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87 Cards in this Set
- Front
- Back
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Which antibody is optimal for an agglutination reaction?
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IgM
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Which test uses particulate antigens to detect Salmonella?
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Widal Test
Ag's - H(flagella) and O (snowflake,granular) |
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Which test uses particulate antigens to detect Rickettsial disease?
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Weil Felix Test
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What term refers to excess antibody inhibiting lattice formation?
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Prozone
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What term refers to excess antigen inhibiting lattice formation?
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Postzone
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Which agglutination test is used for the detection of primary atypical pneumoniae?
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Cold agglutination Test
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Antigen + latex particle
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Passive Agglutination
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What disease is characterized by inflammation-> joint cartilage -> Ab to synovial cavity -> enzymes damage Fc of IgG -> new Ag created -> Ab formed.
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Rheumatoid Arthritis; This detects antibody.
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The Ab formed against Rheumatoid Arthritis:
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Rheumatoid Factor
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This passive agglutination technique is used for the antigen detection in various organisms. The test is as follows: unknown culture + dead staph cells = protein A coated with specific enzymes.
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Co-agglutination
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What is the name for the passive Hemagglutination technique in which an RBC absorbs a polysaccharide Antigen. The RBC is treated with chemicals to reveal new protein receptors.
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Tannic Acid AKA Boyden AKA "Tanned cell" Technique
(if Ag attached passive if Ab attached reverse passive) |
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An agglutination inhibition test for human chorionic gonadotropic is essentially a test for what?
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Pregnancy. No agglutination= postive test.
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Which test is characterized by serum + RBC = Hemagglutination
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Paul Bunnell
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What is the procedure for agglutination by viruses?
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Virus + RBC = HA. AB forms complex with virus preventing lattice formation.
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In a precipitation the ___ is the precipitin and the ____ is the precipitinogen.
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Antibody, antigen
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What does a precipitation reaction consist of?
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Soluble Ag + Ab
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Which test is used to demonstrate toxin production by cornybacterium diptheria?
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Elck Test
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Explain Immunoelectrophoresis:
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Graber and Williams; electrophoresis + precipitin in agar= electrophoretic disperal of Ag and then immunodiffusion reaction.
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Which electrophoresis technique is used to reveal Ags in a particular specimen?
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Immunoelectrophoresis
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Explain counterelectrophoresis:
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Nakamura; Ab have little electric charge and migrated toward cathode; Ag have greater mobility and migrate toward anode.
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What are some of the advantages of using counterelectrophoresis?
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It's fast, sensitive, and you can use large # of speciments.
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Explain Rocket Electrophoresis:
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This is a combination of immunot electrophoresis and counter electrophoresis. Ag migrates to electrical field applied to gel that contains Ab. Ag combine w/ Ab during electrophoresis-> ppt resembles rocket -> quantitative technique.
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Explain Fluorescent Ab Technique:
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Ab + fluorescent = fluorescence
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Most fluorescents label what?
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Albumins
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What are some advantages of using immunofluorescence?
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Detection of Ag or Ab is rapid, procedures are shortened, pure cultures are not required, sensitive, low cost.
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Explain Flourescytometry:
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suspension labeled w/ flourescent monoclonal Ab -> passes across laser beam -> population counted.
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Explain Radioimmunoassay:
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Very sensitive assay used to measure minute amounts of Ag or Ab.
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What are some advantages and disadvantages of radioimmunoassay?
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Advantages: sensitive, detection of Ag and Ab
Disadvantages: Expensive equip, safety |
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Explain Ezyme Linked Immunoabsorbent Assay:
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Ab labelled with enzyme + Ag + substrate for enzyme = color change.
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What are some ezymes used for elisa?
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horseradish, peroxidase, beta galactosidase, phosphatase.
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What are some advantages of Elisa?
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Safe, stable reagents, reproducibility, inexpensive, many sera @ 1 time.
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Explain indirect elisa, double Ab sandwich, and competetive elisa:
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indirect: detect of Ab. Ag + Ab (unknown) + (Ab + enzyme) + substrate = color change. Double Ab sandwich: Ab + Ag (unknown)+ unlabelled specific Ab and Ab-enzyme or anti-species + substrate = color change. Competetive: Ab incubated w/ sampe containing Ag -> Ab-Ag mixture added to Ag coated microtiter wells -> the more Ag is sample the less free Ab will be available to bind Ag-coated well.
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In general, oraganisms that infect blood are likely to evoke ____ response. Organismas that infect tissues are likely to evoke ___cellular response.
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Humoral; cellular
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What is the path of bacterial infection?
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infection - attachment to cell- proliferation - invasion of tissues - toxin damage to cells.
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What is specific immunity for bacterial infections?
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phagocytosis= organisms stimulates Ab prod-AgAb complex= increase phagocytosis. Toxin neutralization= Ab+toxin blocks rxn- forms complex with Ab- susc to phago.
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What is a toxoid
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A detoxified toxin
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What is cell mediated response for bacterial infection?
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mac engulf and process Ag= sens T cells; some org destroyed by mac others are not. Result = granulomas, cytolytic activity with activated Tc cells.
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Explain Ab dependent toxicity:
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Ab marks cell and NK cells detect change in cell. This is a type of specific viral immunity
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What is neutralization?
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Ig binds to virus and blocks the spread of virus to other cells.
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What is opsonization?
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Viral aggregates + complement; this is easier to phagocytize.
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Explain cell mediated viral immunity:
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cytolysis by Tc cells.
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Explain Immunoparisitology:
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Organisms produce chronic disease state; spread by invertebrate vectors.
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Explain cell mediated Parasitic Immunity:
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protozoans (plasmodium,toxoplasma) = surface Ag = Th and Tdth
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Define Affinity:
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Strength of a single Ag=Ab bond
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Define Avidity:
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Strenth at which a multivalent Ab binds to a multivalent Ag.
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What are some examples of Bacterial Vaccines?
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DPT, TAB, Meningococcal, Hemophilus, pneumococcal, choler, plague, anthrax.
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What are some examples of viral vaccines?
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HB, Polio, Rabies
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Which vaccines are generally killed?
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Bacterial vaccines
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What are disadvantages of viral vaccines?
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infectious virus present, spread of vaccinated person to susceptible person, contaminationg viruses present,genetic change could take place, vaccine susceptible to heat.
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Which vaccines are generally attenuated?
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Viral vaccines
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What are the two stages of graft rejection?
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Sensitized (leukocytes from donor move to lymphnodes and stimulate Th cell proliferation)/ effector (Populatation of effector cells migrate to graft to mediate rejection)
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Explain Hyperacute graft rejection:
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Never accepted by new host.
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Explain acute rejection:
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first set: appears tissue will take - fever,trans fails- T cells produce lymphokines - blood supply cut- cells die.
2nd set: Retransplant- Ab+NK+T cells - destroy graft blood supply. |
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Explain Chronic rejection:
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Months to years- Walls of blood vessels become blocked by proliferation of smooth muscle cells. Neutrophils then mononuclear cells-capillary endothelium destroyed-blood clots-tissue death.
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Explain lymphoagglutination:
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Lymphs from donor and recipient tested w/ monoclonal Abs directed against class I Ag.
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Explain lymphocytotoxicity teset:
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lymphs from donor and recipient tested w/ monoclona Abs directed against class Ig- complement added= lysis
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Explain Mixed lymphocyte culture:
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In vitro culture of leukocytes from donor or recipient.
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Explain two way mixed lymphocyte culture:
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Lymphocytes placed in culture - lymphs increase in sized w/in 5 day incubation - this determines if recipient is acting against donor.
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Explain one way mixed lymphocyte culture:
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Donor lymphocytes are poisoned with mitomycin C- mix with recipient cells-transformed cells become index of recipient response.
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What can be used to prevent rejection non specifically?
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Corticosteroids (inhibit B and T cells non selectively; Cytotoxic drugs (Act on nucleic acid synthesis/activity); Azathioprine (incorporated into DNA dividing cells-prevent further proliferation).
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What is the immune response to tumors?
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Nk and cytotoxic T cells
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What are some RNA oncogenic viruses?
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leukemia, sarcoma, mammary tumor
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What are some DNA oncogenic viruses:
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Herpes (frog and monkey), Burkitts lymphoma (malig of jaw and face), Hodkins (lymph nodes and spleen), lymphoma
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Define neo antigens:
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Altered form of previously existing Ag
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Explain Grave's disease:
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Ab to thyroid stimulating hormone. Can bind to TSH receptor to stimulate secretion of hormone.
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Explain Hashimoto's thyroiditis:
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Ag= thyroid gland-lymphs and macs= inflammation-goiter-complement mediated lysis- destruction of thyroid cells-hypoactive thyroid.
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Explain myexedema:
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Ab+cellular rxn-cytotoxic responses-destruction of glandular tissue- thyroid shrinks.
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Explain Myesthenia gravis:
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Muscle weakness-skel muscles fatigue- auto ab to acetylcholine receptors protein- reduction in # of receptors.
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Explain autoimmune anemias
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Pernicious (intestinal protein), hemolytic anemia (ab to RBC Ags binds to RBC)
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Good Pasture's Syndrome
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Kidney disease. Ab against glomerular basement.
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Explain Insulin Dependent Diabetes:
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Autoimmune rxn to insulin producing cells; destroys b cells; decrease in insulin production; increase in blood glucose.
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Post-strep diseases:
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Kidney and heart; cross reactive type of Ab. Group A strep contain Ag that are cross reactive w/ kidney and heart.
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Explain Systemic lupus erythematous:
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Development of autoAbs against nucleic acids; Auto Abs form immune complexes that deposit in organs-inflamm rxns-destruc of cells in organs=damage to glomerular nephron-threatening kidney failure
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Explain multiple sclerosis
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Myelin sheaths destroyed-slower nerve impulses- Ab + complement=destruction of myelin sheath. Dia: increased IgG in myelin sheath.
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Explain Rheumatoid Arthritis:
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Inflammation of connective tissue-joints=may lead to death.
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Explain Scleroderma:
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Tightening of skin= over production of collagen in connective tissue.
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Explain Bruton type hypogammaglobulinemia:
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Sex linked disease; male infants suffer from chronic bact infection; B cells fail to develop.
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Explain DiGeorge's syndrome:
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Person born with little or no thymus gland. T cells markedly reduced. B cells are present, but Ab levels are very low. Not inherited like Nezelof's.
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Explain Nezelof's syndrome:
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Inherited thymic disorder; T cell def disorder that results in abnormal Ig sythesis. Decrease in T cells but not be cells.
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Explain Wiskiott-Aldrich syndrome:
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bleeding-reduced platelets-recurring inf-eczema-fatal injection of lymphoid malignancy.
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Explain leprosy:
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T cells depressed- lymphocytes not responsive to mitogens.
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Explain Bare lymphocyte syndrome:
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No class II MHC molecules
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Explain Chronic granulomatous disease:
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Phagocytic disfunction of certain enzymes. cells fail to generate toxic species.
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Explain Chediak-Higashi syndrome:
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Fragile lysosomal membranes which do not degranulate properly.
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Describe the 3 types of anaphylaxis:
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local (allergies;mild; sneezing,itching,food); systemic (severe; life threatening, shock), Cutaneous (skin rxn-rapid-few minutes)
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What are some mediators involved in Type I hypersens?
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Histamine-released by cell degranulation-vasodilation, musc contraction. Serotonin-same as histamine but seen in rats. SRS-A, ECF-A (in nasal secretions), Prostaglandins, Cytokines (released by mast cells and eosinophils.
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Describe Type II hypersensitivity:
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Rxns against blood cells. Rxns against tissue Ags. Transfusion Rxn-incompatible blood.
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