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48 Cards in this Set
- Front
- Back
Natural killer cells:
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large granular lymphocytes in peripheral blood
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IgM and IgG synthesis:
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begin after birth
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Class I MHC:
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present on nucleated cells
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APCs:
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B cells, macrophages, dendritic cells
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CD4 cells:
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secrete cytokines (IL-2 leads to proliferation of CD4/CD8 T cells; y-interferon activation of macrophages); help B cells become antibody producing plasma cells
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y-interferon:
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(sec by CD4), leads to activation of macrophages (pg 43)
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CD8 cells:
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kill virus-infected, neoplastic, and donor graft cells
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B cells:
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Differentiate into plasma cells that produce immunoglobulins to kill encapsulated bacteria, Act as APCs that interact with CD4 cells
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Natural killer cells:
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Kill virus-infected and neoplastic cells
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Macrophages:
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Involved in phagocytosis and cytokine production, Act as APCs
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Dendritic cells:
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Skin (Langerhans' cells), germinal follicles, Act as APCs
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GVH reaction:
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jaundice, diarrhea, dermatitis
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Antiacetylcholine receptor:
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Myasthenia gravis
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Anti-basement membrane:
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Goodpasture syndrome
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Anticentromere:
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CREST syndrome
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Antiendomysial and antigliadin
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Celiac diease
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Anti-insulin
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Type 1 diabetes
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Anti-intrinsic factor:
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Pernicious anemia
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Anti-islet cell:
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(no disease listed)
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Anti-parietal cell:
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(no disease listed)
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Antimicrosomal:
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Hashimoto's thyroiditis
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Antithyroglobulin:
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(no disease listed)
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Antimitochondrial:
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primary biliary cirrhosis
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Antimyeloperoxidase:
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Microscopic polyangiitis
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Antiproteinase 3:
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Wegener's granulomatosis
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Antiribonucleoprotein:
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Mixed connective tissue disease
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Anti-thyroid-stimulating hormone receptor:
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Grave's disease
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Most common cardiac finding in SLE:
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fibrinous pericarditis with effusion
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Procainamide:
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most common drug associated with drug-induced lupus
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Drug-induced lupus:
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antihistone antibodies
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Systemic sclerosis:
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excess collagen deposition
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Raynaud's phenomenon:
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most common initial sign of systemic sclerosis
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Systemic sclerosis:
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anti-topoisomerase antibodies
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CREST syndrome=
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calcinosis, Raynaud's phenomenon, esophageal dysfunction, sclerodactyly, telangiectasia
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MCTD- Mixed conn tissue dlo:
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antiribonucleoprotein antibodies
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Bruton's agammaglobulinemia:
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Defects: Failure of pre-B cells to become mature B cells (opsonization effect), Mutated Tyrosine kinase. Clinical features: Sinopulmonary infections.
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IgA deficiency:
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Defects: Failure of IgA B cells to mature into plasma cells. Clinical Features: Sinopulmonary infections, giardiasis.
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Common variable immunodeficiency:
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Defects: Defect in B-cell maturation to plasma cells, Adult immunodeficiency disorder.
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DiGeorge syndrome:
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Failure of third and fouth pharyngeal pouches to develop, Thymus and parathyroids fail to develop
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Severe Combined immunodeficiency (SCID):
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Defects:Adenosine deaminase deficiency; adenine toxic to B and T cells. Clinical features: Defective CMI, decrease immunoglobulins
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Wiskott-Aldrich syndrome:
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Defects: Progressive deletion of B and T cells. Clinical features: Symptom triad: eczema, thrombocytopenia, sinopulmonary infections. Defective CMI, decrease IgM, normal IgG, increase IgA and IgE.
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Ataxia-telangiectasia:
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Defects: mutation in DNA repair enzymes, Thymic hypoplasia. Clinical Features: Cerebellar ataxia, telangiectasias of eyes and skin.
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Anti-gp120 for HIV:
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detected in ELISA test screen
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Hereditary angioendema:
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deficiency of C1 esterase, Continued C1 activation decreases C2 and C4 and increases their cleavage products, which have anaphylatoxic activity. Normal C3.
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C2 deficiency:
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Most common complement deficiency, septicemia, lupus-like syndrome
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C6-C9 deficiency:
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increased susceptibility, Neisseria gonorrhoeae, N. meningitidis
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Paroxysmal nocturnal hemoglobinuria:
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Defect in molecule anchoring decay accelerating factor (DAF), normally degrades C3 and C5 convertase. COmplement-mediated intravascular lysis of red blood cells (hemoglobinuria), platelets, and neutrophils.
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Amyloid:
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abnormal folding of protein
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