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Step 1 11.15.12

Immunology II

QuestionAnswer
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
Created by: tjs2123