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109 Cards in this Set

  • Front
  • Back
Two main components of inflammation
Vascular wall response and an inflammatory cell response
Acute inflammation
Involves fluid exudation and polymorphonuclear cell emigration
Chronic inflammation
Involves lymphocytes and macrophages and inducing blood vessel proliferation and scarring
n inflammatory extravascular fluid that has a high protein concentration and cellular debris; specific gravity above 1.020
An extravascular fluid with low protein content and specific gravity below 1.012; an ultrafiltrate of blood plasma resulting from elevated fluid pressures of diminished osmotic forces
Three major components of acute inflammation that cause clinical presentation
Alterations in vascular caliber leading to increased blood flow, structural changes in the microvasculature permitting plasma proteins and leukocytes to leave the circulation to produce inflammatory exudates, and leukocyte emigration from blood vessels and accumulation and site of injury
Vascular changes during inflammation
Vasodilation (increases hydrostatic pressure) and increased vascular permeability (decreases plasma osmotic pressure)
When fluid loss causes concentration of red blood cells and increased blood viscosity (when white cells accumulate along the endothelium [margination]) and begin to emigrate through the vessel wall
Causes of increased vascular permeability
Formation of endothelial gaps in venules (immediate transient response)(caused by endothelial cell contraction [IL1, TNF, IFN gamma effect cytoskeleton, long lived]), Direct endothelial injury (A,C,V, immediate sustained response), Delayed prolonged leakage (V,C, apoptosis/cytokine effects), Leukocyte-mediated endothelial injury, Increased transcytosis (V, vesiculovacuolar organelle), Leakage from new blood vessels
Bind through lectin domain
Immunoglobulin family molecules
ICAM-1 and VCAM-1; bind integrins on leukocytes
Mucin-like glycoproteins
Ligands for leukocyte adhesion molecule CD44; include heparin sulfate
Receptor: Sialyl-Lewis X, PSGL-1; Role: Rolling (neutrophils, monocytes, lymphocytes)
Receptor: Sialyl-Lewis X; Role: Rolling, adhesion to activated endothelium (neutrophils, monocytes, T-cells)
Receptor: CD11/CD18 (LFA-1, Mac-1) (integrins); Role: Adhesion, arrest, transmigration (all leukocytes)
Receptor: VLA4 (integrin); Role: Adhesion (eosinophils, monocytes, lymphocytes)
Receptor: L-selectin; Role: lymphocyte homing to high endothelial venules
Receptor: CD31; Role: leukocyte migration through endothelium
How chemokines and cytokines affect adhesion and transmigration
Redistribution of preformed adhesion molecules to the cell surface, Induction of adhesion molecules on endothelium, Increased avidity of binding
Chemotaxis receptors
G-protein coupled, cause polymerization of actin and facilitation of cell movement
Leukocyte activation
Production of arachidonic acid metabolites, degranulation and secretion of lysosomal enzymes, cytokine secretion, increased adhesion molecule expression and increased integrin avidity
Receptors involved in leukocyte activation
G-protein coupled, toll like receptors, receptors for opsonins, receptors for cytokines
Important recognition proteins for phagocytosis (4)
Fc fragment, C3b (opsonizers) Macrophage mannose and scavenger receptors
Killing and degredation of phagocytosed particles (mechanism)
Activation of NADPH oxidase, converts oxygen to superoxide anion, produces hydrogen peroxide, lysosomal myeloperoxidase converts hydrogen peroxide and chlorine into HOCl
Oxygen independent methods of microbial killing
Bactericidal permeability increasing protein, lysozyme, lactoferrin, major basic protein, defensins
Leukocyte released products that can cause tissue damage
Lysosomal enzymes (frustrated phagocytosis, premature fusion of lysosomes with forming phagosomes, when lysosomes arae damaged by ingested material), oxygen-derived active metabolites, products of arachidonic acid metabolism
Leukocyte adhesion deficiency type I
Defective synthesis of B2 integrins (LFA-1 and Mac-1)
Leukocyte adhesion deficiency type II
Defect in fucose metabolism causing loss of sialyl Lewis X
Genetic defects in phagolysosome formation
Chediak-Higashi syndrome
Genetic defects in microbicidal activity (genes encoding NADPH)
Chronic granulomatous disease
Acquired deficiencies of neutrophils
General principals surrounding the chemical mediators of inflammation
Mediators originate either from plasma of from cells, plasma forms must be activated, cell forms are sequestered in intracellular granules or are synthesized de novo, production of active mediators is triggered by microbial products or by host proteins, such as the proteins of the complement, kinin, and coagulation systems, that are themselves activated by microbes and damaged tissues; mediators bind to speciic receptors on target cells, one mediator can stiumulate the release of other mediators by target cells themselves, once activated and released from the cell most of these mediators are short-lived
Histamine source (3)
Mast cells (main), platelets, basophils
Histamine release from mast cell granules caused by? (6)
Physical injury, immune reactions, anaphylatoxins (complement fragments), histamine-releasing proteins derived from leukocytes, neuropeptides, cytokines
Serotonin source (2)
Platelets and enterochromaffin cells
Causes of serotonin release (2)
Platelet aggergation, PAF
Histamine and serotonin effects
Vasodilation and increased vascular permeability
Two general categories of the biologic function of complement
MAC induced cell lysis, and complement fragment induced changes in vascular permeability, chemotaxis, and opsonization
C3a, C5a, C4a (2): Vascular phenomena
Vascular phenomena: Stimulate histamine release (anaphylatoxins), C5a activated lipoxygenase pathway of arachidonic acid
Complement mediated leukocyte adhesion, chemotaxis, and activation
Complement mediated phagocytosis
C3b and iC3b
C3 and C5 activation
Can be by several proteolytic enzymes present within the inflammatory exudate
Complement regulating factors
Decay accelerating factor (cell-associated) and C1 inhibitor (circulating)
Paroxysmal nocturnal hemoglobinuria
Caused by defects in DAF; characterized by recurrent complement-mediated red cell lysis and anemia
Hereditary angioneurotic edema
Caused by C1 inhibitor deficiency; characterized by episodic, potentially life-threatening edema
Purpose of the kinin system
To produce vasoactive peptides (bradykinin) from kininogens by the action of proteases called kallikreins
Bradykinin functions
Increases vascular permeability and causes contraction of smooth muscle, dilation of blood vessels and pain when injected into the skin
Inactivation of bradykinin
Kininase, inactivation during passage of plasma thought the lung by angiotensin-converting enzyme
Kinin cascade
Factor XII to factor XIIa by surface activation;
Prekallikrein to kallikrein by factor XIIa;
High-mol-weight kininogen to bradykinin by kallikrein
What acts as a cofactor in the activation of Hageman factor?
High mol weight kininogen
What is a potent activator of Hageman factor?
Kallikrein; allows for autocatalytic amplification of the initial stimulus
What has chemotactic activity and can also directly convert C5 to C5a?
Clotting system: intrinsic pathway
Activated by Hageman factor, leads to activation of thrombin, cleavage of fibrinogen, and generation of the fibrin clot
Formed during intrinsic pathway; induces vascular permeability and are chemotactic for leukocytes
Thrombin inflammatory properties
Increased leukocyte adhesion to endothelium via binding to specific protease-activated receptors (platelets, endothelial, and smooth muscle cells)
Activation of Hageman factor
When it encounters collagen or basement membrane or activated platelets; conformational change that exposes an active serine center
The main link between coagulation system and inflammation
Fibrinolytic system
Activated by factor XIIa, produces plasmin to degrade fibrin
PAR-1 induction of inflammation
Mobilization of P-selectin, production of chemokines, expression of endothelial adhesion molecules; induction of cyclooxygenase-2 and production of prostaglandins; production of PAF and nitric oxide; and changes in endothelial shapes
Plasmin functions
Degrades fibrin; cleaves C3, fragments then form fibrin split products that increase vascular permeability and activating Hageman factor
Systems initiated by Hageman factor
Kinin system, clotting system, fibrionlytic system. complement system
Lipid short range signaling molecules from cell membrane derived arachidonic acid, generated by cells responding to activating stimuli
Major enzyme classes that synthesize eicosanoids
Cyclooxygenases (prostaglandins, thromboxanes) and lipoxygenases (leukotrienes and lipoxins)
Prostaglandin I2
Prostaglandin E2
Vasodilation, sensitivity to painful stimuli, can mediate fever
Thromboxane A2
Leukotrienes C4, D4, E4
Increase vascular permeability, cause vasodilation
Leukotrienes B4
Powerful chemotactic agent
Endogenous negative regulators of leukotriene action
Platelet activating factor:
Produced by?
Phospholipid derived mediator produced by mast cells and other leukocytes; Causes platelet aggregation/release, bronchoconstriction, vasodilation, increased vascular permeability, increased leukocyte adhesion, leukocyte chemotaxis
Cytokines produced by?
Lymphocytes and macrophages
IL-1 and TNF secretion
From macrophages, stimulated by endotoxin, immune complexes, toxins, physical injury and a variety of inflammatory products
IL-1 and TNF acute phase reactions
Fever, increased sleep, decreased appetite, increased acute phase proteins, hemodynamic effects, neutrophilia
IL-1 and TNF endothelial activation effects
Increased leukocyte adherence, PGI synthesis, procoagulant activity, and IL-1, IL-8, IL-6, and PDGF; Decreased anticoagulant activity
IL-1 and TNF fibroblast effects
Increased proliferation, collagen synthesis, collagenase, protease, PGE synthesis
IL-1/TNF leukocyte effects
Increased cytokine secretion, priming
CXC chemokines
IL8; recruitment of neutrophils
CC chemokines
Recruitment of monocytes, eosinophils, basophils, and lymphocytes; eotaxin, monocyte chemoattractant protein, macrophage inflammatory protein-1 alpha, RANTES
Cx3C chemokines
Fractalkine (in two forms); Cell surface form: firm lymphocyte and monocyte adhesion; Soluble form: chemoattractant for lymphocytes and monocytes
C chemokines
Specific for lymphocytes
NO functions
Vasodilation, inhibit platelet aggregation and adhesion, kill certain microbes and tumor cells
NO synthesis
From arginine, molecular oxygen, NADPH and other cofactors by nitric oxide synthase
Antimicrobial activity of NO (4)
Reactive nitrogen intermediates, formation of antimicrobial metabolites by interaction between NO and reactive oxygen species, production increased during host response to infections, genetic inactivation of iNOS enhances microbial replication
Specific (secondary) granules
Lysosomal granules in neutrophils that contain lysozyme, collagenase, gelatinase, lactoferrin, plasminogen activator, and histaminase
Azurophil (primary) granules
Lysosomal granules in neutrophils that contain myeloperoxidase, bactericidal factors, acid hydrolases, and a variety of neutral proteases
Alpha1-antitrypsin; inhibit lysosomal enzymes to keep the inflammatory response in check
Substance P
Neuropeptide that mediates vascular permeability, transmits pain signals, regulates blood pressure, and stimulates immune and endocrine cell secretion
Hypoxia-induced factor 1 alpha
Produced by cells deprived of oxygen; can induce the inflammatory response on its own
Mediators of vasodilation (3)
Prostaglandins, NO, histamine
Mediators of increased vascular permeablity
Vasoactive amines, C3a and C5a, bradykinin, leukotrienes C4, D4, E4, PAF, substance P
Mediators of chemotaxis, leukocyte recruiment and activation
Leukotriene B4, chemokines, IL-1, TNF, bacterial products
Mediators of fever
IL-1, TNF, prostaglandins
Mediators of pain (2)
Prostaglandins, bradykinin
Mediators of tissue damage
Neutrophil and macrophage lysosomal enzymes, oxygen metabolites, NO
Serous inflammation
Marked by an outpouring of a thin fluid that is either derived from the plasma or the secretions of mesothelial cells lining the peritoneal, pleural, and pericardial cavities (effusion)
Fibrinous inflammation
Great vascular permeability that results in an exudate rich in fibrinogen. When vascular leaks are large enough or a procoagulant is present
Suppurative/purulent inflammation
Characterized by the production of large amounts of pus or purulent exudate consisting of neutrophils, necrotic cells, and edema fluid
Pyogenic bacteria
Bacteria that produce a localized suppuration
A local defect, or excavation, of the surface of an organ or tissue that is produced by the sloughing of inflammatory necrotic tissue
What chronic inflammation is typified by
Infiltration with mononuclear inflammatory cells, tissue destruction, attempts at healing
Cell types involved in chronic inflammation (4)
Monocytes, lymphocytes, eosinophils, mast cells
Major basic protein
A cationic molecule contained in granules in eosinophils. It is toxic to parasites but also lyses mammalian epithelium
Granulomatous inflammation
A distinctive pattern of chronic inflammatory reaction characterized by focal accumulation of activated macrophages, which often develop an epithelial like appearance
A focus of chronic inflammation consisting of a microscopic aggregation of macrophages that are transformed into epithelium like cells surrounded by a collar of mononuclear leukocytes, principally lymphocytes and occasionally plasma cells
Giant cells
Fused epithelioid cells in the periphery of in the center of granulomas
Foreign body granulomas
Incited by relatively inert foreign bodies; caused by fibers that are large enough to preclude phagocytosis and do not incite any specific inflammatory or immune response
Immune granulomas
Caused by insoluble particles that are capable of inducing a cell-mediated immune response; produces a granuloma when the inciting agent is poorly degradable or particulate
Reactive/inflammatory lymphadenitis
The constellation of lymph nodal histologic changes
Clinical and pathologic changes associated with the acute phase response
Fever, acute phase proteins, leukocytosis, increased pulse and BP, decreased sweating, rigors, chills, anorexia, somnolence, malaise