It does not have to do with increased membrane permea
Edema
Accumulation of fluid in the interstitial or serous cavities, either exudate or transudate
Purulent exudate
inflammatory exudate rich in leukocytes, the debris of dead cells debris and microbes
Hallmark of acute inflammation
The production of protein rich exudate- edema
Factors for vascular leakage
increased formation of interendothelial spaces in venules elicited by many chemical mediators: histamine, bradykinin, leukotrienes, the neuropeptide substance P.
•2.Direct endothelial injury by apoptosis
delayed prolonged leakage, and affecting ve Ike’s and arterioles
3. Leukocyte mediated endothelial injury
4. Increased transcytosis: vesiculovacuolar organelles are located around the intercellular junctions and cause leakage from the vessel via vegf
5. Newly formed blood vessel have immature intercellular junctions and therefore they are prone to vascular leakage
Cellular components of acute inflammation
- neutrophils
- macrophages
-chemical mediators - chemical substances that drive the inflammation
How do leukocytes leave the vascular system
They secrete collagenases
Chemotaxis
Unilateral movement of leucocytes toward a chemical attractant.
Components of acute inflammation
A. Changes in vascular calibre that lead to increased blood flow.
•B. Increased vascular permeability allowing plasma protein and leucocyte to leave circulation through structural changes in microvasculature
•C. Leukocyte emigration (extravasations),accumulation at site of injury, activation to eliminate offending agent (phagocytosis)
Causes of acute inflammation
Infections: bacterial, viral, fungal, parasitic and microbial toxins
•Tissue necrosis : ischemia (myocardial infarct), trauma, hypoxia and physical and chemical injury (thermal injury, burns,frostbite, irradiation,environmental chemicals).
•Foreign bodies: splinters, dirts, sutures.
•Immune reactions: hypersensitivity reactions or autoimmune diseases.
Chemotactic factors
Bacteria products.
•Complement component - C5a
•Arachidonic acid metabolites esp. leukotiene B4(LBT4), HETE-hydroxyeicosatetraenoic acid and kallikrein.
•Cytokines -IL8.
Phagocytosis
Ingestion of particulate material by phagocytic cells(neutrophils & monocyte-macrophages).
Opsonisation
the coating of a particulate material by substances called opsonin to facilitate phagocytosis.