Inflammation and Wound Healing (1c) Flashcards
Definition of inflammation
Response of body tissue to immune reactions, injury, or ischemic damage
Acute and Chronic
Acute inflammation overview
8-10 days from onset to healing
Immediate response by tissue, an innate component of immune response, aimed at removing harmful stressors and minimizing tissue damage
5 cardinal signs of inflammation
Redness Heat Swelling Pain LOF
Endothelial cells in inflammation
Produce antiplatelet and antithrombotic agents, vasodilators and constrictors.
Provide selectively permeable barrier
Regulate leukocyte extravasation
Synthesize and release inflammatory mediators
Produce growth factors which aid in angiogensis and ECM synthesis
CSF (colony stimulating factors) for producing non RBCs
Platelets
Initial cessation of bleeding
Release 300+chemical mediators
Affect endothelial function such as increasing vascular permeability, altering chemotactic, adhesive and proteolytic functions
Neutrophil
A leukocyte involved in phagocytosis which arrives in first 90 minutes.
Surface receptors are involved in their activation.
Ingest bacteria and dead tissue
Monocytes/macrophages
Monocytes are larger WBCs than neutrophils, and become macrophages with inflammatory stimuli.
Both ingest microbes/dead tissue (monophages much more than neutrophils)
Both produce postaglandins, leukotriens, platelet activating factor, cytokines and growth factors.
They can surround and wall off material than can’t be digested
Eosinophils
Large role in allergic reactions, and contain a protein toxic to parasitic worms too big to be phagocytized
Basophils/Mast cells
Release histamine when bound to IgE
Poons notes just say heparin
Vascular stage of inflammation
Vasodilation and increased permeability is a result of chemical mediators (histamine and nitric oxide) which allows protein rich fluid (exudate) into extravascular spaces. This results in increased concentration of RBCs, leukocytes, platelets, and clotting factors.
This allows initiation of clotting processes, dilution of offending agent, and limits systemic spread
Vascular stage of inflammation continued
The loss of plasma proteins reduces intracap osmotic pressure causing the edema, pain and impaired function.
How is the increased permeability in the vascular stage created?
Binding of chemical mediators (histamine, bradkinin, leukotrines) cause contraction of endothelial cells and separation of intercellular junctions
Cellular stage of inflammation
Mast cells are first to react by releasing chemical mediators immediately
Mast cells and macrophages already positioned
Cell stage leukocyte response (after initial mast cell/macrophage response)
- Margination and adhesion to endothelium
- Transmigration across endothelium
- Chemotaxis
- Activation and phagocytosis
Margination and adhesion (step one in leukocyte cell response)
Margination - chemical mediators cause leukocytes to slow and adhere to endothelium, and move along it periphery of blood vessels
Adhesion - cytokines released to tightly bind leukocytes.
Transmigration (step 2 in leukocyte cell response)
Adhesion of leukocytes and chemical mediators cause endothelial cells to shrink and open gaps, this allows leukocytes to extend pseudopodia between endothelial cells and transmigrate into ECM
Chemotaxis (step 3 in cell leukocyte response)
Chemokines (small proteins directing leukocytes) bacterial and cell debris cause purposeful and energy-directed movement of leukocytes to desired areas
Activation (part of step 4 in cell leukocyte response)
Specific receptors activate monocytes/neutrophils and macrophages. Activated by bacteria and or cell debris
Phagocytosis (other part of step 4 in cell leukocyte response)
Agent is engulfed by pseudopod and trapped in cytoplasmic vesicle, which may merge with lysosomes that help kill and digest insulting agent.
*This can produce ROS as byproduct
Plasma derived mediators (3)
from liver
Acute-phase proteins
Factor XII
Complement proteins
Cell derived mediators (2)
Preformed and newly synthesized
Acute phase proteins (from plasma derived mediators)
Fever and inflammation
Factor XII (from plasma derived mediators)
Clotting/fibrinolytic system Kinin system (bradykinin)
Compliment proteins (from plasma derived mediators)
Activation of complement system
Preformed mediators (from cell derived mediators)
Mast cells (release histamine)
Platelets (serotonin)
Neutrophils/macrophages (lysosomal enzymes)
Newly synthesized (cell derived mediators)
Leukocytes (prostaglandin/ leukotriens/PAF)
Leukocytes/macrophages (NO and oxygen derived free radicals)
Macrophages/leukocytes/endothelial cells)
