Inflammation and Immune Response Quiz 2

Inflammation and Vascular Physiology Overview

• Specific gravity (SG) is the ratio of the weight of a solution to an equal volume of water, with pure water having a SG of 1.000.
• Hydrostatic pressure is the pressure exerted by a fluid on the walls of its container and drives fluid out of the circulatory system.
• Plasma oncotic pressure, generated mainly by albumin, pulls fluid into the circulatory system.
• Inflammation is a protective response of living tissue to injury, closely linked to the repair process.
• The cardinal features of inflammation include redness, swelling, warmth, pain, and loss of function.
• Triggers of inflammation encompass infections, trauma, physical and chemical agents, foreign bodies, and more.
• Acute inflammation has a rapid onset and short duration, with excessive fluid in tissues and emigration of neutrophils.
• Chronic inflammation has a slower onset and longer duration, involving lymphocytes, macrophages, and tissue changes.
• Neutrophils, lymphocytes, eosinophils, monocytes, and basophils are types of leukocytes (white blood cells).
• Monocytes are precursors of macrophages, which are key in the inflammatory response.
• Diseases caused by inflammatory reactions involve vascular changes, cellular events, leukocyte recruitment, and chemical mediators.
• Vascular changes in acute inflammation include vasodilation, increased permeability, stasis, and escape of exudate into injured tissue.

Leukocyte Activation and Phagocytosis in Acute Inflammation

• Leukocyte activation involves 5 essential responses, including the production of arachidonic acid metabolites, degranulation, activation of oxidative burst, secretion of cytokines, and an increase in binding affinity of adhesion molecules.
• Phagocytosis involves recognition and attachment, engulfment, and killing and degradation of offending agents through oxygen-dependent and oxygen-independent mechanisms.
• Chemical mediators of inflammation can originate from plasma or cells, and most act by binding to specific receptors on target cells.
• Released mediators can cause a secondary wave of mediator release and act on one type of target cell or a variety of different types.
• The principal mediators of inflammation can be cellular or plasma proteins/systems, including histamine, serotonin, lysosomal enzymes, arachidonic acid metabolites, and plasma proteins such as Factor XII activation, kinin, and complement C3 and C5 cleavage.
• Vasoactive amines like histamine and serotonin are preformed and primarily found within mast cells, causing arteriolar dilatation and increasing vascular permeability.
• Arachidonic acid metabolites are produced by various cell types and can be metabolized by two enzymatic pathways, leading to the production of prostaglandins, leukotrienes, and lipoxins with various inflammatory effects.
• Cytokines and chemokines are proteins that mediate/regulate immune/inflammatory reactions and act as chemoattractants for leukocytes, with major roles in acute inflammation.
• Cytokines like TNF and IL-1 and chemokines like C-X-C and C-C have specific roles in acute inflammation, affecting different cell types and anatomic regions.
• The production of arachidonic acid metabolites by leukocytes and the action of cytokines and chemokines play crucial roles in the acute inflammatory response.
• The acute inflammatory response involves a complex interplay of leukocyte activation, phagocytosis, and the action of various chemical mediators, cytokines, and chemokines.
• Understanding the mechanisms of leukocyte activation, phagocytosis, and the roles of chemical mediators, cytokines, and chemokines is essential in comprehending the pathophysiology of acute inflammation.

Test your knowledge of inflammation and vascular physiology with this quiz covering topics such as specific gravity, hydrostatic pressure, plasma oncotic pressure, triggers of inflammation, leukocyte activation, phagocytosis, and the role of chemical mediators, cytokines, and chemokines in acute inflammation.