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22 Cards in this Set
- Front
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how do you control mature lymphoid cells from reacting to self antigens
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tolerance- state of unresponsiveness which is specific for a particular antigen, and is induced by prior exposure to that antigen. The most important form of tolerance is self-tolerance to prevent autoimmune responses.
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Tolerance Maintenance
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Clonal Deletion- like in the thymus if the cells show too much affinity to self, but it's not completely efficient.
Clonal anergy- cell is turned off Suppression- via regulatory T cells |
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Central Tolerance is where? Peripheral Tolerance is where?
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Central- thymus and bone marrow; where deletion happens
Peripheral-elsewhere where mature T and B cells are; where anergy, deletion and suppression happens |
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General predisposition of autoimmune diseases has this genetic component
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MHC genes are ass'd with autoimmune diseases
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Systemic Lupus Erythematosus
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autoimmune disease that involves chronic, systemic inflammation.
-anti-nuclear antibodies (ANA) -antibody against ds DNA -increased serum complement levels -immune complex deposition -mad autoantibodies -malar rash |
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Rheumatoid Arthritis
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chronic, recurrent, systemic inflammatory disease of joints.
-rheumatoid factor (abnormal Ab against Fc region of IgG) -immune complexes -joint inflammation -symmetrical joint problems -morning stiffness |
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Insulin-dependent diabetes mellitus (IDDM)
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autoantibodies and autoreactive T cells are produced against the beta cells of the pancreatic islets of langerhans, resulting in diminished insulin production and chronic hyperglycemia.
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Hashimoto's Thyroiditis
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-excessive thirst, polyuria, weight loss, lethargy
-inflamm disorder of thyoid -cellular infiltration of thyroid -high titer auto-Abs -enlarged thyroid (goiter) and abnormal thyroid function |
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Addison's Disease
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-abdo discomfort, malaise, weight loss, hyperpigmentation, low cortisol levels and Abs to the adrenal cortex
-adrenal insufficiency -autoAbs against adrenal cells -hypotension, anorexia, malaise, hyperpigmentation |
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Polyglandular Autoimmune Syndromes
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-circulating autoantibody against multiple endocrine glands
-type I, II, and III -may have multiple endocrine diseases |
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Grave's Disease
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Auto-Ab develop that stimulate thyroid function
-hyperthyroidism -Auto-Ab against TSH receptor -Proptosis (bug-eyes) |
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Goodpasture's Syndrome
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-affects young males,
Triad: pulmonary hemorrhage, glomerulonephritis, circulating antibody to basement membranes -lungs and kidneys -Ig and complement deposits - |
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Bloddy diarrhea, tenesmus, fever, weakness, doesnt skip large intestine. disease of mucosa
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Ulcerative colitis
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abdominal pain, diarrhea, malabsorption, from mouth to anus
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Crohn's Disease
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Immune Hemolytic Anemias
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immunologic reactions against rbs proteins, usually mediate by antibody, complement, or phagocytes. may be from drugs that bind to rbc membranes , inducing Ab responses, and cause immune-mediated destruction of the rbc.
-fatigue, from complement (intravascular) or phagocytic cells (extravascular) |
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Which is warm-antibody types? Which is cold-antibody types?
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Warm- IgG (70% of hemolytic anemias)
Cold- IgM (16%) |
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Direct Coomb's Test
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add Ag to in vivo antibody-coated RBCs, see agglutination
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Indirect Coomb's Test
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uncoated RBCs added with serum with Ab to RBC, then you get coated RBC, then you add that with anti-Ig, then wait for agglutination
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Myasthenia Gravis
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Type II hypersensitivity
Autoreactive Abs against the ACh receptors in the NMJ. complement is activated, and the post-synaptic membrane is dunzo. you then present with muscle weakness. |
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Name 3 inflammatory vasculitides
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1. giant cell arteritis
2. wegener's granulomatosis 3. henoch-schonlein purpura *all have inflammation of the blood vessels |
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Pemphigus Vulgaris
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an immunobulloud disease
-blistering diease of skin and mucous membranes -auto-Ab against keratinocyte antigens |
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Multiple Sclerosis
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-inflammatory demyelination of the CNS, progressive motor weakness, parethesias, visual impairment, ataxia
-oligoclonal Ig bands in CSF -HLA Ag associations -altered immunoregulatory T cell populations |