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51 Cards in this Set
- Front
- Back
define inflammation?
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vascular and cellular response of local tissue to injury resulting in accumulation of fluid and leukocytes in extravascular tissues (a delivery system)
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what does inflammation consist of?
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hemodynamic and vascular events, inflammatory mediators from blood plasma (humoral) and cells (cellular), cellular infiltration
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what initiates inflammation?
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infectious agent, mechanical, chemical, or immunological injury
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what are two basic features of inflammation?
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nondiscering and stereotyped
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how is inflammation protective?
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destroys, dilutes, walls off agent of injury, set stage for repair of injured tissue by regeneration or repair
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how is inflammation harmful?
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hypersensitivity reactions (drugs, insect bites, toxins), chronic inflammation diseases (rheumatoid arthritis, immune complex glomerulonephritis, pemphigus vulgaris), fibrosis/scarring
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what occurs if there is a failure of response with inflammation?
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infections unchecked, wounds unhealed, permanent festering sores
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what are the cardinal signs of inflammation?
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heat (calor), swelling (tumor), redness (rubor), pain (dolor), loss of function (functio laesa)
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what does the suffix -itis indicate?
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inflammation of an organ
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what does the suffix -sis indicate?
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any abnormal process or condition affecting an organ
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what is the term for the inflammation of the spinal cord?
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myelitis
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what is the term for the inflammation of the vein?
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phlebitis
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what is the term for the inflammation of the lips?
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chelitis
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what is the term for the inflammation of the bone marrow?
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osteomyelitis
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what is the term for the inflammation of the cecum?
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cecitis or typhlitis
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what is the term for the inflammation of the oviduct?
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salpingitis
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what is the term for the inflammation of the lung?
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pneumonia/pneumonitis
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what is acute inflammation?
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exudative process designed to dilute (increase fluid in tissue space) and remove (via influx of inflammatory cells) injurious agents
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what is chronic inflammation?
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proliferative response, includes process of repair; scarring, neovascularization, reconstruction of damaged tissue
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what is the clinical course for acute inflammation?
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min-48hours
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what is the cellular response to acute inflammation?
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neutrophils
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what is the vascular response to acute inflammation?
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increased permeability and vasodilation
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what is the matrix of acute inflammation?
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edema and fibrin
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what is the clinical course for subacute inflammation?
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poorly defined, 3-7days
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what is the cellular response to subacute inflammation?
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neutrophils and macrophages and lymphocytes
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what is the vascular response to subacute inflammation?
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increased permeability, endothelial hypertrophy, hyperplasia
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what is the matrix of subacute inflammation?
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edema and fibrin
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what is the clinical course for chronic inflammation?
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7days-yrs
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what is the cellular response to chronic inflammation?
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macrophages, lymphocytes, plasma cells
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what is the vascular response to chronic inflammation?
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neovascularization
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what is the matrix of chronic inflammation?
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collagen (fibrous)
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what are the vascular events in acute inflammation?
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hemodynamic adjustments, increased vascular permeability, exudate (inflammatory edema) formation
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what occurs in tissues without adequate perfusion during acute inflammation?
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cannot support inflammatory response (lack of vascular events) and there is no inflammation in dead/avascular tissue)
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what hemodynamic adjustments occur in acute inflammation?
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(1) transient arteriolar vasoconstriction (inconsistent) (2) arterioles dilate first followed by adjacent capillaries resulting in (a) increased blood flow (active hyperemia; redness, heat) that brings in inflammatory mediators and leukocytes (b) local hemoconcentration and slowing of blood flow in capillaries and venules (passive hyperemia or congestion)
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what causes increased vascular permeability during acute inflammation?
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intercellular gaps form in post-capillary venules and endothelial cell injury
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what causes intercellular gaps to form in post-capillary venules?
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mast cell degranulation that causes endothelial contraction (receptor-mediated) via an immediate transient response caused by mediators (histamine, serotonin, bardykinin, kinins, leukotrienes, lymphokines, PAF, fibrinopeptides and delayed (4hrs) and prolonged (>24hrs) do to cytoskeletal reorganizaiont (IL1/TNF, hypoxia)
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what are the mediators of intercellular gaps in post-capillary venules?
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histamine, serotonin, bardykinin, kinins, leukotrienes, lymphokines, PAF, fibrinopeptides
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what causes direct endothelial injury resulting in increased vascular permeability?
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endotoxin, radiation, NO, O2, radicals, chemicals
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what type of process is the direct endothelial injury?
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necrosis
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in direct endothelial injury, toxins, burns, and chemicals occur where?
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immediate prolonged inflammation in any vessel type
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in direct endothelial injury, leukocyte-dependent injury (vasculitis, immune-mediated) occurs where?
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mostly post-capillary venules
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what are the patterns of vascular leakage responses?
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immediate transient (mins), delayed prolonged, immediate prolonged
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what causes and where does immediate transient vascular leakage occur?
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histamine on postcapillary venules
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what causes and where does delayed prolonged vascular leakage occur?
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damaged but not necrotizing effect on endothelial cells (UV radiation sunburn) all vessel types
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what causes and where does immediate prolonged vascular leakage occur?
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agents causing direct endothelial damage and death (burn) all vessel types
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when does exudate (inflammatory edema) formation occur?
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severe damage to vascular permeability; leakage of blood coagulation proteins (fibrinogen) into tissue space which polymerizes to fibrin
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when is exudate (inflammatory edema) formation seen clinically?
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when local lymphatic drainage is saturated and backs up
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how might exudate (inflammatory edema) formation be spread?
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lymphatics may also serve to spread inflammatory process to regional lymph nodes resulting in lymphadenitis then systemic inflammation
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what is permeability?
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fluids and proteins leak into surrounding extravascular tissues carrying acute phase proteins, complement, fibrinogen, fibronectin, antibodies
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the early vascular events of inflammation provide the physiologic basis for what?
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lewis triple response reaction, an example of mild acute inflammation
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what is the lewis triple response reaction?
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(1) red line appears (arteriole dilation) (2) red halo around line called a flare (hyperemia) (3) swelling around line, blanching of original mark (edema)
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