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122 Cards in this Set
- Front
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humoral immune response |
-antibody production
-B lymphocyte recognize thru receptor -present to T cell -T cell drives B cells to make plasma cells -plasma cells make antibodies |
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cell mediated - B cells (process) |
-start in bone marrow -gene arrangement -make successful b cell recepter (bcr) -training for self tolerance
-makes immunogloblins |
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cell mediated - T cells (process) |
-start in bone marrow -gene arrangement -successful t cell receptor (alpha&beta) -move to thymus -educate/train for tolerance to self in thymus -move to secondary lymphoid glands |
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T cells - cell types involved |
-process -linear, short, proteins -CD8: cytolytic T cells (Tc) -CD4: helper T cells (Th) |
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B cells - cell types involved |
-process -immunogloblins -not linear protein but 3D |
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CD8: |
-cytolytic T cells
-killer -problem = blow up = necrosis |
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CD4: |
-helper T cells -help things happen -make cytokines of all kinds -influences macrophages and other T cells (Th1- help make macrophage better & Th2- B cell presenting antigen) |
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antigen |
-recognized as non-self
-foreign substance
-substance that cause your immune system to produce antibodies against it |
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B cells act in humoral immunity and produce...
B cells don't require...
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-antibodies
-MHC presentation |
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antibody |
protein produced by body's immune system |
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autoimmune disorder |
when antibody mistakenly produced because it considers a healthy tissue a harmful substance |
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3 major functions of antibody |
-complement activation
-opsinization
-neutralization |
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macrophages do what to antigens? |
both phagocytize (devour) and present antigens |
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other antigen presenting-self cells (APCs): |
-dendritic cells (DC) -follicular dendritic cells (FDCs) -B cells |
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immunity |
protection against infection |
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3 things about human immunity |
1. recognition to "non-self" (antigen)
2. highly specific response to non-self
3. memory (lead to good memory) |
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the part of an antigen that is recognized |
epitope |
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Endogenous: -heterologous -autologous -homologous |
-cross react with others
-loss of tolerance
-distinguish tissues |
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dendritic cells (DC) |
-interdigitating cells (interlock like fingers)
-captures & present antigens to T cells
-found in T cell zones in lymphoid tissues |
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follicular dendritic cells (FDCs) |
-trap antigens bound to AB or complement and display to B cells
-found in germinal centers of lymphonodes and spleen
|
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B cells recognize antigen via... and
present it to... via... |
-BCR (b cell receptors)
-helper Ts
-MHC II |
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MHC Class I (MHC I) |
-presented on nucleated cells, -signals CD8+ T cells, -heavy alpha chain and beta 2-microglobulin chain |
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MHC CLASS II (MHC II) |
-Signal CD4+ helper cells, -antigen is consumed, processed, and presented, -two peptide chains of more equal size |
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Name five different types of anitbodies |
1. IgG (gamma) 2. IgA (alpha) 3. IgM (mue) 4. IgE (epsilon) 5. IgD (delta) |
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IgG (gamma) |
-serum & tissue -readily diffuses -only one that crosses the placenta (active transport) -Antibody which neutralizes toxins and opsonizes bacteria
|
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IgA (alpha) |
-seretion/mucus -found in circulatory system -Antibody found in mucosa, tears, sweat, bile, and breast milk. -Stops bacteria and viruses from entering epithelium |
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IgM (mue) |
-1st to respond when Bcell trigger -lots of binding sites (10) -activates complement cascade -stays in vascular -neutralizes -Antibody that is first after immunization
|
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IgE (epsilon) |
-mast cells & allergies -Antibody whose Fc fragment binds to receptors on mast cells, involved in releasing granules (histamine, leukotrienes, eosinophils), -involved in parasite infections and hypersensitivity |
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IgD (delta) |
-surface receptors -signaling mech. & not in circulation -Antibody that helps with antigen recognition and activation along with IgM |
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primary and secondary lymphoid tissue
examples of each |
primary: generates lymphocytes ex- bone marry & thymus
secondary: maintain mature naive lymphocytes & initiate adaptive immune response ex- spleen skin |
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Antigens have to be presented to _____ by MHC molecules |
T cells |
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killer T cells |
hunt down and destroy cells that are infected with toxics |
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helper T cells |
-required for all adaptive immune responses -activate B cells to secrete antibodies, macrophages destroy ingested microbes -help activate cytotoxi T cells to kill infected target cells
|
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humoral respones follwing hypersensitivity |
type I - Anaphylactic type II - antibody dependent type III -immune complex-mediated |
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cellular response follwing hypersensitivity |
type IV (cell mediated) |
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type I (anaphylactic)
& example |
-immune isn't really doing anything wrong -excessive IgE -allergic reactions -mast cells are triggered --> running nose -ex: hay fever, anapylaxis --> bee sting, pollen |
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type II (antibody dependent)
& example |
-antibody mediated cell lysis -igM/igG/complement cascade
-ex: hemolytic disease of new borns - mom has antibodies against newborns platelets/rbc = death |
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type III (immune complex-mediated)
& example |
-immune complex deposition: release of lysosomal contents from neutrophils, histamines, aggregation platelets -IgG & IgM
-ex: autoimmune disease: rheumatoid arthritis, SLE, drug induced |
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type IV (cell-mediated)
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-no Ig involvement -cell mediated, inflammation response (swell)
-caused by microbial agents: bacteria, viruses, fungi |
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hypersensitivity reaction of Hay Fever |
type I |
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hypersensitivity reaction of anaphylaxis --> bee sting, pollen |
type I |
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hypersensitivity reaction of SLE and Type I diabetes (IDDM) |
type II |
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hypersensitivity reaction of Hemolytic Desease of New Borns (HDN) |
type II |
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hypersensitivity reaction of neonatal isothrombocytopenia (NIST) |
type II |
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hypersensitivity reaction of adverse transfusion outcome |
type II |
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hypersensitivity reaction of rheumatoid arthritis |
type III |
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hypersensitivity reaction of SLE |
type III |
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hypersensitivity reaction of drug induced |
type III |
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hypersensitivity reaction of bacteria: TB, Leprosy |
type IV |
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hypersensitivity reaction of viruses: small pox, herpes, measles |
type IV |
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hypersensitivity reaction of fungi: candidiasis, hisoplasmoisis |
type IV |
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hypersensitivity reaction of poison ivy |
type IV |
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autoimmunity |
the failure of an organism in recognizing its own constituent parts as "self," (antibody=good) which allows an immune response against its own cells and tissues |
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define "self" and why it needs tolerance to self |
body’s own cells are self. ( nonself : foreign cells) |
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loss of self tolerance results to |
autoimmunity |
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systemic lupus erythematosus (SLE) is primarily humoral or cell mediated? |
cell mediated |
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who/when usually gets systemic lupus erythematosus (SLE) |
mostly female in late adolescents, early adulthood |
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causes of systemic lupus erythematosus (SLE) |
-lesions caused & excessive autoantibody production -diagnostic nightmare: move around your body & always a diff antigen -schizophrenic immune system |
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Rheumatoid arthritis (RA) humoral or cell mediated? |
cell mediated |
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pathogenesis (development) of rheumatoid arthritis (RA) |
1. release of lysosomal content 2. release of histamines 3. aggregation of platelets |
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anergy: |
lack of costimulatory molecules on tissues that may present self results in inactivation of Ts that interact with these "self" tissues |
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seclusion |
tissues exclude the immune cells all together so self-reaction isn't a problem unless the tissue is damaged and proteins are released
ex: lens of eye |
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mechanisms - loss of self-tolerance and developing autoimmunity (1) |
1. previously secluded tissue proteins are exposed |
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mechanisms - loss of self-tolerance and developing autoimmunity (2) |
2. alteration of tissue antigens
-injury, infection, environmental insults, drugs |
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mechanisms - loss of self-tolerance and developing autoimmunity (3) |
3. exposure to 'shared' determinants: exogenous antigens similar to self antigens |
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mechanisms - loss of self-tolerance and developing autoimmunity (4) |
4. idiotype bypass
-idiotype: AG-binding sites that are unique to that AB or BCR -this is disregulated either on the T or BCR |
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mechanisms - loss of self-tolerance and developing autoimmunity (5) |
5. inappropriate la expression MHC-!! presenting self antigen where they should be down regulated |
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mechanisms - loss of self-tolerance and developing autoimmunity (6) |
impaired t cell regulation |
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many autoimmune disease are more common in |
females than male |
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systemic lupus erythematosus (SLE)
autoantibodies: |
(ANA) antinuclear antibodies |
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systemic lupus erythematosus SLE
symptoms... |
-butterfly rash on face -youngish female -pain/swelling joints -chest pains -photosensitivity |
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systemic lupus erythematosus SLE
immune complex deposition causes... |
organ damage (especially skin, joints, kidney) |
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systemic lupus erythematosus SLE genetic predisposition: |
HLA DR2
DR3
BW15 |
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systemic lupus erythematosus SLE
death usually caused by... |
renal failure
heart problems/infection |
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hashimoto's thyroiditis
organ specific: |
thyroid |
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hashimoto's thyroiditis
autoantibodies to thyroid tissues lead to... |
destruction of thyroid epithelial cells |
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hashimoto's thyroiditis
___ cell mediated: |
T cell mediated
-CD8+ cell death -ADCC |
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hashimoto's thyroiditis
sympotoms: |
-enlarged thyroid -hypothyroidism -usually middle-aged woman
|
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rhematoid arthritis
is mainly ___ disease |
joint |
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rhematoid arthritis
what causes it |
immune complex deposition and damage from cytokines |
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rhematoid arthritis
more likely in ___ & age range: |
(3-5x likely) women
20-40 yr. old |
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autoimmune hemolytic anemia
autoantibodies: |
normal red blood cells |
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autoimmune hemolytic anemia
can be ____ or related to _____ or due to _____ |
-idiopathic
-autoimmune disorder
-druge (a-methyldopa) |
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autoimmune hemolytic anemia
results in... |
opsonization of rbcs and their phagocytosis |
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autoimmune hemolytic anemia
are consumed ____ or ____ into ______ which are removed by ____ |
-macrophages, nibbled
-spherocytes
-spleen |
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autoimmune hemolytic anemia
results in... |
mild anemia (may have splenomegaly) |
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Systemic Lupus erythematosus (SLE):
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multisystem autoimmune disease which the lesions are caused by immune complex deposition & characterized by excessive autoantibody production. |
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Autoimmune hemolytic anemias:
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occurs when antibodies directed against the person's own red blood cells (RBCs) cause them to burst (lyse), leading to insufficient plasma concentration. The lifetime of the RBCs is reduced. |
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Rheumatoid arthritis (RA): |
is a long-term disease that leads to inflammation of the joints and surrounding tissues. It can also affect other organs. |
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Hashimoto’s thyroiditis:
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autoimmune disease in which thyroid gland is attacked by a variety of cell- and antibody-mediated immune processes. |
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State role of MHC in the immune response Antigen presenting cells present antigen via MHC to the immune system |
o Class 1: endogenous (from within the cell) o Class 2: exogenous, only seen on APC |
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Specific immune deficiency:
|
-afferent: antigen presentation and recognition
-efferent: t cell activation and antibody production |
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Nonspecific immune deficiency |
- complement
- phagocytosis |
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immune deficiency
-primary: |
-congenital (having since birth) -genetically determined -fortunately rare -appear early in life |
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immune deficieny
-secondary |
-acquired -secondary to therapy or other disease |
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primary immune deficiencies Severe Combined Immunodeficiency (SCID)
-affects both... -thymus is... -other lymphoid tissue is...
|
-T and B cell function -hypoplastic -atrophic |
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primary immune deficiencies Severe Combined Immunodeficiency (SCID)
no antibodies + no cell mediated response = |
infant with severe, recurrent infections often due to opportunistic pathogens |
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primary immune deficiencies Severe Combined Immunodeficiency (SCID)
2 common genetic defects: |
1. ADA deficiency: build up of A and dATP, lymphocyte death and decrease dna synthesis
2. common gamma chain defect: defective receptors for cytokines, decrease proliferation of T and B precursors |
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primary immune deficiencies Severe Combined Immunodeficiency (SCID)
treatment... |
bone marrow transplant |
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primary immune deficiencies
list 2 other primary immune deficiencies: |
1. DiGeorge syndrom: thymic develop. defect
2. Bruton disease: x-linked agammaglobulinemia Pre-Bs fail to mature/get blood, low plasma immunoglobulin, infection by bacteria P. carinii |
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secondary immune deficiencies
possible causes |
-age -malnutrition -neoplasia of immune system -immune suppression -infection |
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chronic granulomatous inflammation
characteristics |
-more macrophages, lymphs & plasma cells -long duration -tissue injury from inflammatory process -ongoing repair (angiogenesis, fibrosis) |
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chronic granulomatous inflammation
examples |
-infections that prolong (TB granulomatous inflammation) -prolonged exposure to injurious agents (toxins) -immune diseases (autoimmune, immune complexes) |
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chronic granulomatous inflammation
list some human health problems that chronic granulomatous inflammation plays role in |
-alzheimer's -type 2 diabetes -atherosclerosis -some cancers |
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chronic granulomatous inflammation
one mediator is _____ and roles... |
macrophages: recruited to site from blood and tissue get rid of microbes & dead cells tissue repair interact with T cells, present antigen & respond to signals from them |
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chronic granulomatous inflammation
2 types of macropages activation which affect downstream behavior |
1. classical (microbes, interferon gamma) inflammation
2. alternative pathway (IL-13, IL-4) tissue repair, firosis, antinflammator |
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chronic granulomatous inflammation
one mediator is _____ and roles... |
lymphocytes: called to inflammation site adaptive immunity (plasma cells) can promote chronic inflammation with macrophages sometimes cd4+ T cells secrete cytokines influcing inflammation |
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chronic granulomatous inflammation
one mediator is _____ and roles... |
eosinophils: -parasites and allergies -protein in granules kills parasites but host cells too |
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chronic granulomatous inflammation
one mediator is _____ and roles... |
mast cells: release histamines |
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chronic granulomatous inflammation
how do we get chronic inflammation? |
-localized -aggregation of large # macrophages -occurs when living pathogen/foreign material cant be eliminated by phagocytosis,killing,digesting |
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List 4 infections that cause granulomas |
1. tuberculosis 2. hansen's disease-leprosy 3. schistosomiasis |
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amyloid
describe physical characteristics of an organ that has significant amounts of amyloid deposition: |
-organ is larger, firmer, and paler -retains fluid due to bad circulation -structural change cause functional change |
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amyloid
describe microscopic features and staining properties of an organ that has significant amounts of amyloid deposition |
-staining properties are known as H and E stain -Hemotaoxic (basic) Eosin (acidic) -esinophilic become pink
-dichrosism congo red -metachromasia methylene blue
|
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amyloid
state unifying feature of amyloid proteins |
-beta sheets -give the staining properties -fibrillar ultra structure -resistant to physiological solvents -resistant to preteolytic digestion |
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amyloid
define primary and secondary amyloidosis |
-primary: absence or a recognizable disease
-secondary: follows or associates with disease |
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amyloid
state origin of amyloid proteins in immune origin amyloidosis |
-systematic -aminoterminal fragment -bence jones protein -Ig light chain |
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amyloid
state origin of amyloid proteins in hemodialysis-associated amyloidosis |
-B2 microglobin (B2 uglobin) |
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amyloid
state origin of amyloid proteins in reactive systemic amyloidosis |
-aa type of amyloid -circulation of acute phase proteins |
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amyloid
state origin of amyloid proteins in hereditary system amyloidosis |
-all autosomal dominant except familial meditrainian |
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amyloid
state origin of amyloid proteins in endocrine-related amyloidosis |
-pancreatic insulits |
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amyloid
state origin of amyloid proteins in intracerebral amyloidosis |
-neuron loss -reactive proliferation of astrocytes -associated with blood vessels |
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state the relationship of SAA with inflammation |
-SAA is high under normal inflammation -SAA under Basal conditions very low: triggers IL1, IL6, TNF-alpha -T is apolopproprotein: HDL -RA and Crohn's Disease |