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It fills in a cut, but it won’t contract and it wont function. for example a MI will cause scar tissue and then it won’t contract.
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Depends on cell type. Myocardium won’t regenerate cell types. Skin cells WILL regenerate.
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what are some things that cause the inflammatory response? |
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Infection, mechanical damage, ischemia, nutrient deprivation, temperature extremes, radiation
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T or F...the inflammatory response will always happen? |
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true, however it's efficiency is always variable. |
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what are the two types of inflammation? |
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what is the vascular response? |
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vasodilation, increased permiability and leakage, wbc adherance to the inner walls, and migration through the vessels |
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what are the two types of lymphocytes? |
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what makes lymphocytes so important? |
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they help with immunity, NOT inflammation |
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requires the immune system, good example is TB, will cause chronic tissue |
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phagocytosis and they cause mast cells to migrate to the injury to release histamine. they are a type of leukocyte |
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T OR F: the inflammatory response is non specific and is a aprt of the vascular component |
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the vascular phase cause hemodynamic changes...what does that mean? |
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it means that it causes vasoconstriction or vasodilation. it changes the way blood circulates. |
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what is the cellular phase? |
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it is the phase that controls the actions of the wbc's. |
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inflammatory mediators are...? |
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increased blood flow to an area. it causes an area congested with blood. |
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what do kinins, histamine and prostagladins do? |
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they increase capillary permiability |
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an increase in capillary permiability causes? |
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fluid exudate production and the vascular response |
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granular, cell derived cells, located in the connective tissue near blood vessels. degranulation causes histamine to be released |
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where are plasma proteins synthesized? |
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vasoactive chemical causes vasodilation and increased permiability. |
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what does histamine bond to? |
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why is the chemotactice factor important? |
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because it will make neutrophil chemotactic factor, which will cause neutrophils to come to the area of injury. |
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eosinophil chemotactic factor of anaphalaxis. attracks eosinophils. |
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what will be be activated once histamine is activated? |
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leukotrienes, prostaglandins, and platelet activating factor. |
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a product of the arachidonic acid from mast cell membranes |
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what causes similar affect to histamine? |
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leukotrienes, but it happens after histamine is released. |
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leukotrienes will cause...? |
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hemodynamic products to increase |
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they are similar to leukotrienes, they induce pain |
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what will stop prostaglandin affects? |
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Definition
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platelet activating factor |
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similar to leukotrienes and platelet activation. they activate neutrophils. it has a clotting factor |
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can destroy pathogens directly. activates every components of the inflammatory response |
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what is coagulation of the clotting system so important? |
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no spreading of germs, it keeps germs where they are to be killed, forms a clot, provides a framework for healing |
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fibrin, an insoluble protein |
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activates and assists inflammatory cells |
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what is the primary kinin? |
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Definition
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what does the kinin system do? |
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dilation of blood vessels, pain, smooth muscle contraction, leukocytes chemotaxis. |
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adherence to leukocytes to endothelial cells |
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emigration of cells through the endothelial junctions |
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aka PMN's. part of early response. short lived and are a part of purulent exodate. |
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produced in the bone marrow, enter circulation and go to the siteof injury. they develope into macrophages. |
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develope from monocytes, arrive 24 hours alter after neutrophils |
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what are the 2 types of cytokines? |
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interferons and interleukins |
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produced by macrophages and lymphocytes in response to a pathogen. |
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interleukin 1 is a proinflammatory cytokine |
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interleukin 10 is an anti inflammatory cytokine |
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protect against viral infections, 2 types (IFN alpha and IFN beta), released by viral double stranded RNA |
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found early and it's mild. never pop a blister, it is msotly white blood cells |
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it can dilute toxins, carry plasma proteins tothe area of injury, and help carry away dead cells and toxins from bacteria. |
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early and usually moderate. pink fluid. |
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usually it's severe. it is an area with a lot of fibrin which can encourage adhesions. |
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what are the signs of inflammation? |
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rubor, calor, doler, tumor, functio laesa |
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because of hyperemia from vasodilation. |
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because of an increase in metabolism at the inflammatory site |
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a change in ph causes nerve stimulation by chemicals. |
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fluid shifts to interstitial spaces. it causes accumulations. |
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what do endothelial cells have that is so important? |
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Definition
it has growth factors that stimulate angionesis and extracellular synthesis. |
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neutrophils and macrophages have manose receptors that bind to? |
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a granulocyte, oxygen dependent that genarte toxic oxygen to engulf pathogens with. |
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what prodces hydrogen peroxide and nitric oxide? why is this so important? |
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neutrophils. it is important because they kill the pathogens |
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an increase in circulating wbc's |
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immature neutrophil are called? |
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derived from bone marrow, exit the circulation at the sign of inflammation and mature into macrophages. |
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what are vasoactive mediators? |
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prostaglandins, leukotrienes, platelet activating factor. they are produced by monocytes and macrophages |
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what engulfs the largest pathogens: neutrophils or macrophages? |
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Definition
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used during allergic reactions and parasites. |
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derived from bone marrow. contains histamine. they bind IgE to receptors which causes release of histamine. |
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what induced vasodilation? |
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Definition
histamine an nitric oxide (they are both mediators) |
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what are the vascular stages? |
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Definition
vasodilation, permiability |
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what happens after vasodilation of the vascular stage? |
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Definition
increased permiability of the microvasculature, and the pouring of exudate (protein rich) into the extravascular spaces. |
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what does the loss of plasma proteins in the vacular stage cause? |
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Definition
it reduces intracapillary osmotic pressure of the interstitial fluid causes fluid to move in the cells which causes swelling |
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what do histamine, bradykinin, and leukotrienes do during the vascular stage? |
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Definition
they cause vascular leakage which causes junctions to form. |
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immediate transient response |
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Definition
occurs with minor injury. reversable and short duration. |
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immediate sustained response |
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serious injuries and it lasts for days. due to direct damage to endothelium. (neutrophils can bind to the endothelium and cause damage) |
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delayed hemodynamic response |
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Definition
due to radiation or burns. it is a delayed response |
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what are the 3 types of vascular responses in response to different severities of injury? |
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Definition
immediate transient responses, immediate sutained response, and delayed hemodynamic response |
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what are the stages of the cellular response? |
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Definition
margination and adhesion of the endothelium, transmigration across the enthelium, chemotaxis , and phagocytosis |
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microbes can bind to bacteria via what receptors? |
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Definition
toll like and manose receptors |
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Definition
binds to h1 cels on the endothelial cells. |
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how many proteins are in the complement system? |
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20 proteins in the plasma proteins |
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causes contraction of smooth muscle, dilation of bloodvessels, and pain when injected. |
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proteins produced by macrophages, and lymphocytes. |
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made by macrophages. encourage adhesions, aggregation of neutrophils. |
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