II - Acute and Chronic Inflammation Flashcards
It is a response of vascularized tissues to infection and damaged tissues that brings cells and molecules of host defense from the circulation to the sites where they are needed, in order to eliminate the offending agents.
Inflammation (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 69
The first step in a typical inflammatory reaction
Recognition of offending agent (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 70
The main components of inflammation
Vascular reaction and cellular response. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 72
The sequential steps in a typical inflammatory reaction
Recognition of offending agent, recruitment of leukocytes and plasma proteins, removal of agent, regulation of response, repair.(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 70
Inflammation which is 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
Initial vascular response to injury
Vasoconstriction.(TOPNOTCH)Robbins Basic Pathology, 8th ed. p.33
Three major components of acute inflammation
Vasodilation, increased permeability, leukocyte emigration. (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 73
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
Denotes an excess fluid in the interstitial tissue or serous cavities
Edema (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
State the molecule in the endothelium responsible for this stage of vascular inflammatory response:Rolling
Selectins (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76
State the molecule in the lymphocyte responsible for this stage of vascular inflammatory response:Firm adhesion
Integrins(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76
State the molecule in the endothelium responsible for this stage of vascular inflammatory response:Transmigration
PECAM-1/CD 31(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 77
State the endothelial adhesion molecule responsible for this stage of vascular inflammatory response:Intercellular adhesion
ICAM -1(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:E-Selectin
Sialyl-Lewis X modified glycoprotein (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:P-Selectin
Sialyl-Lewis X modified glycoprotein (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:ICAM-1
Integrins (TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76
State the lymphocytic adhesion molecule counterpart of the following endothelial receptors:CD-31
CD-31(TOPNOTCH) Robbins Basic Pathology, 9th ed. p. 76
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 leukocytesB. Regulation of responseC. Recognition of injurious agentD. Removal of agentE. 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 Pseudomonas infection.
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
Sequential steps in phagocytosis
Recognition and attachment of particle to be ingested, engulfment and formation of phagocytic vacuole, killing or degradation of ingested material. (TOPNOTCH) Robbins Basic Pathology, 9th ed. P.78
First step in phagocytosis
Recognition and attachment of particle to be ingested(TOPNOTCH) Robbins Basic Pathology, 9th ed. P.78
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