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48 Cards in this Set

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