Lecture 4 - Inflammation Flashcards
Define inflammation.
The body’s natural response to harmful stimuli, such as pathogens, damaged cells, or irritants. A protective mechanism aimed at removing harmful stimuli and initiating tissue repair.
List the cardinal signs of inflammation.
Redness, swelling, edema, loss of function, heat
The purpose of inflammation is to ______ and _______ the injuries agent. There are both ____ and _____ forms of inflammation.
localize; eliminate; acute; chronic
Describe acute inflammation and list the types of responses.
Immediate & early response to tissue injury; vasodilation, vascular leakage & edema
Describe the process of acute inflammation.
Bacteria trigger macrophages to release cytokines & chemokines, vasodilation & increased vascular permeability cause redness/heat/swelling, inflammatory cell migrate to tissue, releasing inflammatory mediators that cause pain
Vasodilation: Mast cells will degranulate and secrete ____ from their _____.
histamine; granules
What does leukocytosis mean?
Increase in white blood cells.
What is hyperemia?
An increase in blood flow to a particular tissue or organ.
What is vasodilation?
Brief arteriolar vasoconstriction followed by vasodilation, accounts for warmth & redness, opens microvascular beds, increased intravascular pressure causes early transudate into interstitium.
What is vascular leakage?
Vascular permeability/leakiness commences (cells, proteins, fluids goes into the surrounding tissues from the blood vessels to localize & eliminate), transudate gives way to exudate, increases interstitial osmotic pressure…edema
Leukocytes leave the vasculature routinely through the following sequence of events:
They are then free to participate in:
Margination and rolling, Adhesion and transmigration, Chemotaxis and activation; Phagocytosis and degranulation, Leukocyte-induced tissue injury
Describe rolling adhesion.
With increased vascular permeability, fluid leaves the vessel causing leukocytes to “marginate” along endothelial surface. As complementary surface adhesion mole.s, they briefly stick & release causing the leukocyte to roll along the endothelium until it eventually comes to a stop as mutual adhesion reaches a peak.
Explain chemotaxis and activation.
Leukocytes extend pseudopods with overlying surface adhesion molecules (integrins) that bind ECM during chemotaxis and undergo activation by preparing AA metabolites from phospholipids. Then prepare for degranulation & release of lysosomal enzymes. Then regulate leukocyte adhesion molecule affinity as needed.
Describe the process of phagocytosis and degranulation.
Once at site of injury, leukocytes recognize &attach to Fc fragments of antibodies and complement components. They engulf and kill microbes. Triggers an oxidative burst engulfment & formation of vacuole which fuses w/ lysosomal granule membrane. Granules discharge within phagolysosome and extracellularly (degranulation).
Describe the degranulation and cleanup.
Reactive end-products are only active within phagolysosome.
Hydrogen peroxide broken down to water and oxygen by catalase.
Dead microorganisms degraded by lysosomal acid hydrolases.
