II - Acute and Chronic Inflammation Flashcards
Initial vascular response to injury
Vasoconstriction.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.33
Inflammation characterized by exudation of fluid and plasma protein and a predominantly neutrophilic leukocyte accumulation.
Acute inflammation(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 71
Inflammation typified by influx of lymphocytes and macrophages associated with vascular proliferation and deposition of connective tissue.
Chronic inflammation(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 71
Five cardinal signs of inflammation
Heat (calor)redness (rubor)swelling (tumor)pain (dolor)loss of function (functio laesa)(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 71
An ultrafiltrate of blood which contains little protein, little or no cellular material and low specific gravity as a result of osmotic or hydrostatic imbalance across the vessel wall WITHOUT increase in vascular permeability.
Transudate. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 73
An extravascular fluid with high protein content. Its presence implies an increased vascular permeability, triggered by tissue injury and ongoing inflammatory reaction.
Exudate(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 73
Effect of histamine on vascular smooth muscle
Vasodilation. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 73
The most common mechanism of increased vascular permeability.
Contraction of endothelial cells resulting in increased interendothelial spaces. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 74
Proliferation of lymphatic vessels and painful enlarged lymph nodes secondary to inflammation.
Reactive or inflammatory lymphadenitis. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 74
Molecules in the endothelium and leukocyte responsible for this stage of vascular inflammatory response: Rolling
P and E-Selectins on endothelium with Sialyl-Lewis-X on leukocyte; Glycam-1, CD-34 on endothelium with L-selectin on leukocyte (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 36 *SEE SLIDE 2.1
Molecules in the lymphocyte responsible for this stage of vascular inflammatory response: Firm adhesion
ICAM-1 on endothelium with CD11/CD18 integrins (aka, LFA-1, Mac-1) on leukocyte; VCAM-1 on endothelium with VLA-4 on leukocyte (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 36 *SEE SLIDE 2.1
Molecules in the endothelium responsible for this stage of vascular inflammatory response:
Transmigration
PECAM-1/CD 31(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77 *SEE SLIDE 2.1
CELLS AND MOLECULES INVOLVED IN: Chronic transplant rejection
Lymphocytes, MACROPHAGES and CYTOKINES (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 41
CELLS AND MOLECULES INVOLVED IN: Acute transplant rejection
Lymphocytes, ANTIBODIES and COMPLEMENT (TOPNOTCH) Robbins Basic Pathology, 9th ed. P 41
The process of leukocyte accumulation at the periphery of blood vessels
Margination(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 75
Arrange the following steps in the inflammatory response: A. Recruitment of leukocytes B. Regulation of response C. Recognition of injurious agent D. Removal of agent E. Resolution
C, A, D, B, E (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 72
Arrange the steps in leukocyte recruitment:A. TransmigrationB. Rolling C. MarginationD. Firm adhesion
C, B, D, A (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 75
Process of coating microorganisms with proteins that facilitate phagocytosis.
Opsonization (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 75
A lymphocyte with ingested microorganism fused with lysosome is called _______.
Phagolysosome(TOPNOTCH)Robbins Basic Pathology, 9th ed. p. 78
The process of migration of the leukocytes through the endothelium.
Transmigration or diapedesis. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76
Process of leukocyte migration toward sites of infection or injury along a chemical gradient.
Chemotaxis (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77
The most important lysosomal enzyme involved in bacterial killing.
Elastase(TOPNOTCH)
A peptide leukocyte granule constituent which kills microbes by creating holes in their membranes.
Defensins(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.40
Predominant form of leukocyte during the first 6 - 24 hours of inflammation.
Neutrophils(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77
Predominant form of leukocyte during 24-48 hrs after the onset of inflammation.
Monocytes(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77
Predominant cellular infiltrate in bacterial infections
Neutrophils(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77
Predominant cellular infiltrate in viral infections
Lymphocytes (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77
Predominant cellular infiltrate in allergic reactions
Eosinophils (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77
Substances responsible for leukocyte-induced tissue injury
Lysosomal enzymes, reactive oxygen and nitrogen species.(TOPNOTCH)
Defective synthesis of CD 18 B-subunit of leukocyte integrins LFA-1 and Mac-1, leading to impaired leukocyte adhesion and migration through endothelium.
Leukocyte adhesion deficiency type 1(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41
Caused by a defect in fucose metabolism resulting in absence of sialyl-lewis X, the oligosaccharide on leukocytes that binds to selectins on activated endothelium.
Leukocyte adhesion deficiency type 2(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41
Results from a defect in the protein involved in membrane docking and fusion.
Chediak-Higashi syndrome(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.41
NADPH deficiency or defect resulting in decreased oxidative burst.
Chronic Granulomatous Disease(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.42
Type of inflammatory mediators that are normally sequestered in intracellular granules and can be rapidly secreted by granule exocytosis or are synthesized de novo in response to a stimulus.
Cell-derived mediators.(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 82
Type of mediators that are produced mainly in the liver and are present in the circulation as inactive precursors that must be activated by proteolytic cleavages to acquire their biologic properties.
Plasma-derived mediators. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 83
The richest sources of histamine
Mast cells (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 83
Causes vasoconstriction or vasodilation: SEROTONIN
Vasoconstriction (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 45
Causes vasoconstriction or vasodilation: PROSTAGLANDINS
Vasodilation (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 46