Karteikarten
Chapter 5
Karten in diesem Stapel (45)
- 1inflammationany injury to vascular tissue activated inflammatory response
- 2classic symptoms of inflammationredness
heat
swelling
pain
loss of function - 3vascular response to inflammationvasodilation
increased vascular permeability
movement of white blood cells - 4vasodilationblood vessel dilation
increases blood flow to injury - 5increased vascular permeabilityleakage of fluid
causes edema at injury - 6movement of WBCsadhere to inner walls of vessels
migrate through the vessels - 7benefits of inflammationprevent infection
limit and control tissue damage
initiate adaptive immune response
initiate healing - 8granulomatosuscapsule that contains the infection
- 9complement systemactivated components can destroy pathogens DIRECTLY
- 10coagulation systemform a fibrinous meshwork at injured or inflamed site
-prevents the spread of infection - 11clotstops bleeding
provides a framework for repair and healing - 12fibrinprimary substance in clotting system
insoluble protein - 13kinin systeminteracts with clotting system
activates and assists inflammatory cells - 14cytokineskinin system
proinflammatory or anti-inflammatory - 15chemokinesinduce leukocyte chemotaxis (WBC)
- 16mast cellsmost important activator of inflammatory response
-contain granules - 17mast cells are found inloose connective tissues near blood vessels near skin and lining of GI and respiratory tract
- 18mast cells activated byphysical injury
chemical agents
immunologic processes - 19degranulation of mast cellsrelease of its contents
- 20synthesis of mast cellsproduce new mediators
- 21histamine released frommast cells
- 22histaminecauses temporary, rapid constriction of smooth muscle and dilation of post-capillary venules
- 23histamine results inincreased blood flow into the microcirculation
- 24histamine binds toreceptors - H1 and H2
pro-inflammatory
anti-inflammatory - 25phagocytosisprocess in which a cell ingests and disposes of foreign material
- 262 most important phagocytesneutrophils
macrophages - 27neutrophilsappear first (24 hours)
- 28steps to phagocytosis1)opsonization, recognition, and adherence
2)engulfment
3)phagosome formation
4)fusion and lysosomal granules
5)destruction of target - 29cellular components of inflammationWBCs or granulocytes
platelets, monocytes, and lymphocytes neutrophils - 30eosinophilsmildly phagocytic
primary defense against parasites
regulate vascular mediators released from mast cell - 31natural killer cellsrecognize and eliminate cells infected with viruses and abnormal host cells, some cancer cells
- 32plateletscytoplasmic fragments formed from megakaryocytes
circulate in blood until needed
interact with components of clotting system - 33monocyteimmature cell in blood
- 34macrophagemature cell in tissues
- 35monocytesproduced in bone marrow
enter circulation
migrate inflammatory site
develop into macrophages - 36macrophages at sitearrive after 24 hours
replace neutrophils - 37macrophage activationincreased size of plasma membrane area
glucose metabolism
increased number of lysosomes
increased secretory products - 38acute inflammationoccurs with all types of cellular and tissue injury
- 39local manifestations of acute inflammationresult from vascular change
leakage of circulating components into the tissue
swelling
pain
heat
redness - 40serous exudatewatery with very few plasma proteins
indicates early inflammation - 41fibrinousthick and clotted
indicated more serious or advanced inflammation - 42purulent of supperative exudateaccumulation of WBC
persistent bacterial infections - 43hemorrhagic exudatebleeding
presence of RBC - 44systemic manifestations of acute inflammationfever
leukocytosis
plasma protein synthesis - 45chronic inflammation> 2 weeks
unsuccessful acute inflammatory response