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NURS232 UNIT I-V
Impaired Immune Response
| Question | Answer |
|---|---|
| What are the major functions of a normal immune system | defense, homeostasis and surveillance |
| what function is responsible for recognition of self vs. non-self and destroying or neutralizing foreign antigens | defense |
| what function is responsible for digestion and removal of damaged cells to allow body cell types to remain uniformed and unchanged | homeostasis |
| when an immune system performs with controlled response it is considered to be working within what function of the normal immune system | homeostasis |
| detection and memory is a part of what normal immune system function | surveillance |
| when mutations are recognized and destroyed this is part of what normal immune system function | surveillance |
| what are the two types of immunity | innate and acquired |
| with type of immunity is responsible for the inflammatory response? | innate |
| which type of immunity is a person born with | innate |
| which type of immunity provides a specific response | aquired |
| acquired immunity can be both | natural and artificial |
| one's innate immunity is influenced by | heredity, age, health, species, race and sex |
| what is the sequential reaction to cell injury | neutralizes and dilutes the causative agent (antigen), removes necrotic materials and establishes an environment for healing |
| mechanism of inflammation is the same regardless of the | injuring agent |
| while the mechanism of inflammation is the same, the intensity of the response depends upon | the extent and severity of the injury and the reactive capacity of the injured person |
| which is the same regardless of the injuring agent: mechanism of inflammation or the intensity of the response | mechanism |
| during the inflammatory response what vascular responses occur? | vasoconstriction, vasodilation,increased capillary wall permeability, viscosity increase and blood clot formation |
| when injured cells release histamine and other chemicals what is the vascular response | vasoconstriction |
| when there is an increased blood flow to the area (hyperemia) what is the vascular response | vasodilation |
| during what vascular response does fluid flow from the vascular space into the surrounding tissue? | increase in capillary wall permeability |
| why does blood flow slow during the inflammatory response? | the blood becomes more viscous |
| what component strengthens blood clot formation | fibrin |
| chemotaxis is a cellular response that | directs migration of WBCs |
| what are the first WBCs to arrive to the injured site? | Neutrophils (phagocytes) |
| how long do neutrophils live? | 24-48 hours |
| when neutrophils die what do they accumulate as? | pus |
| in response to the movement of neutrophils what does the bone marrow do? | releases more WBCs |
| if the demand for WBCs exceed supply what is released? | bands |
| the monocytes are formed in the bone marrow and matured into macrophages in the | tissue |
| monocytes arrive how long after injury | 3-7 days |
| what is the primary function of a monocyte/macrophage | clean the area of inflammatory debris, start the healing process and present antigens to the t & b lymphocytes |
| what type of cell is responsible for cleaning the arrea of inflammatory debris? | monocytes/machrophages |
| which cell arrives first on the scene of inflammation? | neutrophils (phagocytes) |
| which cell presents antigens to the T & B lymphocytes | monocytes/macrophages |
| monocytes transform to what in the tissue | macrophages |
| which WBC is responsible for orchestrating the healing process | monocytes/macrophages |
| the directional migration of WBCs is referred to as | chemotaxis |
| which types of WBCs have selective roles in inflammation with allergic reactions | eosinophils/basophils |
| eosinophils/basophils control the effects of | histamine and serotonin |
| the effects of histamine and serotonin during the inflammatory response is controlled by | eosinophils/basophils |
| what are the major chemical mediators involved in an inflammatory response? | histamine, complement system, prostaglandins & leukotrienes, and cytokines |
| the source for histamine is | mast cells and basophil granules |
| the mast cell/basophil granule is a _______ for histamine while the eosinophils/basophils _______ the effects of histamine | source; control |
| histamine is responsible for what biologic activities? | increase in vascular permeability, constriction of smooth muscles, stimulation of irritant receptors |
| the release of histamine in the body is seen as what clinical outcomes | edema of the airways, bronchial constriction, uticaria, angioedema, pruritis, N/V, diarrhea, shock |
| an increase in vascular permeability causes | edema of airways, angioedema, shock |
| because histamine also affects the bowels what clinical signs will be evident | n/v, diarrhea |
| histamine causes uticaria and pruritis because it | stimulates irritant receptors |
| the complement cascade has 2 pathways | classic and alternative |
| the classic pathway begins with what component? | C1 fixation to antigen-antibody complex |
| the alternative pathway begins with what component? | C3 activated without C1 fixation |
| which pathway does not include a C1 fixation? | alternative pathway |
| which pathway attacks bacteria and fungi | alternative |
| which pathway begins with the fixation of C1 to an antigen-antibody complex? | classic |
| classic complement begins with | c1 fixation |
| what are the complement functions | chemotaxis, anaphylaxis, opsonization and cytolysis |
| which complement function increases release of histamine | anaphylaxis |
| which complement function speeds phyagocytosis | opsonization |
| which complement function destroys cells | cytolysis |
| which complement function calls cells in | chemotaxis |
| prostaglandins induce inflammation and contribute to an increase in | blood flow, edema, pain and fever |
| which type of cell is responsible for edema, pain and fever | prostaglandins |
| a prostaglandin is a potent | pyrogen |
| prostaglandins sensitize | pain receptors |
| prostaglandins potentiate the effects of | histamine |
| prostaglandins contribute to vasodilator and | capillary permeability |
| leukotrienes form the slow reacting substance of | anaphylaxis |
| which type of cell forms the slow reacting substance of anaphylaxis | leukotrienes |
| which type of cell is the "communicator" during an inflammatory response? | cytokines |
| which type of cell regulates movement, proliferation and differentiation of leukocytes and other cells | cytokines |
| interleukins, interferons, tumor necrosis factor and colony-stimulating facotrs and erythropoietin are common | cytokines |
| interleukins are a common | cytokine |
| tumor _______ factor is a common type of cytokine | necrosis |
| colony-______ factors and erythropoietin are common cytokines | stimulating |
| the clinical manifestations of inflammation are categorized as | local, regional and systemic |
| redness, swelling, heat, pain and loss of function are ______ clinical manifestations of inflammation | local |
| regional clinical manifestations of inflammation include | lymph nodes |
| leukocytosis is a __ clinical manifestation | systemic |
| leukocytosis is a WBC count greater than | 10,000 |
| leukocytosis and fever are what category of clinical manifestations of inflammation? | systemic manifestations |
| what affect does an increased temp have during the inflammatory process? | kills microbes, increases phagocytosis, increases proliferation of T cells and enhances interferon |
| what affect does fever have on phagocytosis | increases it |
| what affect does fever have on the proliferation of T cells? | increases |
| an increased temperature increases | phagocytosis, proliferation of T cells and interferons |
| The types of inflammation are acute, sub-acute and | chronic |
| acute inflammation is healed in | 2-3 weeks |
| a sub-acute inflammation lasts | weeks to months |
| infective endocarditis is an example of what type of inflammation? | sub-acute |
| chronic inflammation may result in | autoimmune disease |
| during chronic inflammation lymphocytes and macrophases cause | damage to tissue which may result in autoimmune disease |
| T cell lymphocytes are produced in the ______ and mature in the ______ | bone marrow; thymus |
| if the thymus gland doesn't work what type of cell is the body lacking? | t-cells |
| if the immune response is not attacking antigens what cell may it be lacking? | t-cells |
| T cells mature in the | thymus gland |
| t cells differentiate into multiple subsets that | coordinate cellular & humoral immunity and directly attack and kill antigens |
| what type of cell directly attacks and kills antigens? | t-cells |
| if there are no T cells there will not be a coordinated | immune response |
| the Cytotoxic T cell (CD8) | kills bad cells and produces memory T cells |
| which T cell produces memory T cells? | cytotoxic T (CD8) |
| which type of T cell kills foreign graft cells? | cytotoxic T (CD8) |
| which T cell subset differntiates into subsets and produce cytokines | helper T (CD4) |
| memory T cells are produced by | cytotoxic T cells |
| the cytotoxic T cell is a natural killer and is the first in the line of defense against | tumor cells and graft cells |
| dendritic cells | capture antigens and transport them to the T cells |
| T cells receive antigens from what type of cell | dendritic |
| how do dendritic cells activate the immune response? | by capturing antigens at the site of contact and transporting it to the T cell with the that specificity to the antigen |
| B cells are involved in | humoral immunity/antibody mediated immunity |
| humoral or cell-mediated | specific response |
| B cells mature and are stored in the | bone marrow |
| b cells migrate to the | spleen and lymphoid tissues |
| b cells stimulated by contact with an antigen change into | plasma cells |
| plasma cells produce | antibodies against the antigen they are stimulated by |
| what type of cell directs/controls B cells | T cells |
| IgG, IgA, IgM....are examples of what? | Immunoglobulin/antibodies produced by plasma cells |
| what are the 5 classes of immunoglobulin/antibodies | IgG, IgM, IgA, IgD, IgE |
| IgG (antiGens) | internal fluids, forms antigen-antibodies |
| IgA (A nose) | secretory, protects mucosal surfaces |
| IgM (Motion) | circulation, starts cascade, autoimmune disorders |
| IgE (snEEze) | basophils and mast cells, mediates allergic reaction |
| IgD (Directs) | B cell surface, activates or suppresses B cells to turn into plasma cells to produce antibodies |
| which type of immunoglobulin is found on the B cell surface? | IgD |
| which type of immunoglobulin is found in the circulation? | IgM |
| which immunoglobulin activates or suppresses B cells? | IgD |
| which immunoglobulin is found in secretory cells? | IgA |
| which immunoglobulin is found in internal fluids and increases serum antibodies? | IgG |
| which immunoglobulin is found in circulation and starts the cascade? | IgM |
| which immunoglobulin is responsible for the passage of antigens from mom to baby | IgG |
| which immunoglobulin stimulates B cells to transform to plasma cells | IgD |
| which immunoglobulin protects mucosal surfaces? | IgA |
| which immunoglobulin is found in tears, saliva and colustrum? | IgA |
| which immunoglobulin forms antigens-antibody complement immune complexes associated with hypersensitivity? | IgG |
| IgM initiates complement cascade; it protects against | virus and bacteria |
| which immunoglobulin is involved in hypersensitivities and autoimmune disorders | IgM |
| which is the first type of antibody to form? | IgM |
| IgM is confined to the | intravascular spaces |
| the primary response to an antigen is evident in | 4-8 days after initial exposure |
| IgM is the first type of antibody | to form |
| during the primary response to an antigen IgM is first then | IgG |
| IgG can move into the | extravascular spaces |
| which is faster: primary response or secondary exposure response? | secondary exposure response |
| the secondary exposure response is faster, stronger and | lasts longer |
| which response is evident in 4-8 days | primary |
| which response is evident in 1-3 days | secondary |
| the T cell is essential to activate components of | immune system |
| cytotoxic t cells directly | attack antigens |
| the lag time of cell mediated and humoral responses | 24-48 hours |
| memory T cells attack specific antigens with | next exposure |
| b cells remain in the | lymphoid tissue |
| b cells are stimulated by antigens to transform in to and to produce what? | plasma cells, produce antibodies to the antigens that stimulated them |
| the effects of aging on the immune system results in high incidence of | cancers and increased susceptibility to infections |
Created by:
Lori Dobrisky
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