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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

Instructions:

Answer 50 questions in 15 minutes.
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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 are the mediators that mast cells release?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
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
pathogenesis
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

2. What are the function of B cells?
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
type four
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

3. What is the main function of TNF alpha? How does it do this?
...
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Increases expression of MHC I and MHC II and also activates NK cells
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)

4. give an example of how influenza does a major antigenic shift.
RNA segment reassortment
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

5. Which is the main antibody in the delayed or secondary response to an antigen?
IgG
Lymphocytes
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

6. 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?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
IgM
CRP - C3b - IgM

7. A lymph node is a ________ lymphoid organ.
Superficial inguinal
secondary
type four
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

8. describe the classic complement pathway.
TGF beta and IL 10
TNF alpha and IL1
Hereditary angioedema; PNH
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

9. Which disease is associated with DR7?
Inferior mesenteric
Chronic granulomatous disease
Steroid responsive nephrotic syndrome
heavy chains

10. If an antigen lacks a peptide component How does the adaptive immunity attack it? What type of response is this called. give an example of bugs that do this. what implications does this have on splenectomy?
IL 4
IgM and IgD
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
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

11. Which disease is associated with HLA A3?
T cell activation; no with CD 4 or CD 8
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
Hemochromatosis
If there is class switching and plasma cell production (that is when memory cells are produced)

12. What do macrophages secrete that activate Th1 cells to secrete interferon gamma?
IgM and IgD
TNF alpha and IL1
Humoral
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

13. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
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
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
MS
If there is class switching and plasma cell production (that is when memory cells are produced)

14. what cell surface marker is used for NK cells as it is unique to them?
IgE
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
CD56
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

15. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

16. What is filgrastim and sargramostim? and What is it used for?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
Popliteal

17. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
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
Rheumatic arthritis
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Cross link

18. The ______ in the BM are DN - the DP are in the cortex of thymus
T cell precursor
Interferon gamma; Th1
Recom IL 11; thrombocytopenia
IL 15; IL 12 - interferon Beta and interferon alpha

19. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Anti alpha subunit 3 of collagen on type IV bm
pentamer
IgM and IgG
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

20. What is the autoantibody for SLE that is nonspecific? Specific?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Yes
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

21. What are some catalase positive organisms?
S. aureus - E. Coli - aspergillus
Macrophages - Dendritic cells - B cells
Axillary
IgM and IgD

22. What is an example of a parasite showing antigenic variation?
Increases expression of MHC I and MHC II and also activates NK cells
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
MHC II - B7

23. Describe the capsular structure of a lymph node; What are the functions of the LN?
neutrophilia!
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
Remove encapsulated bacateria
Cyclosporine - OKT3

24. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Its a serine protease that activates apoptosis; NK and CD8
except hyperacute
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

25. What kinds of receptors activate innate immunity?
Bind FcG for antibody dependent cellular cytotoxicity
TLR ad nuclear receptors
pentamer
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

26. The idiotype; the Fc portion determines the...
isotype
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 cells react to the angtigen and activate leukocyted (macrophage acitivation)
IgAs in mothers breast milk!

27. which of the hypersensitivity reactions is not Ab mediated?
MHC I; from RER with help of the B2 microglobulin
Brain - eyes - placenta/fetus - testicles; because they can have an antigen in there and not get attacked by immune system because dont have contact with immune system via blood and lymph; if an infection occurs such that trauma results in exposure t
Type IV
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

28. What lymph node drains the thigh?
Antimicrosomal and antithyroglobulin
Axillary
The igA found in breast milk
Superficial inguinal

29. Which diseases are associated with DR4?
DM type I and RA
pathogenesis
carboxy terminal
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

30. What is digoxin immune Fab used for?
Soluble C3 spontaneously hydrolyzes spontaneously to C3b and opsonizes microbial and host cell surfaces and accumulates on surfaces; C3b activates C5 convertase which leads to MAC activation
Antidote for digoxin intoxication
False! B cell class switching requires a second signal
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

31. Which type of selection of thymic development provides central tolerance?
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
except hyperacute
Negative selection
2 heavy chains and two light chains

32. How is the antigen loaded onto a MHC II?
MS
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
IgA
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

33. What are the symptoms of serum sickness?
IL 5
Paracortex; viral infection
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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

34. what ensure that a memory response is generated?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Sinusitis - otitis media - pneumonia
neutrophilia!
If there is class switching and plasma cell production (that is when memory cells are produced)

35. What are the two signals to kill for NK cells?
Celiac
Local infection/inflammation; infection of the ln itself; metastasis
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells

36. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
Secretory component
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
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

37. What happens in a deficiency of C3?
acute phase reactants
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
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
mesenchymal

38. How does igA cross the epithelium?
By transcytosis
CRP - C3b - IgM
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
lowest concentration

39. Name 5 ways Antibody diversity is generated?
Alternative splicing of mRNA
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
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
All MHC 1/CD8

40. What are the autoantibodies for wegeners granulomatosis?
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
Fc
Receiving preformed Antibodies
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

41. What is the common variable immunodeficiency ? How is it different from Brutons?
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
neutrophilia!
The igA found in breast milk
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

42. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
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
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Antimicrosomal and antithyroglobulin

43. What are the autoantibodies for drug induced lupus?
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
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Antihistone

44. In general What are T cells good for?
pathogenesis
RNA segment reassortment
Anti viral and anti tumor
T

45. what cell surface proteins are on all APCs?
All MHC 1/CD8
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
MHC II - B7
TGF beta and IL 10

46. What is the pathology of acute transplant rejection? is it reversible?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

47. What is anergy? why does this occur?
IgM
cannot cross placenta
except hyperacute
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

48. What is the pathogenesis of a candida skin test?
When you select for which MHC it will have; take out the lymphs that self react
Delayed type hypersensitivity
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
encapsulated

49. IgE has the ___________ in the serum
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
lowest concentration
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
N. meningitidis - H. influenzae - S. pneumonia - Salmonella d/t lack of C3b opsonization for MAC d/t lack of complement activation d/t lack of IgM; MAC is needed by encapsulated avoid by humoral and cell mediated through their capsule

50. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
Recom IL 11; thrombocytopenia
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
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma