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65 Cards in this Set

  • Front
  • Back
Histamine sources
Mast cells, platelets, basophils
Nitric Oxide Sources
Mast cells, platelets, basophils
Heparin sources
Mast cells, basophils
Kinins (bradykinin) sources
Circulating alpha-2 globulins,
neutrophils,
parenchymal cells
Histamine actions
Cause endothelium to become sticky and adhese to neutrophils and macrophages
Nitric oxide action
Mediate sm muscle contraxn and pain. Cause endothelium to become sticky.
Heparin action
Prevents early coagulation to allow fluids out-activates antithrombin III (inhibts intrinsic), and inhibits platelet formation
Kinin (brady) action
Vasodilation,
inc cap perm,
mediate pain,
stim histamine release, activate eicosanoid cascade.
Eicosanoids, namely leukotrienes, are made from what?
Cell membranes of neutrophils, basophils, eosinophils, macrophages, mast cells.
LTB4 action
Chemotaxis
make neutrophils stickier
-promote resp burst and stimulate enzyme release by neutrophils
Stim Ig produxn by B lymphocytes
LTC4, LTD4, LTE4 actions
Inc cap perm:
Cause enothelium to contract and round up
Chemotaxis for neutrophils
Stim produxn of O2 metabolites and release of enzymes by WBCs
Chemotactic for eosinophils
Stim phospholipase
Eicosanoid prostaglandin source
Macrophages
Platelets
Eicosanoid prostaglandin action
Vasodilation
Pain mediation
PGE's induce release of neutrophils into the circulation from bone marrow and peripheral storage pools
Acute phase protein-serum amyloid A's source
Hepatocytes
Serum amyloid A action
Induce adhesion to and migration of leukocytes through endothelium
Alters cholesterol metab in macrophages
Acute phase protein fibrinogen source
Hepatocytes
Fibrinogen action
Walls off bacterial agents
Forms meshwork/scaffolding for healing process to start
Increases RBC aggregation
Acute phase protein Complement proteins source
Hepatocytes and macrophages
complement protein action
Form lytic complex to poke holes in target cells
Opsonization of bacterial cells
Chemotaxis for neutrophils
Fragments inc vasc perm
Iron binding proteins (lactoferin) source
Neutrophils
Iron binding protein lactoferin action
Remove Fe from Fe-transferin in tissue fluids
Produces oxidizing agents
Fibronectin (plasma soluble form) source and action
Hepatocytes
Opsonize bacterial cells
activates macrophages to phagocytose
Causes macrophages to express Fc and C3 rcptrs
Fibronectin (insoluble form) action
Links cells to ec matrix
Maintain cell shape
Promote fibroblast growth
Promote platelet adhesion
serves as connector btwn fibrin and macrophage during repair
Attracts fibroblasts into a wound and tethers them there
IFN alpha source
WBCS
Fibroblasts
IFN alpha action
Slow virus spread till Ab's made
Inhibit protein syntheses in adjacent cells: stim expression of enzyme that degrades mRNA
Inhibit produxn of enzyme that starts translation
IFN beta source
WBCs
Fibroblasts
IFN beta action
Slow the spread of virus till Ab's made
Inhibit protein expression in adjacent cells (enzymes for degrading mRNA and inhibiting translation)
IFN gamma source
Lymphocytes
IFN gamma action
Stim NK cells
Cause inflamm cells to express Fc and C3b
Activate macrophages by stim NO synthetase and inducing syn of enzymes tha are antiprotozoal in nature.
Enhance Ag processing and recognition
IL 1 source
Endothelium
Macrophages
IL 1 action
Acute phase protein syn
Cause sticky endothelium
Stim neutrophil migration
Immunological rxns
stim hypothalmus to produce
fever by stimulating PG
produxn and release
Stim sleep cntr and ACTH
release
Stim PG produxn and resp
burst
Act alons w/ IFNgamma and
IL2 to enhance inflamm
and immune response
Bone and cartilage resorptn
by stimulating osteoclast
IL 1RA source
activated macrophages
IL 1RA action
Competes with IL 1 for IL 1 rcptr. Modifies and dampens inflamm response
IL 2 and IL 15 souces
Ag-stimulated T cells
IL 2 and IL 15 action
Stim helper T cells (TH 1 cells) and B-cell proliferation.
Enhance activity of cytotoxic T cells and NK cells
IL 3 source
Activated T cells
IL 3 action
Hemopoietin (stimulates stem cells for all cell lines)
Stim mature mast cells and macrophages to divide and prvnt immature death.
IL 4 and IL 13 action
Suppress inflammation (w/10)
and enhance immunity
Activate T hlprs to stim B cells to produce Ab
Note: IgE synthesis depndnt on 4
IL 5 action
Stim eosinophils proliferation during paasitic infxns.
Only Il specific for eosinophils
IL 6 source
T cells, stromal cells, epithelial cells, and other inflamm cells
IL 6 action
Stim hepatocytes to make acute phase proteins
Stim IgA produxn
persistant IL 6 results in bone marrow produxn shift from neutrophils to macropgs
IL 8 source
Macrophages, endothelium, fibroblasts
IL 8 action
Stim neutrophils migration into site of inflamm by:
Adhesion expression on neutrophils
Stim neutrophil activation and degranulation
IL 10 source
Helper T cells
IL 10 action
Inhibit inflammation
Works w/ 4 and 13 to dampen macrophage and neutrophil response
Stim B and T cells
Inhibit macrophages from making proinflamm ck's
IL 12 source
Macrophages
Neutrophils
B cells
IL 12 action
Stim cell mediated immunity
Stim T helprs that reg cell mediated immunity
Stim NK cells
Stim IFN gamma release
IL 13 action
Binds T cells responsible for mediating the hyperresponsiveness of airways (asthma)
IFN alpha source
Activated macropgs
Neutrophils
Lymphocytes
NK cells
Enothelial cells
TNF alpha action
Promotes scar formation
Acts w/ IL1 to make fever
Makes enothel sticky
Directly kill certain bact
Cachetin
TNF beta source
Lymphocytes
TNF beta action
Lymphotoxin
Kills infected cells
Needed for normal lymphoid dvlpmnt
Chemokine MIPs source
Activated macrophages
MIP action
Stim lymphocytes and macrophages
Activate fibroblasts
Chemokine MCP-1 source
Endothelium
Sm muscle
Activated macrophages
MCP-1 action
Attracts macrophages to inflammation site
Chemokine Granulysin source
Cytotoxic T cells
Granylysin action
Kills pathogenic bact
Chemokine VEGF source
Most tissue cells, not endothelium
VEGF action
Angiogenesis in wound healing
Increases vascular permeability
Chemokine PDGF source
platelets
endothelium
macrophages
PDGF action
Induces fibroblasts, monoctes and sm muscle cells into lesion
Chemokines EGF and FGF source
Epithelium
Macrophages
Platelet activating factor source
WBCs
Platelets
Vascular endothelium
Platelet activating factor action
Cause platelets and WBCs to aggregate and adhere to vasc endothelium
Causes WBCs to release enzymes and free radicals
Inc vasc permeability