Inflammation and Immune Response Quiz 3

Inflammation and Vascular Physiology Overview

• Specific gravity (SG) is the ratio of the weight of a solution to the weight of an equal volume of water.
• Maple syrup has a higher specific gravity than water.
• Hydrostatic pressure drives fluid out of the circulatory system.
• Plasma oncotic pressure is generated by large plasma proteins like albumin and pulls fluid into the circulatory system.
• Inflammation is the reaction of vascularized living tissue to local injury or invasion and is a protective response that may sometimes harm the host.
• Inflammation consists of a vascular reaction and a cellular reaction.
• Cardinal features of inflammation include redness, swelling, warmth, pain, and loss of function.
• Triggers of inflammation include infections, trauma, physical and chemical agents, foreign bodies, and hypersensitivity reactions.
• Acute inflammation has rapid onset and short duration, while chronic inflammation has slower onset and longer duration.
• Types of leukocytes involved in inflammation are neutrophils, lymphocytes, eosinophils, monocytes, and basophils.
• Acute inflammation involves vascular changes such as vasodilation, increased permeability, and stasis due to loss of fluid from vessels.
• Mechanisms of increased vascular permeability during acute inflammation include endothelial cell contraction, direct endothelial cell injury, leukocyte-mediated endothelial injury, increased transcytosis, and leakage from new blood vessels.

Understanding Vascular Permeability, Edema, Transudate, and Exudate

• Immature endothelial cells in new vessels have small size and do not come in contact with one another, leading to endothelial gaps that allow exudate to escape until the cells mature.
• Edema is a component of inflammation due to excessive fluid within tissues or body cavities, caused by cells leaking out of vessels.
• Two types of edema are exudate and transudate, with different characteristics and causes.
• Transudate is a filtrate of plasma resulting from abnormal increase in hydrostatic pressure or decrease in plasma oncotic pressure, associated with low protein content and specific gravity.
• Exudate, also known as inflammatory edema, results from increased blood vessel permeability characteristic of inflammation, containing high protein content, specific gravity, and cellular debris.
• Pus is an exudate rich in neutrophils, dead cell debris, and often microbes.
• Formation of exudates and transudates occurs due to changes in hydrostatic pressure, osmotic pressure, and vascular permeability in the vascular bed during inflammation.
• Acute inflammation involves cellular events and leukocyte recruitment, including adhesion, transmigration, chemotaxis, recognition, activation, and termination.
• Leukocyte recruitment in acute inflammation involves key steps such as margination, rolling, activation, firm adhesion, transmigration, and chemotaxis.
• Leukocyte adhesion to endothelium is mediated by complementary adhesion molecules on leukocyte membranes and endothelial cells, involving selectins and integrins.
• Firm adhesion of leukocytes occurs after activation and is mediated by integrins, leading to subsequent transmigration through endothelial gaps in venules.
• Chemotaxis involves leukocytes moving within tissues along a chemoattractant gradient toward the site of injury, induced by exogenous and endogenous chemical mediators.

Leukocyte Activation and Removal of Offending Agents

• Leukocyte activation involves responses such as production of arachidonic acid metabolites, degranulation, activation of oxidative burst, secretion of cytokines, and increased binding affinity of adhesion molecules.
• Phagocytosis process includes recognition and attachment, engulfment, and killing and degradation through oxygen-dependent and oxygen-independent mechanisms.
• Chemical mediators of inflammation can originate from plasma or cells, and act by binding to specific receptors on target cells.
• Released mediators can cause a secondary wave of mediator release, and most mediators are short-lived.
• Mediators can be cellular or plasma proteins/systems, and include histamine, serotonin, lysosomal enzymes, arachidonic acid metabolites, and plasma proteins like factor XII, kinin, and complement C3 and C5.
• Principal roles of mediators in inflammation include vasoactive actions, chemoattraction, and regulation of immune/inflammatory reactions through cytokines and chemokines.
• Histamine, primarily found within mast cells, causes arteriolar dilation, increased vascular permeability, and redistribution of P-selectin.
• Arachidonic acid metabolites, produced by various cell types, are involved in pathways such as cyclooxygenase and lipoxygenase, generating prostaglandins, leukotrienes, and lipoxins with diverse effects on inflammation.
• Cytokines like TNF and IL-1 mediate and regulate immune/inflammatory reactions, while chemokines act as chemoattractants for leukocytes and organize cell types in different anatomic regions.
• Prostaglandins cause pain and fever, vasodilatation, inhibit platelet aggregation, or promote it, while leukotrienes and lipoxins have specific effects on vascular permeability, bronchospasm, and neutrophil function.
• The inflammatory process involves a complex interplay of various mediators, cells, and systems, with the potential for harmful effects when imbalanced or deficient.
• Understanding the roles and actions of chemical mediators in inflammation is essential for comprehending the pathophysiology of acute and chronic inflammatory diseases.