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Test your basic knowledge |
USMLE Step 1 Immunology
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Study First
Subjects
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health-sciences
,
usmle-step-1
Instructions:
Answer 50 questions in 15 minutes.
If you are not ready to take this test, you can
study here
.
Match each statement with the correct term.
Don't refresh. All questions and answers are randomly picked and ordered every time you load a test.
This is a study tool. The 3 wrong answers for each question are randomly chosen from answers to other questions. So, you might find at times the answers obvious, but you will see it re-enforces your understanding as you take the test each time.
1. What is a factor that is a predictor for a bad transplantation?
T cell dysfunction
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
delayed!
2. What are the three types of lymphocytes?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
B - T - and NK cells
IL 1 and IL 6
The igA found in breast milk
3. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Type II hypersensitivity - complement dependent resulting in phagocytosis of RBCs coated with C3b by fixed macrophages in the spleen; Group O mother has anti A - B - IgG Abs that cross placenta and attach to fetal blood group A or B RBCs
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
4. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
A B and T cell disorder; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig
Anemias (esp due to renal failure)
Glycoproteins; HLA
5. So antibodies are the effectors for the humoral response. List some of their functions.
No! That is why they are different from T cells - they can recognize antigens in free solution; if a bug has a peptide fragment that a mature naive B cell recognizes it will bind to it and cause activation - it then gets activated into a plasma cell!
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
6. which of the hypersensitivity reactions is not Ab mediated?
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep
Type IV
Interferon gamma; Th1
7. What does IL 2 do?
A B and T cell disorder; X linked recessive; progressive deletion of B and T cells; thrombocytopenic purpura - infections - eczema; high IgE and IgA but low IgM
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Activates cytotoxic CD 8 T cells as second signal
In the germinal center of secondary follicles (In the paler center)
8. What is colostrum?
The igA found in breast milk
IgAs in mothers breast milk!
Capsule of lymph node is made up of type III collagen (made by reticulin fibers!) - extension of this collagen extends into the splenic tissue as trabeculae; nonspecific filtration of lymph by Macrophages - Antibody production (via activation) - stor
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen
9. What is a type I hypersensitivity reaction? What is atopic?
acute phase reactants
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
10. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
IL 4 - 5 - 10 - 6
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep
Paracortex; viral infection
Paracortex
11. Which is the most abundant antibody in blood?
IgG
cannot cross placenta
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Delayed type hypersensitivity
12. What is oprelevkin? and What is it used for?
Sinusitis - otitis media - pneumonia
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Recom IL 11; thrombocytopenia
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
13. Only the _______ contribute to the Fc region
heavy chains
IL 4 - 5 - 10 - 6
Closed circuit where go directly to veins and open where squeeze out of capillary sinusoids and interact with either PALS or with macrophages in the cords of Billroth (for antigen immune function or for blood cleaning or for both) and squeeze back in
For some reason a mature naive B lymphocyte got away from tolerance and the result was a production an Ab on its surface with an Fab region that recognized the alpha 3 collagen subunit on the BM as non self. It then gets activated by a Th2 cell (enti
14. what ensure that a memory response is generated?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Interferon gamma; Th1
If there is class switching and plasma cell production (that is when memory cells are produced)
DM type I and RA
15. What kinds of receptors activate innate immunity?
cannot cross placenta
TLR ad nuclear receptors
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
16. Which disease is associated withB B27?
Pernicious Anemia and Hashimotos
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a
Cross link
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
17. which immunodeficiency presents with delayed separation of the umbilicus? ataxia? telangiectasia?albinism? anaphylaxis on exposure to blood products with IgA? tetany?retained primary teeth? peripheral neuropathy?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Inferior mesenteric
IgE; by activating eosinophils
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
18. What is the defect in hyper IgM syndrome? What are the lab results?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Local infection/inflammation; infection of the ln itself; metastasis
By transcytosis
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
19. What are the autoantibodies for type I diabetes mellitus?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Anti glutamate carboxylase and anti insulin
They directly stimulate Macrophages by binding CD14; also the alternative complement pathway binds to these host surfaces and induces MAC complex; also TLRs exist for endotoxins; also IgM though not an opsonin can act as a pentamer and trap the antig
When you select for which MHC it will have; take out the lymphs that self react
20. other than C3a - what other complement acts as an anaphyloxin?
A chemotactic factor for neutrophils
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
IgG
C5a
21. What are the autoantibodies for autoimmune hepatitis?
Anti smooth muscle
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
T cell activation; no with CD 4 or CD 8
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
22. which antibodies can bind complement?
Antimicrosomal and antithyroglobulin
Superior mesenteric
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs
IgM and IgG
23. What does granzyme do? who secretes it?
Influenza; antigenic shift; antigenic drift
Its a serine protease that activates apoptosis; NK and CD8
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
type four
24. What are the autoantibodies for wegeners granulomatosis?
Hemochromatosis
IgM or IgG antibodies coat the antigen and result in activation of MAC complex via the classical pathway OR fixed macrophages in the spleen phagoctyose the opsonized (C3b or igG) antigens - ex penicillin reaction; IgM AIHA - anti B IgMs in a group A
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
If there is class switching and plasma cell production (that is when memory cells are produced)
25. IgM can fix complement but...
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
cannot cross placenta
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
26. What is the common variable immunodeficiency ? How is it different from Brutons?
Defect in B cell maturation; idiopathic - presents at older age and normal number of B cells and hyperplastic germinal centers because B cells can be activated but can not produce Abs
IgM
Daclizumab; prevent ACUTE rejection of renal transplant
Chronic granulomatous disease
27. What is the clinical use for azathioprine?
Yes
Its main effect is a defect in Ab opsonization for killing
...
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
28. What are superantigens? give two examples.
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen
IgM
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
29. Describe the interstitial tissue of a spleen including the sinuses. What type of cells are found in the four structures (cortex - paracortex - medulla and sinuses)?
The interstitial tissue of a lymph node is structured into the cortex on the outside Which is densely cellular which transitions into the paracortex Which is less dense and then the medulla Which is least dense. The cells that inhabit these tissues a
Its main effect is a defect in Ab opsonization for killing
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
T cell activation; no with CD 4 or CD 8
30. What are the autoantibodies for pemphigus bulgaris?
Antidesmoglein
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
dimer
31. hat is the presentation of Jobs syndrome or Hyper IgE?
delayed!
Activates cytotoxic CD 8 T cells as second signal
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
IL 1 and IL 6
32. What is MHC II made out of? Where is it found? What does it bind to? What type of antigens does it present?
DM type I and RA
IL 15; IL 12 - interferon Beta and interferon alpha
...
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
33. What are the T cell functions?
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Anti IF
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
34. What are the autoantibodies for Mixed connective tissue disease?
When you select for which MHC it will have; take out the lymphs that self react
IgE; by activating eosinophils
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Anti U1 RNP (ribonucleoprotein)
35. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
opsonizes
This means that MHC can not recognize it and thus will not be phagocytosed. The humoral response rescues - IgM is the primary response attack. Since there is no class switching (without MHC activation no CD40 L and interleukins to activate!) then the
IL 4
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
36. What are the autoantibodies for polymyositis and dermatomyositis?
Type IV
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Anti Jo -1
Paracortex
37. what will NK cells do to cells covered in IgG Ab? why?
Kill them because they have CD16 on them that recognize the FcG portion
Cyclosporine - OKT3
Antibody mediated cytotoxicity; either complement dependent or complement independent
Interferon gamma and IL 2
38. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Humoral
heavy chains
Paracortex
39. IgM can exist as a _______ also
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Th2; Th1
pentamer
NK cells
40. which of the transplant rejections is antibody mediated? why does it occur?
B - T - and NK cells
Fc
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
41. From where do cytokines come from?
Lymphocytes
Binds to Mtor which (like tacrolimus and cyclosporine just in a different pathway) inhibits IL 2 production and thus t cell proliferation in response to IL 2 producton
B - T - and NK cells
Rheumatic arthritis
42. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Delayed type hypersensitivity
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Cells that stil have weird parts of their membrane that macrophages usually bite off
Wiskott Aldrich syndrome
43. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
TNF alpha and IL1
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
44. What is the clinical use for sirolimus? what should you combine it with?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Antibody mediated cytotoxicity; either complement dependent or complement independent
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
45. What do mature naive B lymphocytes express?
Antidesmoglein
IgM and IgD
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
False! B cell class switching requires a second signal
46. The two heavy chains of an antibody contribute to the...
Fab portion
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Cells that stil have weird parts of their membrane that macrophages usually bite off
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
47. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Defect in LFA 1 integrin (CD 18) protein on phagocytes (neutrophils!); recurrent bacterial infections - severe gingivitis - poor wound healing - absent pus formation - and delayed separation of the umbilicus; neutrophilia
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
High endothelial venules are post capillary cuboidal endothelial cells that contain specific adhesion molecules for lymphocytes with specific binders that allows for lymphocytes to drain out of the vasculature into the lymph node structure (this is h
In any situation where immunologically competent cells are transplanted into immunologically crippled recipient; graft rejects all the cells due to foreign proteins resulting in severe organ dysfunction
48. What are the autoantibodies for pernicious anemia?
Wiskott Aldrich syndrome
Anti IF
Give a vaccine with a peptide comp from it that the cell mediated immunity otherwise cant get to! like h.influenzae vaccine. then class switching and memory response can occur
...
49. How does igA cross the epithelium?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
By transcytosis
Its a serine protease that activates apoptosis; NK and CD8
50. What are some sinopulmonary infections?
Sinusitis - otitis media - pneumonia
IL 4 - 5 - 10 - 6
Cells that stil have weird parts of their membrane that macrophages usually bite off
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak