Immunology day 2
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| Which antibodies can be given passively? | To Be Healed Rapidly: Tetanus, Botulinum, HBV, RabiesI | ||||
| Isotype switching is mediated by | CD40 ligan, IL-4, IL-5, Il-6 | ||||
| IgA functions | Prevents attachment of bacteria and viruses to mucous membranes, does not fix complement | ||||
| Defect in tyrosine kinase gene (BTK). Name disorder, what you would see, lab findings, inheritance? | (decreased production) Bruton's agammaglobinulinemia. Recurrent bacterial infections after 6 month (maternal IgG levels decline). Low B cells, normal pro-B cells. X linked | ||||
| Thymus and parathyroids fail to developt owing to failure of development of 3/4 pouch. Name disorder, what you would see, lab findings, inheritance | (Decreased production). CATCH-22 (Cardiac defects, abnromal facies, thymic hypoplasia, cleft palate, hypocalcemia (tetany), microdeletion of 22). Will have recurrent fungal/viral infections. 22q11 deletion | ||||
| Name the multiple causes of SCID and labs for each. | Causes: Failure to synthesize MHC II (noraml immature T cells), defective IL-2 receptor (normal Pro-T cells, X-linked), ADA deficiency (only stem cells present) | ||||
| No rejection of allografts | SCID | ||||
| Patient with SCID will present: | Recurrent viral, bacterial, fungal, protozoal infections. No rejection of allografts, high incidence of malignancy, GVH disease, FTT) | ||||
| Decreased activation of T cells is a result of what deficiency? What cells are deficient? | IL-12; causes disseminated mycobacterial infections due to decreased TH1 resposne | ||||
| decreased activation of B cells results in what disorder? presentation, lab values | hyper-IgM syndrome; CD40L on CD4 T helper cells --> inability to class switch. Presents with pyogenic infections. High IgM, low IgG, IgE, IgA | ||||
| Disorder= high IgM, low IgG, IgE, IgA, Disorder= high IgE, IgA, low IgM, Disorder = High IgE | Hyper-IgM syndrome, Wiskott-Aldrich syndrome, Job's syndrome | ||||
| Defect in the ability to mount an IgM response to capsular polysaccharides of bacteria. Disorder, mechanism, presentation, lab, genetics | Wiskott-Aldrich syndrome (decreased activation of B cells), "WIPE" = pyogenic Infections, thrombocytopenic Purpura, Eczema, high IgE, IgA, X-linked | ||||
| Neutrophils fail to respond to chemotactic stimuli | Job's syndrome (decreased activity of neutrophils), Failure of IFN-gamma production by helper T cells. (FATED) Coarse facies, cold staphylococcal abcesses, retained primary Teeth, high igE, Dermatologic problems (eczema) | ||||
| Defect in LFA-1integrin (CD_) proteins on ___ | CD18, phagocytes; LAD defciency (phagocyte cell deficiency). Early recurrent bacterial infections, absetn pus formation, neutrophila, delayed seperation from umbilical cord | ||||
| Defect in microtubular function and lysosomal emptying of phagocytic cells. Presentation, genetics | Chediak-Higashi (phagocytic cell deficiency). Recurrent pyogenic infections, by staph, strep, partial albinism, peripheral neuropathy, autosomal recessive | ||||
| Defect in microbiocidal activity of ____. Describe presentation. Describe diagnostic test | NADPH oxidase. Chronic granulomatous disease (deficiency of phagocytes). Presents with marked susceptibility to S. aureus, E. coli, Aspergilllus. Negative nitroblue tetrazolium dye reduction test | ||||
| Chronic mucotaneous candidiasis is a dysfunction in what cell type? | T cell dysfunction against candida. Presents with skin and mucous membrane candida infections | ||||
| Deficiency in a class of immunoglobulins | Selective immunoglobulin deficiency. Selective IgA deficiency is the most common; Presents with sinus, lung infections, milk allergies, diarrhea. | ||||
| milk allergies, diarrhea due to - | IgA deficiency | ||||
| Anaphylaxis to bloo products | IgA deficiency | ||||
| Defect in DNA reapir enzymes. Its associated with what deficiency? presents with what problems? | Ataxia telangiectasia; associated with IgA deficiency. cerebellar problems, spider angiomas (due to ATM gene) = autosomal recessive, tumor suppressor | ||||
| decreased plasma cells but normal B cells | Common variable immunodeficiency; present in 20s-30s; increased risk of autoimmune disease, lymphoma. | ||||
| Bugs that have antigenic variation include | salmonella (flagellar), borrelia, Neisseria (pilus), Virus (shift=rearrangment, drift=random mutation), trypanosomes (african sleeping sickeness)- programmed rearrangement | ||||
| Anergy: | self-reactive molecules become non-reactive with costimulatory molecule | ||||
| Types that have granulomatous disease | Tuberculosis, Fungal (histo), syphillis, leprosy, Cat scratch, sarcoid, crohn's, berylliosis (non-caseating) (aerospace/nuclear industry) | ||||
| Define granuloma | Nodular collection of specialized macrophages (epitheliod cells) surrounded by a rim of lymphocytes) | ||||
| Desribe progression of granuloma | APC eats antigen; presents on MHC II--> matched with CD4; TH1 stimulates IFN gamma--> monocyte --> macrophage--> epitheliod cell --> giant cell | ||||
| Components of granuloma | epitheliod cell, giant cell, fibroblasts, lymphocytes. | ||||
| Difference between Langhans cells and foreign body | Langhans= multiple nuclei in horseshoe conformation; Foreign body = scattered nuclei | ||||
| Radioimmunosorbent test | Type I (detects specific igE antibodies in serum agasint specific allergies) | ||||
| Coomb's: Direct/Indirect; hypersensitivity __ | Direct: detects IgG/C3b attached to RBC; Indirect: detects antibodies in serum (Rh anti-D); II | ||||
| Immunofluoresecnt staining | III | ||||
| Alternative pathway is part of ___ immune system. Eg: | LPS, gram -; innate | ||||
| Classical pathway is part of ___ immune system; it involves | C1-C4 = viral neutralization; adaptive | ||||
| Mannose binding lectin pathway | Used for binding to sugars on surface | ||||
| C3b =, c3a = c5a = | C3b = opsonization, c5a, c3a = anaphylotoxins, c5a = neutrophil chemotaxis | ||||
| Deficiency of c1 esterase leads to | hereditary angioedema = problem with classical system; C1 esterase= noramlly controls complement; without it you'll have a decrease in C2-C4, increased cleavage products --> anaphylaxis (swelling of face/oropharynx) | ||||
| C2 deficiency | Association with septicemia (S. pneumoniae), lupus like syndrome in cildren | ||||
| C6-C9/C5-8 deficiency | Increased susceptibility to Neisseria/mengitidis | ||||
| DAF function | (decay accelerating factor): prevents complemetn activation of self cells | ||||
| DAF deficiency | due to a defect in the the anchoring of the particle; leads to complement mediated lysis for RBCs and paroxysmal nocturnal hemoglboinuria (platelets, neutrophils, hemoglobinuria) | ||||
| Function of interferons: | induce production of ribonuclease that inhibits viral protein synthesis by degrading viral mRNA. Also activates NK cells to kill virus-infected cells | ||||
| Alpha/beta interferons ___-, while gammma does ___ | alpha/beta = inhibit viral protein synthesis, gamma= increases MHC I/II expression and antigen presentation on cells |
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Created by:
ddecampo
on 2009-05-12