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186 Cards in this Set
- Front
- Back
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function of lymph node?
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nonspecific filtration by macrophage
storage and activation of B and T cells antibody production |
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function of follicle in lymph node
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site of B cell localization and proliferation
in outer cortex, 1' follicle dense and dormant 2' follicles have pale central germinal centers and active |
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function of medulla in lymph node
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medullary cord - closely packed lymphocytes and plasma cells
medullary sinus - communicate w/ efferent lymphatics and contain reticular cells and macrophages |
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function of paracortex in lymph node
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houses T cells
high endothelial venules present enlarges in extreme cellular response |
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to which lymph node do these parts drain?
upper limb, lateral breast |
axillary
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to which lymph node do these parts drain?
stomach |
celiac
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to which lymph node do these parts drain?
duodenum, jejunum |
superior mesenteric
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to which lymph node do these parts drain?
sigmoid colon |
colic - inferior mesenteric
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to which lymph node do these parts drain?
rectum (lower part), anal canal above pectinate line |
internal iliac
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to which lymph node do these parts drain?
anal canal below pectinate line |
superficial inguinal
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to which lymph node do these parts drain?
testes |
superficial and deep plexuses -> para aortic
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to which lymph node do these parts drain?
scrotum |
superficial inguinal
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to which lymph node do these parts drain?
thigh (superficial) |
superficial inguinal
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to which lymph node do these parts drain?
lateral side of dorsum of foot |
popliteal
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thoracic duct drains every lymph node in our body except?
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right arm and right half of head (drain to right lymphatic duct)
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what's a sinusoid of spleen?
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long vascular channels in red pulp with fenestrated barrel hoop basement membrane. macrophages found nearby.
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in what part of the spleen are T cells found ?
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periarterial lymphatic sheath (PALS) and red pulp of the spleen
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in what part of the spleen are B cells found?
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follicles within the white pulp of the spleen
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what do macrophages in the spleen remove?
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encapsulated bacteria
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what's the fxn of thymus?
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site of T cell differentiation and maturation
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where does the thymus arise from? (embryology)
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epithelium of 3rd branchial pouch
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what's in the cortex of thymus?
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immature T cell
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what's in the medulla of thymus?
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mature T cell, epithelial reticular cells and contains Hassall's corpuscle
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what is positive selection?
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if T cell can hind to MHC, T cell survives. if not, T cell dies
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what is negative selection?
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eliminating T cells that are reactive to own antigens
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where in the thymus do positive/negative selection occur?
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positive - thymic cortex
negative - corticomedullary jxn |
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what is innate immunity?
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receptors that recognize pathogens are germline encoded.
fast and non specific. no memory neutrophil, macrophage, dendritic cell, complement |
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what is adaptive immunity?
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receptors that recognize pathogens undergo VDJ recombination during lymphocyte development.
response is slow on first exposure, but memory response is faster and more robust. T cell, B cell, circulating Ab |
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where do T cell precursors come from?
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bone marrow
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which surface antigen is specific for cytotoxic T cell?
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CD8
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which surface antigen is specific for helper T cell?
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CD4
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helper T cell is divided into these two cells?
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Th1, Th2
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Th1 cell function?
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make IL2, IFN gamma and activate macrophages & CD8 T cell
inhibited by IL4 |
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Th2 cell function?
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make IL4, IL5 and help B cells make antibody (IgE >IgG); inhibited by IFN gamma
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MHC is encoded by which gene?
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heman leukocyte antigen (HLA) gene
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types of MHC I genes?
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HLA-A, B, C
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MHC I is expressed on which cells?
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almost all nucleated cells
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fxn of MHC I?
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antigen is loaded in RER.
mediates viral immunity pairs with beta2-microglobulin |
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types of MHC II genes?
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HLA-DR, DP, DQ
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MHC II is expressed on?
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only antigen presenting cells (APC)
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fxn of MHC II?
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antigen is loaded in an acidified endosome
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fxn of B cell?
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make Ab
IgG opsonize bacteria, virus |
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type I hypersensitivity (allergy) is mediated by which Ig?
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IgE
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type II hypersensitivity(cytotoxic), and type III (immune complex) mediated by which Ig?
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IgG
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hyperacute organ rejection is mediated via what molecule?
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antibody
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fxn of T cells?
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CD4 T cells help B cells make Ab and produce gamma interferon.. which activates macrophages
CD8 cells kill virus infected cells directly |
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type IV (delayed type) hypersensitivity is mediated by?
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T cells
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acute and chronic organ rejection mediated by?
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T cells
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helper T cell's CD4 binds to what on APCs?
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MHC II
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cytotoxic T cell CD8 binds to ?
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MHC I on virus infected cells
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3 antigen presenting cells?
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macrophage
B cell dendritic cell |
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what's the role of CD3 complex?
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cluster of polypeptide associated w/ a T cell receptor. important in signal transduction
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what's a costimulatory signal?
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CD28 on helper T cell binding to B7 on APC. needed to activate helper T cell along with MHC II - CD4 binding
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how does cytotoxic t cell activation occur?
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MHC I binding of TCR/CD8, and IL-2 from Th cell (helper cell) activate Tc cell to kill virus infected cell
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what part of Ab bind to antigen?
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variable light/heavy chain
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Fc portion of Ab does what?
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fixes complement (only IgM and IgG)
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3 functions of Ab?
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opsonization, neutralization, complement activation
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Ab diversity generated by? (4 mechanism)
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recombination: VJ (light) VDJ (heavy)
random combination of heavy and light chains somatic hypermutation addition of nucleotides to DNA during recombination by terminal deoxynucleotidyl transferase |
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Mature B cell express which Ig on their surface?
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IgM and IgD
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what is isotype switching?
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mediated by cytokines and CD40 ligand, they switch into plasma cells that secrete IgA, IgE or IgG
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fxn of IgG?
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main Ab in 2' response. fix complement, corsses placenta, opsonize bacteria, neutralize bacterial toxins and viruses
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fnx of IgA?
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prevents attachment of bacteria and viruses to mucous membranes. monomer or dimer. found in secretions
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fxn of IgM?
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produced in the 1' response to an antigen. fixes complement but does not cross the placenta. antigen receptor on surface of B cell. monomer on B cell or pentamer
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fxn of IgD?
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unclear. found on the surface of many B cells and in serum
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fxn of IgE?
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mediates immediate hypersensitivity (type I) by inducing the release of mediators from mast cells and basophils when exposed to allergen. mediates immunity to worms by activating eosinophils.
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fxn of IL-1?
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secreted by macrophage.
cause acute inflammation induce chemokine production to recreit leukocytes, activates endothelium to express adhesion moleculess |
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fxn of IL-2?
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secreted by Th cells.
stimulates growth of helper and cytotoxic T cells |
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fxn of IL-3?
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secreted by activated T cells
supports the growth and differentiation of bone marrow stem cells. has a fxn similar to GM-CSF |
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fxn of IL-4?
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secreted by Th2 cells promotes growth of B cells. enhances class switching to IgE and IgG
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fxn of IL-5?
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secreted by Th2 cells
promotes differentiation of B cells. Enhances class switching to IgA. stimulates production and activation of eosinophils |
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fxn of IL-6?
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secreted by Th cells and macrophages.
stimulates production of acute phase reactants and immunoglobulins. |
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fxn of IL-8?
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secreted by macrophages.
major chemotactic factor for neutrophils. |
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fxn of IL-10?
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secreted by regulatory T cells
inhibits actions of activated T cells |
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fxn of IL-12?
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secreted by B cells and macrophages.
activates NK and Th1 cells |
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fxn of gamma interferon
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secreted by Th1 cells.
stimulates macrophages. |
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fxn of TNF?
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secreted by macrophages
mediates septic shock. causes leukocyte recruitment, vascular leak. |
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cell surface proteins on helper T cell?
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CD4, TCR, CD3, CD28, CD40L
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cell surface proteins on cytotoxic T cells?
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CD8, TCR, CD3
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cell surface proteins on B cells?
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IgM, B7, CD19, CD20, CD21, CD40, MHC II
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cell surface proteins on macrophages?
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MHC II, B7, CD40, CD14. receptors for Fc and C3b
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cell surface proteins on NK cells?
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receptors for MHC I, CD16, CD56
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all cells except mature red cells
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MHC I
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membrane attack complex defends against what type of bacteria?
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gram negative bacteria
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two path ways of activation of complement system?
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classic pathway
alternative pathway |
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complement classic pathway is activated via?
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IgG or IgM
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complement alternative pathway is activated via?
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molecules on the surface of microbes (esp endotoxin)
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two primary opsonins in bacterial defense?
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C3b and IgG
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which two molecules help prevent complement activation on self cells?
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decay accelerating factor (DAF), and C1 esterase
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complement that neutralize virus?
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C1, C2, C3, C4
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complement associated with anaphylaxis?
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C3a, C5a
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membrane attack complex (MAC) is composed of what complements?
fxn of MAC? |
C5b-9.
cytolysis |
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this complement is a chemotactic factor for neutrophil
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C5a
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deficiency of C1 esterase inhibitor causes?
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hereditary angioedema
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deficiency of C3 leads to ?
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severe, recurrent pyogenic sinus and respiratory tract infection
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deficiency of C6-8 leads to?
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neisseria bacteremia
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deficiency of decay accelerating factor (DAF) leads to?
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complement mediated lysis of RBCs and paroxysmal nocturnal hemoglobinuria (PNH)
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role and mechanism of interferons?
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place uninfected cells in an antiviral state.
interferons induce the production of a ribonuclease that inhibits viral protein synthesis by degrading viral mRNA (but not host mRNA) activates NK cells to kill virus infected cells |
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alpha and beta interferon fxn?
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inhibit viral protein synthesis
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gamma interferon fxn?
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increase MHC I and MHC II expression and antigen presentation in all cells
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active immunity vs passive immunity?
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active - induced after exposure to foreign antigens. slow onset, long lasting (memory)
passive - based on receiving preformed Ab from another host. rapid onset. short life span of Ab (half life = 3 weeks) |
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preformed antibodies are given after exposure to what agents/viruses?
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tetanus toxin, botulinum toxin, HBV or rabies
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3 bacteria that has antigenic variation to invade host immune response?
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salmonella (2 flagellar variant), borrelia (relapsing fever), neisseria gonorrhea (pilus protein)
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virus that has antigenic variation?
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influenza (antigenic shift and drift)
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parasites that have antigenic variation?
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trypanosome (programmed reacrrangement)
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what is anergy?
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self reactive T cells become non reactive without costimulatory molecule thus lack of response to foreign substance. B cells also become anergic, but tolerance is less complete than in T cells
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type I hypersensitivity causes?
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anaphylaxis, atopy
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mechanism of type I hypersensitivity?
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free antigen cross links IgE on presensitized mast cells and basophils triggering release of vasoactive amines (histamine). reaction develops rapidly after antigen exposure due to preformed antibody
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mechanism of type II
(ab mediated) hypersensitivity? |
IgM or IgG bind to fixed antigen on enemy cell leading to lysis (by complement) or phagocytosis
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mechanism of type III (immune complex mediated) hypersensitivity?
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antigen-antibody complexes activate complement, which attracts neutrophils.
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what is serum sickness?
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immune complex disease(type III) in which Ab to the foreign proteins are produced (takes 5 days). Immune complexes form and are deposited in membranes where they fix complement (leads to tissue damage)
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what is arthus reaction?
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a local subacute Ab-mediated hypersensitivity (type III) reaction. intradermal infection of antigen induces Ab, which form antigen antibody complexes in the skin. characterized by edema, necrosis, and activation of complement
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mechanism of type IV hypersensitivity?
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delayed T cell mediated. sensitized T lymphocytes encounter antigen and then release lymphokines (leads to macrophage activation)
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which type hypersensitivity causes these diseases?
hemolytic anemia idiopathic thrombocytopenic purpura erythroblastosis fetalis rheumatic fever goodpastures's bullous pemphigoid graves disease myasthenia gravis |
Type II
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which type hypersensitivity causes these diseases?
T1DM MS guilllain Barre hashimoto GvHD PPD (test for TB) contact dermatitis |
type IV
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which type hypersensitivity causes these diseases?
SLE rheumatoid arthritis polyarteris nodosum poststrep glomerulonephritis serum sickness arthus reaction hypersensitivity pneumonitis |
type III
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which type hypersensitivity causes these diseases?
anaphylaxis allergic rhinitis |
type I
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what disease is caused by decreased production of B cells?
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bruton's agammaglobulinemia
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characteristics of bruton's agammaglobilinemia?
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X linked recessive. defect in tyrosine kinase. low levels of all classes of Ig. decrease in B cells. recurrent bacterial infections after 6 months of age. (when maternal Ab depletes) occurs in boys (X-linked)
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what disease is caused by decreased production of T cells?
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thymic aplasia (digeorge syndrome)
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characteristics of digeorge?
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thymus and parathyroids fail to develop owing to failure of development of 3rd and 4th pharyngeal pouches. presents w/ tetany due to hypocalcemia. recurrent viral and fungal infections. congenital defects of heart and great vessels. 22q11 deletion
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what disease is caused by decreased production of B cells and T cells?
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severe combined immunodeficiency (SCID)
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characteristics of SCID?
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defect in early stem cell differentiation. recurrent viral, bacterial, fungal and protozoal infection. multiple etiology (e.g. failure to synthesize MHC II, defective IL2 receptors or adenosine deaminase deficiency)
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what disease is caused by decreased activation of T cells?
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IL-12 receptor deficiency
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characteristics of IL-12 receptor deficiency?
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presents with disseminated mycobacterial infections due to decreased Th1 response
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what disease is caused by decreased activation of B cells? (two)
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hyper IgM syndrome
Wiskott-Aldrich syndome |
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characteristics of hyper IgM syndrome
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defect in CD40L on CD4 T helper cells leads to inability to class switch. presents early in life w/ severe pyogenic infections. high levels of IgM. very low IgG,A,E
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characteristics of wiskott-aldrich syndrome?
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X linked defect in ability to mount an IgM response to capsular polysaccharides of bacteria. elevated IgA, normal IgE and low IgM.
Triad - recurrent pyogenic infection, thrombocytopenic purpura, eczema |
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what disease is caused by decreased activation of macrophages?
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job's syndrome
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characteristics of job's syndrome?
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failure fo IFN gamma production by helper T cells. PMN fail to respond to chemotactic stimuli.
presents with - coarse facies, cold (noninflamed) staph abscess, retained 1' teech, increased IgE, dermatologic problems |
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what disease is caused by phagocytic cell deficiency? (3)
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leukocyte adhesion deficiency syndrome (type 1)
chediak-higashi disease chronic granulomatous disease |
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characteristics of leukocyte adhesion deficiency?
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defect in LFA-1 integrin proteins on phagocytes. presents early w/ recurrent bacterial infections, pus formation, and delayed separation of umbilicus
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characteristics of chediak higashi disease?
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autosomal recessive. defect in microtubular function and lysosomal emptying of phagocytic cells. presents w/ recurrent pyogenic infection by staph and strep. partial albinism, peripheral neuropathy
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a patient presents w/ marked susceptibility to opportunistic infections, esp S aureus, e coli, aspergillus. Dx confirmed w/ negative nitroblue tetrazolium dye reduction test
what disease? |
chronic granulomatous disease
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chronic granulomatous disease mechanism?
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defect in phagocytosis of neutrophils owing to lack of NDAPH oxidase activity or similar enzymes
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patient presents with skin and mucous membrane candida infection, due to idiopathic dysfunction of T cells. what disease?
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chronic mucocutaneous candidiasis.
T cell dysfunction specifically against candida albicans |
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pt presents w/ sinus and lung infection. milk allergy and diarrhea present. what disease?
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selective immunoglobulin deficiency (idiopathic dysfunction of B cells)
possibly due to a defect in isotype switching. IgA def most common |
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pt presents w/ cerebellar problems and spider angioma.
what disease? |
ataxia-telangiectasia (idiopathic dysfunction of B cells)
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mechanism of ataxia telangiectasia
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defect in DNA repair enzymes w/ associated IgA deficiency
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a young pt in 20s has decreased plasma cell but normal # of circulating B cells. decrease in Igs.
what disease? |
common variable immunodeficiency (idiopathic dysfunction of B cells)
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what disease?
antinuclear antibody (ANA) |
SLE
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what disease?
anti-dsDNA, anti-smith |
specific for SLE
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what disease?
antihistone |
drug induced lupus
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what disease?
anti IgG |
rheumatoid arthritis (rheumatoid factor)
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what disease?
anticentromere |
scleroderma (CREST)
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what disease?
anti Scl70 |
scleroderma (diffuse)
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what disease?
antimitochondrial |
1' biliary cirrhosis
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what disease?
antigliadin |
celiac disease
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what disease?
anti basement membrane |
goodpasture's
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what disease?
anti-epithelial cell |
pemphigus vulgaris
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what disease?
antimicrosomal, antithyroglobulin |
hashimoto's thyroiditis
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what disease?
anti Jo-1 |
polymyositis, dermatomyositis
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what disease?
anti SS-A (anti Ro) |
Sjogren's syndrome
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what disease?
anti SS-B(anti Ra) |
sjogren's syndrome
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what disease?
anti U1 RNP |
mixed connective tissue disease
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what disease?
antiglutamate decarboxylase |
T1DM
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what disease?
anti smooth muscle |
autoimmune hepatitis
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what disease?
c-ANCA |
wegener's granulomatosis
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what disease?
p-ANCA |
other vasculitides (than wegener, SLE, goodpasture)
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HLA-B27 associated with what diseases?
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prosirasis, ankylosing spondylitis, IBD, reiter's syndrome
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HLA-B8 associated with what diseases?
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graves disease, celiac sprue
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HLA-DR2 associated with what diseases?
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multiple sclerosis, hay fever, SLE, goodpastures
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HLA-DR3 associated with what diseases?
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T1DM
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HLA-DR4 associated with what diseases?
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rheumatoid arthritis, T1DM
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HLA-DR5 associated with what diseases?
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pernicious anemia -> B12 deficiency, hashimoto's thyroiditis
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HLA-DR7 associated with what diseases?
|
steroid responsive nephrotic syndrome
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what is syngeneic graft?
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from identical twin or clone
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mechanism, clinical use and toxicity of cyclosporine?
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mech - bind to cyclophilin. complex blocks the differentiation and activation of T cells by inhibiting calcineurin, thus preventing the production of IL2 and its receptor
clinical - suppresses organ rejection after transplant. selected autoimmune disorders toxicity - predisposition to viral infection and lymphoma. nephrotoxic(preventable w/ mannitol diuresis) |
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mechanism, clinical use and toxicity of tacrolimus (FK506)?
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mech - similar to cyclosporine; binds to FK binding protein, inhibiting secretion of IL2 and other cytokines
clinical use - potent immunosuppressive used in organ transplant recipients toxicity - nephrotoxicity, peripheral neuropathym HTN, pleural effusion, hyperglycemia |
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mechanism, clinical use and toxicity of azathioprine?
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mech - antimetabolite precursor of 6-mercaptopurine that interferes w/ metabolism and synthesis of nucleic acids. toxic to proliferating lymphocytes
clinical use - kidney transplant, autoimmune disorders toxicity - bone marrow suppression. active metabolite mercaptopurine is metabolized by xanthine oxidase; thus toxic effect increase by allopurinol |
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mechanism, clinical use and toxicity of muromonab-CD3 (OKT3)
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mech - monoclonal ab binding to CD3 on T cell surface. blocks cellular interaction w/ CD3 responsible for T cell signal transduction
clinical - immunosuppression after kidney transplant toxicity - cytokine release syndrome, hypersensitivity reaction |
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mechanism, clinical use and toxicity of sirolimus (rapamycin)
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mech - binds to mTOR. inhibit T cell proliferation in response to IL-2
clinical use - immunosuppression after kidney transplantation in combination w/ cyclosporine and corticosteroids toxicity - hyperlipidemia, thrombocytopenia, leukopenia |
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mechanism of mycophenolate mofetil
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inhibits de novo guanine synthesis and blocks lymphocyte production
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mechanism of daclizumab
|
monoclonal ab w/ high affinity for IL2 receptor on activated T cells
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clinical use of aldesleukin (IL-2)
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renal cell carcinoma,metastatic melanoma
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clinical use of erythropoietin (epoetin)
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anemia (esp in renal failure)
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clinical use of filgrastim (G-CSF)
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recovery of bone marrow
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clinical use of sargramostim (GM-CSF)
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recovery of bone marrow
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clinical use of alpha interferon
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hep B, C, kaposi's sarcoma, leukemia, malignant melanoma
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clinical use of beta interferon
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multiple sclerosis
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clinical use of gamma interferon
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chronic granulomatous disease
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clinical use of oprelvekin (IL-11)
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thrombocytopenia
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clinical use of thrombopoietin
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thrombocytopenia
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what is hyperacute rejection?
|
Ab mediated due to presence of preformed antidonor Ab in the transplant recipient. occurs within minutes after transplant
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what is acute rejection?
|
cell mediated due to cytotoxic T lymphocytes reacting against foreign MHCs. occurs weeks after transplant. reversible w/ cyclosporine/OKT3
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what is chronic rejection?
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Ab mediated vascular damage (fibrinoid necrosis); occurs months to yrs after transplantation. irreversible
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what is GvH disease
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grafted immunocompetent T cells proliferate in the irradiated immunocompromised host and rejects cells w/ foreign proteins resulting in severe organ dysfunction.
Sx - maculopapular rash, jaundice, hepatosplenomegaly and diarrhea |
