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69 Cards in this Set
- Front
- Back
what might result if a T cell does not receive the correct co-sitmulation from a APC presenting self peptide during peripheral tolerance
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T cell anergy - cant react to that Ag
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what happens if a APC presents a T cell with self peptide during peripheral tolerance and there IS co-stimulation
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activation induced cell death of T cells
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you see acute malar rash in what disease
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systemic lupus erythematosus (fixed erythema, flat or raised ver malar eminencies - butterfly)
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what disease might cause Libman-Sacks vegtations
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SLE - they are wiry depositis on any valve of heart - exposed to flow or not - larger than thos in r. heart disease
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Five patterns of nephritis
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1. normal 2. mesangial lupus glomerulonephrities 3. focal proliferative 4. diffuse proliferative 5. membranous
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wire loops are seen in what kind of glomerulinephritis
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membranous - thickening of the capillary wall
seen in glomerulonephritis caused by SLE |
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which stage of glomerulonephritis includes epithelial cresnants
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diffuse proliferative - presense of fibrinoid necrosis and hyaline thrombi indicate active disease as well as marked increase in cellularity
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In what disease might you see symmetric synovitis in the early stages
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rheumatoid arthritis
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"pannus" - what are the three types of cells you would see in this type of inflammation?
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fibrocellular mass of synovium and synovial stroma consisting of inflammatory cells (T cells, macrophages, plasma cells), granulomatous tissue and fibroblasts whih cause erosion of underlying cariglage.
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pannus eventually bridges remaining bone and forms
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fibrous andylosis which is evetually replaced by bone
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what infiltrate would see subsynovially with RA
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dense lymphoid aggregate
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firm nodules, nontender, round and oval, arise in the skin in the subcuatnwous tissue and have cetnral zone of fibrinoid necorosis all are signs of
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RA
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a product of chronic inflammatory activity against mamy stimuli and microscopically characterized by amorphous, eosinophilic, hyaline, EC substane
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amyloidosis
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Amyloid type whose major protein compoenent is K or gamma light chains and includes multiple myeloma
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primary (AL)
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what is the main protein component in secondary amyloidosis
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protein A
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What is the main protien component in neuropathic (portugal, sweeden, Japan) familial amyloidosis
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Transthyretin (prealbumin) - also the main compoenent in cardiopathic familial amyloidosis
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what is the main component in nephropathic familial mediterranean fever
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protein A (it is a type of familial amyloidosis though)
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what is the main protein component in dialysis amyloidosis
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B2-microglobulin
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how does the AL protein form
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carcinogen? - monoclonal B-lymphocyte proliferation - plasma cells - light chains - limited proteolysis
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how does AA protein form
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chronic inflammation - macrophage activaiton - IL 1 and 6 - liver cells - SAA protein - limited proteolysis
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diabetes mellitus - type I involves MHC locus on chromosome? and Insulin/ IGF-2 locus on chromosome?
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MHC locus is on chr. 6 and Insulin / IGF-2 locus is on chromosome 11
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is a rare, chronic disease characterized by excessive deposits of collagen in the skin or other organs.
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scleroderma (can be diffuse or systemic
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win what layer does the dense collagen deposit in scleroderma
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dermis - you see a thinning of the epidermis. this all starts at the fingers and other distal regions of upper extremities.
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what might the impact on the interlobular arteries in a reanl manifestation of systemic sclerosis
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intimal thickening due to the deposition of mucinous or finely collagneous matrix
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chronic granulomatous disease, wiskott-aldrich syndrome, sever combined immunodeficiency, agammaglobulinaemia, and X linked lymphoproliferative syndrome are all associated with what chromosome
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X
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X linked agammaglobulinemia or Bruton is what defect
which chains are absent which chains are present? |
there is a block in the production of Ab light chains, heavy chains made. low or absent IgG
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Btk (B-cell tyrosine kinase) mutation underlies what disease
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Brutons
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what kind of infections would a pt with Brutons be more suseptible to
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bacterial
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pts with what disease have a high risk of developing poliomylitis from the vaccine
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brutons
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this disease has three types
1. with predominant B cell defect 2. dereased Th, increased T suppressor 3. with autoAb to T or B cells |
common variable immunodeficiency
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what kind of infections are pts with common variable immunodeficiecy disease prone to
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bacterial, hypogammaglobulinemia,
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vurrca vulgaris might arise if a pt has
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common variable immunodeficiency
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what causes DiGeorge syndrome
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3rd and 4th pharyngeal pouches are malformed
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disease where thymus and parathyroids are abent
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DiGeorge
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pts with DiGeorge syndrome have high susceptibility to what kind of infections
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viruses and fungi
cardiac malformation are very common |
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lymphopenia characterized by low or absent T cells and frequently low/absent B cells may be caused by
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SCID
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those pts with SCID have an increased chance of what kind of infection
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viral, bacterial, and fungal
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most SCID is X linked and due to the defect in what kind of receptor
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IL-7 receptor which leads to poor lymphoid tissue formaion
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the most comomon complement deficiency is a deficiency in
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C2 - 50% homozygotes develop SLE like disease
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amyloide linked with myeloma and B cell tumor
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AL
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Amyloid protein linked with reactive chronic inflammation
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Protien A
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Amyloid protein linked with chronic renal failure
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B2 Microglobulin
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Amyloid protein linked with cerebral Plaques in Alzeimers
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APP - Amyloid Precurser protein
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in a congo red stain amyloid glows bright apple green due to
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the dye binding to unique molecular conformation seen in all forms of amyloid (B-pleated sheets)
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stain for SLE which involves Abs to non-DNA constuents and is LEAST specific
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specked pattern - speckles observed
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stain for SLE which includes nucleolar RNA stain and observed discrete spots of flourescence in nucleus
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Nucleaolar pattern
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stain for SLE using flourescence indicating double stranded DNA
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Rim/Peripheral staining
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homogeneous diffuse nuclear staining for SLE involves Abs to what three constiuants
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chromatin, histones, and double st. DNA
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SLE's genetic trait involves contributions from MHC or non-MHC genes
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both support genetic predisposition
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angioedema
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swelling of blood vessels
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four stages of RA
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1. antigen processing
2. antigen presentaiton of RF-specific B cell to T cell 3. angiogenesis 4. collagenase activation lysosomal enzymes metalloproteinases serine proteases cathepsins tissure destruction (invading pannus) |
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what is the rheumatoid factor?
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IgM against Fc component of IgG antibodies
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what type of hypersensitivity is RA
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type III
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what are the symptoms of RA
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fatigue, weight loss, myalgias, excessive sweating, low grade fevers, morning stiffness, lymphadenopathy
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expression of what adhesion molecule is a key step in the accumulation of inflammatory cells in RA
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ICAM
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diabetes mellitus is caused by
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immunological destruction of B cell of islet
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characterized by dry eyes and mouth - caused by immunological destruction of the lacrimal and salivary glands
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sjogren syndrome
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what type of hypersensitvity is sjogren syndrome
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type III
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what type of hypersensitivty is scleroderma
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type III
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how do fibroblasts and myofibroblasts contribute to systemic sclerosis
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ecm abnormalities and fibrosis
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how do endothelial cells contribute to systemic sclerosis
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vasculopathy (Raynaud's and Nailfold capillaries)
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what are the four complications linked with systemic sclerosis
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pulmonary fibrosis
pulmonary hyertensiion skin disease renal crisis |
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how does the dermis and epidermis change in scleroderma
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dermis thickens (dense collagen put down) and epidermis thins (begins with distal appendegaes)
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what is hashimotos thyroditis caused by
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defect in T cells - there is antithyroid Ab
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disease which influences B cells differentiating into plasma cells
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common variable
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disease where cardiac malformations are very common and the principle cause of death
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DiGeorge disease
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disease which may be due to ADA deficiency
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SCID
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disease of complement that leads to decreased complement activity and absence of specific components
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C1-C4 - leads pt to be more suseptible to bacterial infections
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leads patent to be more suseptable to severe neisseria infections
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C5-C9 absence
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