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Step 1 11.15.12
Immunology II
| Question | Answer |
|---|---|
| How is passive immunity articially acquired, what is its onset and duration? | receive preformed Ab like IgA in breat milk, antitoxin or just Ig. rapid onset but short half life |
| How is active immunity acquired, what is its onset and duration? | exposure to foreign Ag from natural infection or vaccines or toxoid. slow onset but long lasting protection |
| In what 4 diseases are Pt given preformed Ab in order to rapidly clear the infection? | tetanus toxin, botulinum toxin, HepB, Rabies |
| What is a Live attenuated vaccine? What type of response does it ellicit? | micro organism has no pathogeneicity but can transiently gorw in host. maily induces a cellular response |
| What are some pros and cons of live attenuated vaccine? | Pro: strong, often life long immunity Con: may revert to a virulent form |
| What tye of vaccine are measels, mumps, polio (Sabin), rubella, varicella, yellow fever? | live attenuated vaccine |
| What is an inactivated or killed vaccine? What type of immunity does it induce? | pathogen is inactivated by heat of chemicals, maintaing surface epitope structure. Induces humoral immunity |
| What are some pros and cons for using an inactivated or killed vaccine? | Pro: stable and safer than killed Con: weaker immune response, usually require a booster |
| What type of vaccines are cholera, influenza, hepA, polio (Salk), and rabies? | inactivated or killed vaccine |
| What is Type I hypersensitivity? What cells mediate it and how fast is the onset? | anaphylactic and atopic. free Ag cross links IgE on presensitized mast cells causing release of histamines. Reaction is rapid to preformed Ab |
| Which types of hypersensitivity are Ab mediated? | I, II, III |
| What is the test for Type I hypersensitivity? | scratch test, radioimmunosorbent assay |
| What are the general characteristics of Type II hypersensitivity? | IgM, IgG bind to fixed Ag on "enemy" cell leading to lysis or phagocytosis. lead to MAC attack |
| What are the 3 mechanisms of Type II hypersensitivity? | 1. Ab opsonizes cells or activates complement 2. Ab recruit neutrophils and macrophages causing tissue damage 3. ab bind to normal receptors and interfere with their fx |
| What test is used for Type II hypersensitivity? | direct and indirect coombs test |
| What is immune complex type III hypersensitivity? | Ag-Ab (IgG) complexes activate complement which attracts neutrophils which release lysosomal enzymes. complex = Ab-Ag-complement |
| What is serum sickness type III hypersensitivity? | Ab to foreign proteins are produced (5 days). Immune complexes form are are deposited on mebranes where they cause damage by fixing complement |
| What most commonly causes type III hypersensitivity serum sickness? What is seens | drugs. see fever uticaria, preoteinuria, lymphadenopathy 5-10 d after ag exposure |
| What is Arthus reaction type III hypersensitivity? What is seen? | local subacute Ab reaction. intradermal injection of Ag induces Ab which from complexes in skin. See edema, necrosis and complement activation |
| What causes the Arthus reaction? | A-Ab complexes. |
| What is the test for Type III hypersensitivity? | Immunoflourescent staining |
| What is type IV hypersensitivity? | Delayed, T cell mediate type. sensitized T cells encounter Ag and release lymphokines, activating macrophages. No ab involved |
| Can type IV hypersensitivity be transferred by serum? | no because it doesnt involve Ab |
| What are 3 manifestations of type IV hypersensitivity? | 4Ts: Tcells, Transplant rejection, Tb skin tests, touching (contact dermatitis) |
| What is the test for Type IV hypersensitivity? | patch test (PPD) |
| What is a useful pneumonic for the 4 types of hypersensitivity? | ACID: Anaphylactic and atopic (I), Cytotoxic (Ab mediated II), Immune complex (III), delayed (IV, cell mediated) |
| What type of hypersensitivity is anaphylaxis from a bee sting, or food or drug allergy? | Type I hypersensitivity |
| What is the presentation of Type I hypersensitivity? | immediate, anaphylactic, atopic |
| What type of hypersensitivity are hay fever, allergies, eczema, hives and asthma? | Type I hypersensitivity |
| What is the presentation of type II hypersensitivity? | tends to be specific to tissue or site where the Ag is found |
| What type of hypersensitivity is erythroblastosis fetalis, acute tranfusion reactions, Rheumatic fever, Goodpastures, Graves, Myasthenia gravis? | Type II hypersensitivity |
| What type of hypersensitivity might be associated with a vasculitis or systemic manifestations? | type III hypersensitivity |
| What type of hypersensitivity mediates SLE, theumatoid arthritis, polyarteritis nodosum, Post strep GN, serum sickness, farmers lung? | Type III hypersensitivity |
| What hypersensitivty mediates swelling and inflammation after a tetanus shot? | Type III hypersensitivity, this is the Arthus reaction |
| What type of hypersensitivity mediates Type I DM, Ms, Guillan -Barre, Hashimoto's thyroiditis, Graft rejection, and contact dermatitis (poison)? | Type IV hypersensitivity |
| What causes an allergic reaction in a blood transfusion rejection, what is seen? | Type I hypersensitivity against plasma proteins. see uticaria, prutitis, wheezing fever |
| How do you treat an allergic reaction to blood transfusions? | antihistamine, this is type I hypersensitivity |
| What is the mech of a anaphylactic rejection of blood transfusion? When might it be seen and what are the Sx | Sever reaction, as in an IgA deficient person must get products lacking IgA. see dysnea, bronchospasm, hypotension, respiratory arrest, shock. |
| What is a febrile non hemolytic transfusion reaction? | Type II hypersensitivity. Host ab against donor HLA ag and leukocytes |
| What are the sx or a febrile nonhemolytic transfusion reaction? | fever, HA, chills, flushing |
| What is an acute hemolytic transfusion reaction? What 2 types of hemolysis could happen? | Type II hypersensitivity. ABO incompatibility causes intravascular hemolyisis. extravascular hemolysis from host Ab reaction against foreign Ag on donor RBCs |
| What are the sx of acute hemolytic transfusion reaction? | fever, hypotensioon, tachypnea, tachycardia, flank pain. hemoglobinemia (if intravascular), jaundice ( if extravascular)( |
| What disorder has anti nuclear Ab (ANA)? | SLE, nonspecific |
| What disorder has anti-dsDNA, anti-Smith ab? | SLE |
| What disorder has antihistone Ab? | drug induced lupus |
| What disorder has anti IgG (rheumatoid factor)? | Rheumatoid arthritis |
| What disorder has anticentromeric Ab? | Scleroderma (CREST) |
| What disorder has Anti-Scl-70 (anti DNA topoisomerase I)? | Scleroderma (diffuse) |
| What disorder has antimitochondrial Ab? | primary biliary disease |
| What disorder has antigliadin, antiendomysial? | Celiac disease |
| What disorder has anti-basement membrane Ab? | Goodpasture's syndrome |
| What disorder has anti-desmoglein Ab? | Pemphigus vulgaris |
| What disorder has antimicrosomial, antithyroglobulin Ab? | Hashimoto's thyroiditis |
| What disorder has anti-Jo-1 Ab? | polymyositis, dermatomyositis |
| What disorder has Anti-SS-A (anti-Ro) Ab? | Sjogren's syndrome |
| What disorder has anti-SS-B (anti-La) Ab? | Sjogren's syndrome |
| What disorder has Anti-U1 RNP (ribonucleoprotein)? | Mixed connective tissue disease |
| What disorder has anti-Smooth muscle Ab? | Autoimmune hepatitis |
| What disorder has anti-glutamate decrboxylase Ab? | Type I DM |
| What disorder has cANCA? | Wegener's granulomatosis |
| What disorder has pANCA? | other vasculitides, prominently microscopic polyangitis |
| What do bacteria cause if a person lacks T cells? | sepsis |
| What types of bacteria are people without B cells vulnerable to? | encapsulated: Strepto, staphylo, haemophilus, Moraxella |
| What types of bacteria are people without granulocytes vulnerable to? | staphy, pseudomonas |
| What types of bacteria are people without complement vulnerable to? | Neisseria (no Mycobacterium avium) |
| What types of viruses are people without T cells vulnerable to? | CMV, EBV, VZV. chronic infection with respiratory/ GI viruses |
| What types of viruses are people without B cells vulnerable to? | enteroviral encephalitis, polio virus (live virus is contraI) |
| What types of fungi/parasites are people without T cells vulneerable to? | Candida, PCP |
| What types of fungi/parasites are people without B cells vulnerable to? | GI giardiasis due to lack of IgA |
| What types of fungi/parasites are people without granulocytes vulnerable to? | Candida, Nocardia, Aspergillus |
| Overall that is the tendency of T cell vs B cell deficiencies in infections? | Lack of T cells= more fungal and viral infections. Lack of B Cell= recurrent bacterial infection |
| What are 4 major B cell immune disorders? | 1. Burton's agammaglobulinemia 2. Hyper IgM syndrome 3. Selective IgG deficiency 4. Common variable immunodeficiency |
| What is the defect and inheritance in Burton's agammaglobulinemia? | Xlinked R(incr in boys). defect in BTK a tyrosine kinase which blocks pro B cells from forming pre B cells |
| What is the presentation in Burton's agammaglobulinemia? What structure might be absent? | recurrent bacterial infections after 6 months (decr maternal IgG) due to opsonization defect. absence of thymic shadow |
| What labs are seen in Burton's agammaglobulinemia? | normal pro-B, decr maturation, decr # of B cells, decr Ig of all classes |
| What is the defect in Hyper-IgM syndrome? | defective CD40L on TH= can't class switch |
| What is the presentation of Hyper-IgM syndrome? | severe pyogenic infections early in life |
| What labs might be seen in Hyper-IgM syndrome? | incr IgM, very Decr IgG, A, E |
| What is the defect in selective Ig deficiency? | defect in isotype switch=a deficeincy is a specific class of Ig |
| What is the presentation of selective Ig deficiency? What reaction is especially worrisome? | sinus and lung infections, mil allergies, diarrhea. anaphylaxis on exposure to IgA containing blood products |
| What labs are seen in selective Ig deficiency? | IgA deficiency is most common. failure to mature into plasma cells. decr secretory IgA |
| What is the defect in common variable immune deficiency (CVID)? | defect in B cell maturation. many causes |
| What is the presentation of common variable immune deficiency? | can be acquired in the 20-30s. incr risk of AID, lymphoma, sinopulmonary infections |
| What labs are seen in common variable immune deficiency? | normal # of B cells, decr plasma cells, Ig |
| What are 4 major T cell immune disorders? | q. Thymic aplasia (DigGeorge) 2. Il-12 receptor deficiency 3. Hyper IgE syndrome (Job's syndrome) 4. chronic mucocutaneous candidiasis |
| What is the defect in thymic aplasia (DiGeorge Syndrome)? | 22q11 delection; failure to develop 3rd and 4th pharyngeal pouches |
| What is the presentation of thymic aplasia (DiGeorge Syndrome)? | tetany(hypocalcemia), reccure viral/fungal infections, CHD, great vessel defects |
| What labs are seen in thymic aplasia (DiGeorge Syndrome)? | thymus and parathyroid fail to develop. decr T cells, decr PTH, decr ca2+. absent thymic shadow on CXR |
| What is the defect in IL-12 receptor deficiency? | decr Th1 response |
| What is the presentation of IL-12 receptor deficiency? | disseminated mycobacterial infections |
| What labs are seen in IL-12 receptor deficiency? | decr IFN-gamma |
| What is the defect in Hyper-IgE syndrome (Job's syndrome)? | TH cells fail to produce IFN-gamma-->neutrophils can't respond to chemotactic stimuli |
| What is a mnemonic for the presentation of Hyper-IgE syndrome (Job's syndrome)? | FATED: coarse Facies,cold, staphylococcal Absesses, retained primary Teeth, incr IgE, dermatologic problems (eczema) |
| What labs are seen in Hyper-IgE syndrome (Job's syndrome)? | incr IgE |
| What is the defect in chronic muccocutaneous cadidiasis? | T-cell dysfunction |
| What is the presentation of chronic muccocutaneous cadidiasis? | Candida albicans infections on skin and mucous membranes |
| What are 3 major B and T cell combined immune deficiencies? | 1. Sever combined immunodeficency (SCID) 2. ataxia-telangiectasia 3. Wiskott-Aldrich syndrome |
| What is the defect in severe combined immunodeficiency (SCID)? | several types: defective IL-2 rector (most common and X linked), adenosine deaminase deficiency, failure to synthesize MHC II Ag |
| What is the presentation of severe combined immunodeficiency (SCID)? | recurrent viral, bacterial, fungal and protozoal infections. no thymic shadow, no germinal centrers in LN bipsy, no B cells on PBS |
| What is the Tx for severe combined immunodeficiency (SCID)? | only bone marrow transplant, no allograft rejection |
| What labs are seen in severe combined immunodeficiency (SCID)? | decr IL-2R= decr T cell activation. incr adenine=toxic to T and B cells (decr dNTPs, decr DNA synth) |
| What is the defect in ataxia-telangiectasia? | defects in ATM gene which codes for DNA repair enzymes |
| What is the presentation of ataxia-telangiectasia? | triad: cerebellar defects (ataxia), spider angiomas (telangiectasia), IgA deficiency |
| What labs are seen in ataxia-telangiectasia? | decr IgA |
| What is the defect in Wiskott-Aldrich syndrome? | X linked recessive defect. progressive deletion of T and B cells |
| What is the presentation of Wiskott-Aldrich syndrome? | Triad TIE: thrombocytopenia purpura, infections, eczema |
| What labs are seen in Wiskott-Aldrich syndrome? | incr IgE, IgA, decr IgM |
| What are 3 major phagocyte dysfunction immune disorders? | 1. Leukocyte adhesion deficiency (type 1) 2. Chediak-Higashi syndrome 3. Chronic granulomatous disease |
| What is the defect in leukocyte adhesion deficiency (type 1)? | defect in LFA-1 integrin (CD18) protein on phagocytes |
| What is the presentation of leukocyte adhesion deficiency (type 1)? | recurrent bacterial infections, absent pus formation, delayed separation of the umbilicus |
| What labs are seen in leukocyte adhesion deficiency (type 1)? | neutrophilia |
| What is the defect in Chediak-Higashi syndrome? | AutoRec. defect in lysosomal trafficking gene (LYST). causes microtubule dysfunction and phagosome/lysosome fusion |
| What is the presentation of Chediak-Higashi syndrome? | recurrent pyogenic infections by Staphy and strep. partial albinism, peripheral neuropathy |
| What is the defect in chronic granulomatous disease? | lack of NADPH oxidase--> decr in ROS and absent respiratory burst in neutrophils |
| What is the presentation of chronic granulomatous disease? | incr susceptibility to catalase + organism (S. aureus, E. coli, aspergillus) |
| What labs are seen in chronic granulomatous disease? | negative nitroblue tetrazolium dye reduction test |
| What is an autograft? | from self |
| What is a syngeneic graft? | from identical twin |
| What is an aloograft? | from nonidentical twin |
| What is a xenograft? | from a different species |
| What is the onset and pathogenesis of hyperacute transplant rejection? | within minutes onset. Type II hypersensitivity (Ab mediated) due to presence of preformed anti donor Ab in transplant recipient |
| What are the major features of hyperacute transplant rejection? | occludes graft vessels, causing ischemia and necrosis |
| What is the onset and pathogenesis of acute transplant rejection? | onset weeks later. cell mediated rejection due to CTL's reacting against foreign MHC's. can reverse with immunosurpression (cyclophosphamide, OKT3) |
| What are the features of acute transplant rejection? | vasculitis of graft vessels with dense lymphocytic infiltrate |
| What is the onset and pathogenesis of chronic transplant rejection? | months to years later, class I MHC nonself is perceived by CTL's as Class I MHC self presenting a non self Ag |
| What are the features of chronic transplant rejection? | irreversible. T cell and Ab mediated vascular damage (obliterative vascular fibrosis), get fibrosis of graft tissue and blood vessels |
| What is the onset and pathogenesis of Graft-versus-host transplant rejection? | variable onset. grafted immunocompetent T cells proliferate in the irradiated ICPT and reject cells with foreign proteins resulting in severe organ dysfunction |
| What are the features of Graft-versus-Host transplant rejection? | maculopapular rash, jaundice, hepatosplenomegaly, diarrhea. usually seen in BM and liver transplant (these organs are rich in lymphocytes). potentially beneficial in BM transplant |
| What is the mech of cyclosporine? | binds to cyclophilis. complex then blocks differentiation and activation of T cells by inhibiting clacineurin, prevent production of IL-2 and its receptor |
| What is the clinical use of cyclosporine? | surpresses organ rejection. also in select AIDs |
| What are the major SE of cyclosporine? | predisposes to viral infection and lymphoma. nephrotixic (prevented with mannitol diuresis), gout |
| What is the mech of tacrolimus (FK506)? | similar to cyclosporine. binds FK-binding protein, inhibiting IL-2 secretion and other cytokines |
| What is the clinical use of tacrolimus? | potent immunosurpression in organ transplant patients |
| What is the SE of tacrolimus (FK506)? | significant: nephrotoxicity, peripheral neuropathy, HTN, leural effusion, hyperglycemia |
| What is the mech of sirolimus (rapamycin)? | inhibits mTOR. inhibits T-cell proliferation in response to IL-2 |
| What is the clinical use of sirolimus (rapamycin)? | immunosurpression after kidney transplant in combo with cylclosporine and steroids. also used with drug eleuting stents |
| What are the major SE of sirolimus (rapamycin)? | hyperlipidemia, thrombocytopenia, leukopenia |
| What is the mech of daclizumab? | MAB with high affinity for IL-2 receptor on activated T cells |
| What is the mech of azathioprine? | antimetabolite precursor for 6-mercaptopurine that interferes with metabolism and synthesis of nucleic acids. toxic to proliferating lymphocytes |
| What is the clinical use of azothioprine? | kidney transplants, AIDs (including GN and hemolytic anemia) |
| What are the major SE of azothioprine? When might they be incr? | bone marrow surpression, active metabolite mercaptopurine is metabolized by xanthine oxidase so toxicites might be incr by allopurinol |
| What is the mech of muromonab-CD3 (OKT3)? | MAB that binds to CD3 epsilon chain on T cells. blocks cellular interaction with CD3 protein responsible for T cell signal transduction |
| What is the clinical use of muromonab (OKT3)? | immunosurpression after kidney transplant |
| What are the major SE of muromonab-CD3(OKT3)? | cytokine release syndrome, hypersensitivity reaction |
| What is aldesleukin used for (IL-2)? | renal cell carcinoma, metastatic melanoma |
| What is Eryhtropoetin used for? | anemias, esp in renal failure |
| What is filgrastim (granulocyte colony stimulating factor) used for? | recovery of bone marrow |
| What is sargramostin (granulocyte-macrophage colony stimulating factor) used for? | recovery of bone marrow |
| What is alpha interferon used for? | Hep B and C, Kaposi's sarcoma, leukemia, malignant melanoma |
| What is Beta interferon used for? | multiple sclerosis |
| What is gamm interferon used for? | chronic granulomatous disease |
| What is Oprelvekin (IL-2) used for? | thrombocytopenia |
| What is thrombopoetin used for? | thrombocytopenia |
| What is the target and use of muromonab-CD3 (OKT3)? | target: CD3, use: prevents acute transplant rejection |
| What is the target and use of daclizumab? | target: IL-2 receptor use: prevent acute rejection of renal transplant |
| What is the target and use of digoxin immune Fab? | target: digoxin use: antidote for digoxin intox |
| What is the target and use of infliximab? | target: TNF-alpha use: Crohn's disease, RA, psoriatic arthritis, ankylosing spondylitis |
| What is the target and use of adalimumab? | target: TNF-alpha use: Crohn's, RA, psoriatic artritis |
| What is the target and use of abciximab? | Target: glycoprotein IIb/IIIa use: prevent cardiac ischemia in unstable angina in patients treated with percutaneuous coronary intervention |
| What is the target and use of trastuzumab (Herceptin)? | target: erb-B2 use: HEr-2 overexpressing breast cancers |
| What is the target and use of rituximab? | target: CD20 use: B-cell non-Hodgkin's lymphoma |
| What is the target and use of omalizumab? | target: IgE use: additional line of tx for sever asthma |
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tjs2123
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