Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Immunology day 2
| Question | Answer |
|---|---|
| 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 |
Created by:
ddecampo
Popular USMLE sets