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69 Cards in this Set

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what might result if a T cell does not receive the correct co-sitmulation from a APC presenting self peptide during peripheral tolerance
T cell anergy - cant react to that Ag
what happens if a APC presents a T cell with self peptide during peripheral tolerance and there IS co-stimulation
activation induced cell death of T cells
you see acute malar rash in what disease
systemic lupus erythematosus (fixed erythema, flat or raised ver malar eminencies - butterfly)
what disease might cause Libman-Sacks vegtations
SLE - they are wiry depositis on any valve of heart - exposed to flow or not - larger than thos in r. heart disease
Five patterns of nephritis
1. normal 2. mesangial lupus glomerulonephrities 3. focal proliferative 4. diffuse proliferative 5. membranous
wire loops are seen in what kind of glomerulinephritis
membranous - thickening of the capillary wall

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