Chapter 1 Inflammatory Response Flashcards
What are the 4 classic signs of acute inflammation
Rubor (red), calor (heat), dolor (pain), and tumor (swelling)
insult or injury results in a rapid and inconsistent transient vaso________ (immediate hemostasis) Vaso_______ is stimulated by vasoactive agensts (cathecholamines, serotonin, bradykinin, and prostaglandins) that are released by the surrounding tissues and norepinephrine.
Within minutes, vaso_____ occurs. This improveves blood flow and local delivery of soluble mediators and inflammatory cells.
Vaso_____ is induced by vascular smooth muscle changes (nitric oxide, histamine, leukotirienes, prostaglandins, and complement factors).
Lymphatic proliferations – to accommodate drainage of edema.
Vasodilation
insult or injury results in a rapid and inconsistent transient vasoconstriction (immediate hemostasis) Vasoconstriction is stimulated by vasoactive agensts (cathecholamines, serotonin, bradykinin, and prostaglandins) that are released by the surrounding tissues and norepinephrine.
Within minutes, vasodilation occurs. This improveves blood flow and local delivery of soluble mediators and inflammatory cells.
Vasodilation is induced by vascular smooth muscle changes (nitric oxide, histamine, leukotirienes, prostaglandins, and complement factors).
Lymphatic proliferations – to accommodate drainage of edema.
Vasodilation is followed by an increase in vascular ______________.
Etiologies
Transcytoplasmic channels - Increase in number and size of intracellular endothelial gaps in the venules (histamine and serotonin). Allows transcytosis of plasma products
Endothelial cell retraction and interendothelial gap formation (hypoxia, endothelial injury, cytokines, and inflammatory mediators).
Loss of serum protein – decreases intravascular osmotic pressure, increases blood viscosity, and increases interstitial osmotic pressure. Leading to edema accumulation and delivery of soluble factors (antibodies and acute phase proteins).
Vasodilation is followed by an increase in vascular permeability.
Etiologies
Transcytoplasmic channels - Increase in number and size of intracellular endothelial gaps in the venules (histamine and serotonin). Allows transcytosis of plasma products
Endothelial cell retraction and interendothelial gap formation (hypoxia, endothelial injury, cytokines, and inflammatory mediators).
Loss of serum protein – decreases intravascular osmotic pressure, increases blood viscosity, and increases interstitial osmotic pressure. Leading to edema accumulation and delivery of soluble factors (antibodies and acute phase proteins).
Fluid loss leads to erythrocyte _______in local vasculature. This combined with a decreased hydrostatic pressure leads to intravascular stasis and congestion. Stasis allows for increased contact among erythrocytes, leukocytes, and the vascular endothelium. Leading to leukocyte _______
Fluid loss leads to erythrocyte concentrating in local vasculature. This combined with a decreased hydrostatic pressure leads to intravascular stasis and congestion. Stasis allows for increased contact among erythrocytes, leukocytes, and the vascular endothelium. Leading to leukocyte extravasation
_______– facilitates leukocyte interaction with endothelial cells, primarily in the systemic postcapillary benules and the pulmonary capillaries.
The intimate association promotes weak, transient interactions between the glycoprotein cell adhesion molecules on endothelial cells (selectins) and their corresponding ligands on inflammatory leukocytes.
These weak bonds break with the rolling of leukocytes along the endothelium at a velocity proportionate to blood flow
Higher affinity interactions develop between endothelial cells and leukocytes.
Formed by ______(proteins) which are on leukocytes and expression and binding affinity increases in the presence of proinflammatory mediators.
Migration – facilitates leukocyte interaction with endothelial cells, primarily in the systemic postcapillary benules and the pulmonary capillaries.
The intimate association promotes weak, transient interactions between the glycoprotein cell adhesion molecules on endothelial cells (selectins) and their corresponding ligands on inflammatory leukocytes.
These weak bonds break with the rolling of leukocytes along the endothelium at a velocity proportionate to blood flow
Higher affinity interactions develop between endothelial cells and leukocytes.
Formed by integrins (proteins) which are on leukocytes and expression and binding affinity increases in the presence of proinflammatory mediators.
____– leukocytes migration following adherence.
Interendothelial junctions of poscapillary venules enable migration along with endothelial cell retraction and cell adhesion molecules.
Once within the interstitial space, leukocyte migration occurs along chemical gradients of ____(bacterial byproducts) and/or ____(complement components, chemokines) chemoattractant agents.
Diapedesis – leukocytes migration following adherence.
Interendothelial junctions of poscapillary venules enable migration along with endothelial cell retraction and cell adhesion molecules.
Once within the interstitial space, leukocyte migration occurs along chemical gradients of exogenous (bacterial byproducts) and/or endogenous (complement components, chemokines) chemoattractant agents.
Neutrophils:
Most numerous circulating _____.
First migratory cell to arrive and take a predominant role in acute inflammation.
Attracted to injury by: _______(cytokines, complement components, bacterial products)
Provide: local killing and degradation of bacterial macromolecules via ________and release of superoxide radicals. They also stimulate further inflammation.
Necrosis and apoptosis occurs and are phagocytized by macrophages. These macrophages then begin to release anti-inflammatory mediators and decrease production of proinflammatory cytokines. Replaced by ______within 24-48 hours.
Sepsis may delay neutrophil apoptosis, prolong proinflammatory state and promote tissue damage.
Most numerous circulating leukocyte
First migratory cell to arrive and take a predominant role in acute inflammation
Attracted to injury by: chemoattractants (cytokines, complement components, bacterial products)
Provide: local killing and degradation of bacterial macromolecules via phagocytosis and release of superoxide radicals. They also stimulate further inflammation.
Necrosis and apoptosis occurs and are phagocytized by macrophages. These macrophages then begin to release anti-inflammatory mediators and decrease production of proinflammatory cytokines. Replaced by macrophages within 24-48 hours.
Sepsis may delay neutrophil apoptosis, prolong proinflammatory state and promote tissue damage.
Macrophages:
Integral to the inflammatory response, wound debridement, and tissue repair
Chemoattractants: cytokins, fibronectin, elastin, complement factors, thrombin, and growth factors attract macrophages.
Debridement occurs through phagocytosis of foreign material, pathogens, and damaged cells. They also secrete ______and elastases that dissolve damaged tissue matrix .
As the acute inflammatory response resolves, macrophages produce growth factors that stimulate fibroblasts to produce collagen aiding in wound repair and healing of the inflamed tissue.
Integral to the inflammatory response, wound debridement, and tissue repair
Chemoattractants: cytokins, fibronectin, elastin, complement factors, thrombin, and growth factors attract macrophages.
Debridement occurs through phagocytosis of foreign material, pathogens, and damaged cells. They also secrete collagenases and elastases that dissolve damaged tissue matrix .
As the acute inflammatory response resolves, macrophages produce growth factors that stimulate fibroblasts to produce collagen aiding in wound repair and healing of the inflamed tissue.
Lymphocytes:
Aquired immunity and protective inflammatory responses
____and ____T cells are major components of cell mediated immunity.
____further differentiate into T helper s.
Th1 – under the influence of IFN- gamma and IL-12 exert influences on macrophages by maximizing the bacterial killing potential of macrophages and stimulating proliferation of cytotoxic T cells.
Aquired immunity and protective inflammatory responses
CD4 and CD8 T cells are major components of cell mediated immunity.
CD4 further differentiate into T helper s.
Th1 – under the influence of IFN- gamma and IL-12 exert influences on macrophages by maximizing the bacterial killing potential of macrophages and stimulating proliferation of cytotoxic T cells.
Mast Cells:
Ubiquitously distributed in all organs and degranulate in response to physical trauma, compliment factors, microbial products, or neuropeptides.
Primary source of ______
Release proinflammatory mediators (serotonin, leukotrienes, prostaglandin, metabolites, heparin, and cytokines.
Overall enhances the local inflammatory response
Ubiquitously distributed in all organs and degranulate in response to physical trauma, compliment factors, microbial products, or neuropeptides.
Primary source of histamine
Release proinflammatory mediators (serotonin, leukotrienes, prostaglandin, metabolites, heparin, and cytokines.
Overall enhances the local inflammatory response
