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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 immune complex disease? give an example.
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
A chemotactic factor for neutrophils
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
Inferior mesenteric
2. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Recom IL 11; thrombocytopenia
3. What is filgrastim and sargramostim? and What is it used for?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Sinusitis - otitis media - pneumonia
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Chronic granulomatous disease
4. which antibodies can bind complement?
IL 5
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
Superficial inguinal
IgM and IgG
5. What bugs can actually infect the lymph node itself?
Steroid responsive nephrotic syndrome
lowest concentration
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
6. What are the autoantibodies for systemic sclerosis?
Celiac
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Anti topoisomerase
pale central germinal centers
7. For which toxins are preformed antibodies (passive) given?
Interferon gamma and IL 2
Tetanus - Botulinum - HBV - Rabies
pathogenesis
Anti topoisomerase
8. Which antibody mediates immunity to worms? how?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
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
IgE; by activating eosinophils
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
9. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
By transcytosis
10. which antibody is involved in the primary response or immediate response to an antigen?
except hyperacute
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
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi
IgM
11. What lymph node drains the testes?
Anti mitochondrial
Para aortic
B - T - and NK cells
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
12. Complements are...
Liver! (they are proteins circulating in the blood)
acute phase reactants
RNA segment reassortment
Kill them because they have CD16 on them that recognize the FcG portion
13. What are the autoantibodies for type I diabetes mellitus?
If there is class switching and plasma cell production (that is when memory cells are produced)
Anti glutamate carboxylase and anti insulin
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Basophils! THey want IG E class switch!
14. What does interferon gamma do to be antiviral?
IgE; by activating eosinophils
Immunoflourescent staining of tissue biopsies
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Increases expression of MHC I and MHC II and also activates NK cells
15. What cytokines to Th2 secrete?
Not thymus - BM
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
IL 4 - 5 - 10 - 6
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
16. Which HLA's are included in MHC I? MHC II?
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17. where do somatic hypermutation and class switching occur?
In the germinal center of secondary follicles (In the paler center)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
18. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
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
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
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
19. What is three common causes of severe combined immunodef? What is the result of all three?
...
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
20. What is the monoclonal antibody to IL2 on activated T cells? What is it used for?
RNA segment reassortment
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
not Ab mediated
Daclizumab; prevent ACUTE rejection of renal transplant
21. what cell surface marker is used for NK cells as it is unique to them?
CD56
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Macrophages - Dendritic cells - B cells
not Ab mediated
22. The lymphocytes are ________ origin
mesenchymal
Yes
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Complement activation (active in both)
23. What do mature naive B lymphocytes express?
Previous transfusion; pregnant woman whose fetus had paternal antigens
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
The patient could become cyanotic in the OR!
IgM and IgD
24. What is colostrum?
The igA found in breast milk
An antigen encounter (presented by APC for Th2) with Th2 will result in it to go to the cortical section and help with B cell activation; Cytotoxic T cell will enter vasculature/efferent lymph to go kill; B cell will wait for Th2 for activation and t
Delayed type hypersensitivity
CD56
25. What is the pathogenesis of a hypersensitivity reaction?
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
T cell precursor
MS - hay fever - SLE - goodpastures
First a B cell gets sensitized to an allergen - after sensitization - it gets induce by Th2 secreting IL4 to class switch from IgM to IgE - next time blood stream is exposed to allergen these antigens cross like IgEs on mast cells and result in chemi
26. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
IL 4 - 5 - 10 - 6
Cross link
27. 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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
mesenchymal
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
28. What type of side chains are found on Fc region of an antibody?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Acts as second signal on B cells to induce class switching to IgE and IgG
Carbohydrate
Anti Jo -1
29. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Anti smooth muscle
Type IV
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
30. What are the autoantibodies for Celiac disease?
Maculopapular rash (palm - soles - back - neck) - jaundice with bile duct necrosis - hepatosplenomegaly - diarrhea; bone marrow and liver transplants (rich with lymphocytes); SCID patient receiving whole blood transfusion
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
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
31. What is the presentation of common variable immunodef? and What are the labs?
Superficial inguinal
Can be acquired in 20s -30s; increased risk of autoimmune disease - lymphoma - Sp infections; normal number of B cells and no plasma cells and immunoglobulin
Its a serine protease that activates apoptosis; NK and CD8
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
32. Which disease is associated with HLA A3?
Hemochromatosis
Interferon gamma; Th1
...
It is a localized type III hypersensitivity reaction to an external antigen; localized instead of systemic; ?; intradermal injection of the antigen results in antibody production and antigen antibody complexes deposit in the skin
33. What is the most common selective Ig deficiency? What is the presentation?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Its main effect is a defect in Ab opsonization for killing
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
34. What is the general structure of an Ab?
Negative nitroblue tetrazolium reduction test
C5a
T cell and antibody mediated vascular damage due to MHC non self being recognized as self by self lymphocytes and resulting in attack of the foreign antigens it presents (all of them); months to years after; no :(
2 heavy chains and two light chains
35. What is chronic mucocutaneous candidiasis d/t?
Acts as second signal on B cells to induce class switching to IgE and IgG
Paracortex
Previous transfusion; pregnant woman whose fetus had paternal antigens
T cell dysfunction
36. What are the PALS?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Increases expression of MHC I and MHC II and also activates NK cells
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
37. What is the most common example of passive immunity?
IgAs in mothers breast milk!
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
opsonizes
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
38. What are the autoantibodies for hashimotos?
Influenza; antigenic shift; antigenic drift
Antimicrosomal and antithyroglobulin
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
39. What are the autoantibodies for drug induced lupus?
Celiac
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Anti IF
Antihistone
40. What is the presentation of hyperIgM syndrome?
Immunoflourescent staining of tissue biopsies
...
Daclizumab; prevent ACUTE rejection of renal transplant
Severe pyogenic infections early in life
41. In general What are T cells good for?
Anti viral and anti tumor
S. aureus - E. Coli - aspergillus
Some microbial surfaces (only) have mannan binding lectin which activates a protease that cleaves C2 and C4 which combine to make C3. the rest follows the alternative pathway
IL 3; supports growth and differentiation of bone marrow stem cells
42. what ensure that a memory response is generated?
False! B cell class switching requires a second signal
Activate macrophages
If there is class switching and plasma cell production (that is when memory cells are produced)
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
43. What is epo used for?
Anemias (esp due to renal failure)
No because no peptide fragment!
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
dimer
44. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
All MHC 1/CD8
Inferior mesenteric
45. What is the pathogenesis of acute transplant rejection? When does it occur?
MHC I; from RER with help of the B2 microglobulin
An acidified endosome with the antigen fuses with the MHC which causes the release of the invariant chain Which is sitting in spot of antigen and stabilizing the MHC II
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Hemochromatosis
46. What is the defect in Leukocyte adhesion defect? What is the presentation? What are the labs?
isotype
Anti mitochondrial
delayed!
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
47. How fast does it occur?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Th cells fail to produce interferon gamma; a lot of IgE
The patient could become cyanotic in the OR!
Negative selection
48. What is serum sickness? give an example.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Type III hypersensitivity where an exogenous antigen results in a systemic antigen antibody complex disease (takes around 5 days after exposure for the Abs to develop); immune complexes then fix in tissue and activate complement resulting in tissue d
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
DM type I
49. What are MHC Class molecules (ie what macromolecule are they made out of)? what gene are responsible for MHC?
Rheumatic arthritis
IgA
Increases expression of MHC I and MHC II and also activates NK cells
Glycoproteins; HLA
50. hat is the presentation of Jobs syndrome or Hyper IgE?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Anemias (esp due to renal failure)
1) VJ light chain random creation 2) VDJ (heavy chain) random creation 3) random combination of light with heavy 4) somatic hypermutation (high frequency mutating that occurs on activation) 5) terminal deoxynucleotidyl transferase (TDT) random additi
except hyperacute