Term
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Definition
| protecttive response intended to eliminate the intial cause of cell injury as well as the necrotic cells and tissues resulting from the original insult. |
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Term
| What does endothelium release in inflammation process? |
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Definition
|
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Term
| What cells are located in the connective tissue for the inflammation process? |
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Definition
| macrophage, lymphocyte, mast cell, monocyte |
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Term
| What does the cell membrane release in the cell membrane? |
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Definition
| leukotrienes from arachidonic acid. |
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Term
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Definition
| neutrophils, eosinophils, basophils, lymphocytes, monocytes, platelets, clotting factors, high-molecular weight kininogen, fibrinolytic factors & complements. |
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Term
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Definition
| endothelial cells, smooth muscle cels, nitric oxide |
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Term
|
Definition
| mast cells, macrophages, lymphocytes, fibroblasts |
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Term
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Definition
| arachidonic acid metabolites: prostaglandins, leukotrienes, lipoxins, & thromboxane |
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Term
| Acute inflammation characterisitics |
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Definition
| minutes to days, blood vessel dilation and leakage, neutrophils entering the surrounding tissues. |
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Term
| Chronic inflammation characterisitics |
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Definition
| lymphocytes, plasma cells, macrophages, healing cells, long term exposure to the noxious agent. |
|
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Term
| What is the primary cellular effectors of acute inflammation? |
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Definition
| polymorphonuclear neutrophil leukocytes. |
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Term
| What cells are involved in chronic inflammation? |
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Definition
| monocytes, macrophages, lymphocytes, and plasma cells. Collectively referred to as mononuclear leukocytes or mononuclear phagocytes. |
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Term
| T/F At any given point an immune reaction is either purely acute or chronic inflammatory phases. |
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Definition
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Term
| Polynuclear neutrophil leukocytes reffer to what immunological cell? |
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Definition
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Term
|
Definition
| redness of an area experiencing increased blood flow during an immune reaction. |
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Term
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Definition
| RBC beome concentrated w/ an increase in viscosity and flow slowly |
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Term
|
Definition
| increased vascular permeability causing fluid to move out & slowing blood flow causes leukocytes to accumulate in the periphery of vessels |
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Term
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Definition
| After increasing vascular permeability, protein-rich fluid moves into the interstitum. |
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Term
| Edema of acute inflammation |
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Definition
| increases in osmotic pressure in interstitial fluid causes outflow of H2O into extravascular space, resulting in edema. |
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Term
|
Definition
| Binds to Integrin in its (high affinity state) on the basal membrane |
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Term
|
Definition
| protein where leukocyte will transmigrate through the membrane into the interstitial space. |
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Term
|
Definition
| when leukocytes stick along the endothelial surface |
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Term
|
Definition
| proteins that are responsible for the rolling of leukocytes. |
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Term
|
Definition
| expressed on endothelium. |
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Term
|
Definition
| expressed on the surface of leukocytes. |
|
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Term
| What inflammatory mediators stimulate the upregulation of selectins? |
|
Definition
| Histamine, thrombin, cytokines (IL-1 & TNF) |
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|
Term
| What proteins are responsible for adhesion of leukocytes on endothelial surfaces? |
|
Definition
| Interaction between integrins on leukocyte cell and integrin ligands expressed on endothelial surfaces. |
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Term
|
Definition
|
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Term
|
Definition
| refers to leukocyte migration toward injyry sites after extravasating from blood vessel. |
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Term
|
Definition
| G-protein activation. Phospholipase C activation. IP3 causes increase in intracellular Ca2+ which triggers the assembly of cytoskeletal contractile elements for formation of pseudopod. |
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Term
| Process of Phagocytosis & degradation |
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Definition
| microbes bind to phagocyte receptors, engulfment of microbes by phagocyte, phagosome fuses with lysosome, degradation of microbes by digestive enzymes & ROS in lysosome. |
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Term
|
Definition
| Prostaglandins, Lipoxins, Nitric Oxide |
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Term
|
Definition
| Prostacyclin (PGI2), PGD2, PGE2, PGF2 |
|
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Term
|
Definition
| Prostagalndin: thromboxane A2 (TXA 2), Leukotrienes (C4, D4, E4). |
|
|
Term
| Increased vascular permeability |
|
Definition
| histamine, bradykinins, leukotrienes, complements (C3, C5a) |
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|
Term
| T/F defects inleukocytes led to incresed infection. |
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Definition
|
|
Term
| Defects in leukocyte function |
|
Definition
| radiation injury, cancer therapy, drug sensitivity, defects in leukocyte adhesion molecules, lack of ability to generate superoxide. |
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|
Term
| Inflammation-induced tissue injury causes |
|
Definition
| Lysosomal enzymes, free radicals, vascula damage to allow diapedesis, phagocytosis of local cells. |
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Term
| Possible outcomes with acute inflammation |
|
Definition
| Complete resolution, Healing by scarring or fibrosis, progression to chronic inflammation |
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Term
|
Definition
| no or minimal tissue damage. |
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Term
| Healing by scarring or fibrosis |
|
Definition
| after substantial loss in connective tissue framework or damage to non-regenerating cells |
|
|
Term
| Progression to chronic inflammation |
|
Definition
| when neutrophils and their fast-acting molecular allies cannot remove the noxious agent. Injurious agent persists over a prolonged period, causing concomitant tissue destruction. |
|
|
Term
| Cardinal signs of acute inflammation |
|
Definition
| Redness, Warmth, Swelling, Pain, Functional loss |
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Term
|
Definition
| Inflammation of prolonged duration. Lacks the vascular changes which are typical of acute inflammation. |
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|
Term
| Characteristics of chronic inflammation |
|
Definition
| mononuclear phagocyte system, tissue destruction by inflammatory cells, repair involving new vessels (angiogenesis), fibrosis: proliferation of fibroblasts, resulting in the accumulation of ECM. |
|
|
Term
| Mononuclear phagocyte system |
|
Definition
| infiltration with mononuclear cells |
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|
Term
| Mononuclear phagocyte system |
|
Definition
| infiltration with mononuclear cells (macrophages, lymphocytes and plasma cells) |
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Term
| Causes of chronic inflammation |
|
Definition
| persistent infections, prolonged expsoure to toxic agents: smoking, chronically elevated plasma lipd levels: atherosclerosis, non-degradable exogenous materials, inahled particulate silica. |
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Term
|
Definition
| immune reactino against self-antigen, multiple sclerosis, rheumatoid arthritis. |
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Term
|
Definition
| Derived ffrom monocytes which are attracted to the area of inflammation. Transformed in the extravascular tissue. |
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|
Term
| Cells involved in chronic inflammation |
|
Definition
| monocytes, macrophages, lymphocytes, plasma cells. |
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|
Term
| Vascular changes during acute inflammation |
|
Definition
| initial vasoconstriction foolowed by vasodilation |
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Term
|
Definition
| redness because of increased blood flow |
|
|
Term
|
Definition
| protein-poor blood fluid moves out of the vessel into interstitial space |
|
|
Term
| Erythrocyte packing: stasis |
|
Definition
| RBCs become concentrated w/ an increse in viscosity and flow slowly. |
|
|
Term
|
Definition
| neutrophilos start to acuumulate along the endothelial surface. |
|
|
Term
|
Definition
| Neutrophiuls migrate through vascular wll into interstitial space. |
|
|
Term
|
Definition
| upon further increasing vascular permeability, protein-rich fluid moves into the interstitum. |
|
|
Term
|
Definition
| an increase in osmotic pressure in interstitial fluid causes outflow of H2O into extravascular space, resulting in edema. |
|
|
Term
|
Definition
| stimjulate the upregulation of selectins such as histamine, thrombin, cytokines (Il-1 & TNF) |
|
|
Term
|
Definition
| occurs through interaction b/n integrins expressed on leukocyte cell surfaces and integrin ligands (VCAM-1) & ICAM-1 expressed on endothelial surfaces. |
|
|
Term
| Where are macrophages tansformed into macrophage? |
|
Definition
|
|
Term
| What particle activates macrophages? |
|
Definition
| Cytokines secreted from activated T cells. |
|
|
Term
| What biologically active products are released by macrophages? |
|
Definition
| Proteases, reactive oxygen species, cytokines (Il-1, Il-6, TNFa), complement components, arachidonic acid metabolites. |
|
|
Term
| What chemicals recruit B & T cells? |
|
Definition
| Adhesion molecules and chemokines that recruit monocytes. |
|
|
Term
| What activates lymphocytes? |
|
Definition
| They are activated by processed antigen fragments present in macrophages. |
|
|
Term
| What do mast cells do in an injury? |
|
Definition
| armed with IgE, produce histamines & metabolites of AA for vascular change. Central players in anaphylactic shock |
|
|
Term
| T/F Neutrophils can further differentiate after arriving at the site of inflammation. |
|
Definition
|
|
Term
| T/F Neutrophils are incapable of cell division |
|
Definition
|
|
Term
| T/F Macrophages are mitotically active |
|
Definition
|
|
Term
| Macrophages do what else besides stereotypical mission |
|
Definition
| Mediate systemic effects like fever, leukocytosis, acute phase response induction. |
|
|
Term
|
Definition
| lymph nodes maay be swollen, tneder sking over node may be reddened and hot. |
|
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Term
|
Definition
| lymphatic vessesl are inflammed. faint obvious throbbing pain along the affected area is common, high fever and chills may be present. |
|
|
Term
|
Definition
| edema caused by the buildup of too much lymph fluid in the tissues. Can result frmo surgery, radiation, infection or trauma. |
|
|
Term
| Acute phase reaction of systemic effects of inflammation |
|
Definition
| fever, drowsiness, malaise, anorexia, hypotension, accelerated degradation of skeletal muscle, increased WBC 15,000-20,000 (bacteria). Leukopenia (viral). Il-1, Il-6, TNF |
|
|
Term
| What is common effect of WBC during systemic effects of inflammation with a virus? |
|
Definition
|
|
Term
| T/F. Longer inflammatory phase, the greater local tissue damage occurs. |
|
Definition
|
|
Term
|
Definition
| anti-inflammatory effects which can limit wound healing and fibrosis. |
|
|
Term
| Labile cel proliferation potential |
|
Definition
| divide continuously to replace older cells undergoing apoptosis. basal cell layer of the epidermis. lining of the respiratory and GI tract. Stem cells. |
|
|
Term
| Stable cell proliferation potential |
|
Definition
| cells that do not normally divide. can be induced to divide by injury: liver cells. |
|
|
Term
| Permanent Cell proliferation potential |
|
Definition
| incapable of regeneration after injury: heart and neurons. |
|
|
Term
|
Definition
| acts like a glue to hold the components of the ECM together. links the ECM to cell via cell surface integrins. |
|
|
Term
|
Definition
| Most abundant glycoproteins in BM. Connects cells to ECM components such as type IV collagen. modulates cell survival, proliferation, differentiation, and motility. |
|
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Term
|
Definition
| cells that make the structural fibes and ground substance of connective tissue such as collagens, elastic fibers, and glycoproteins. tissue damage stimulates fibroblasts to unergo mitosis, increase the number of fibroblasts. |
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|
Term
| Repair by connective tissue |
|
Definition
| Severe or persisten tissue injury to both parenchymal cells and stromal framework limits/ prevents regeneration of original tissue. Repaire occurs by replacing the injured/ dead parenchyme with connective tissue resulting in firbrosis and scarring. |
|
|
Term
| Sequential process involved in fibrous repair |
|
Definition
| Formatino of granulation tissue, angiogenesis, migration of fibroblasts & ECM deposition (Scar formation). |
|
|
Term
|
Definition
| specialized tissue characteristic of healing at injured sites. pink/red, soft with a granular appearance. composed of porliferating fibroblasts and new capillaries. progressively lays down ECM. |
|
|
Term
|
Definition
| refers to formatino of new blood vessels. |
|
|
Term
| Two processes for angiogenesis |
|
Definition
| mobilizing endothelial precursor cells from bone marrow to an injured site. Sprouting new blood vessesl from preexisting blood vessels. |
|
|
Term
|
Definition
| excess amount of cllagen synthesis |
|
|
Term
|
Definition
| excess accumulation of granulation tissues. |
|
|
Term
| Pathway for Angiogensis from preexisting blood vessels |
|
Definition
| Increased permeability of vessel by VEGF->migration of enothelial cells toward angiogenic stimulus->proliferation of endothelial cells behind the leading edge->Recruitment of smooth muscle cells->maturation to functional vessels. |
|
|
Term
| Pathway of EPC angiogenesis |
|
Definition
| growth factors (PDGF,bFGF,TGF-B) secreted from activated endothelial cell & other inflammatory cells, migratino and proliferation of fibroblasts, diposition of ECM, decrease proliferating fibroblasts, gradual regression of vasculature, vascular scar formation. |
|
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Term
|
Definition
| continuous modification and remodeling of scar ECM after its synthesis and depostion. outcome of ECM in each stage is balanced by synthesis. enzymes degrade collagens and other components of ECM called matrix metalloproteinases depend on zinc ion for their activity. tightly regulated in tissues since they have potential damdage tissues. |
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