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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. describe the classic complement pathway.
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Remove encapsulated bacateria
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

2. What are C1 - C2 - C3 - C4 important for?
Anti Jo -1
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
TLR ad nuclear receptors
Viral neutralization of igM and IgG!

3. What lymph node drains the anal canal (below the pectinate line)?
Severe pyogenic infections early in life
Anti Ach receptor
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

4. The pathogenesis of contact dermatitis is ________ hypersensitivity
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Fab portion
type four
active complement pathway

5. The two heavy chains of an antibody contribute to the...
Fab portion
Yes
B - T - and NK cells
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

6. what happens in a deficiency of C1 esterase inhibitor? DAF?
Hereditary angioedema; PNH
...
Bind FcG for antibody dependent cellular cytotoxicity
isotype

7. What is an example of a parasite showing antigenic variation?
All MHC 1/CD8
Axillary
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

8. What is recomb gamma interferon used for?
When you select for which MHC it will have; take out the lymphs that self react
Steroid responsive nephrotic syndrome
Chronic granulomatous disease
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

9. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
2 heavy chains and two light chains
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
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

10. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Activates Th1 helper cells; Macrophages
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
CRP - C3b - IgM

11. ________ regulate the cell mediated response.
Humoral
Into cortex and medulla; cortex is where immature T lymphocytes enter - at the corticomedullar junction is where positive and negative selection occur; and at the medulla is where the mature T lymphs - reticulin cells and hassalls corpuscles are (dea
Antibody mediated cytotoxicity; either complement dependent or complement independent
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!

12. 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
IgG
IgA
Liver! (they are proteins circulating in the blood)

13. what secretes IL 4?
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
Basophils! THey want IG E class switch!
A recomb cytokine of IL 2; RCC and metastatic melanoma
Receiving preformed Antibodies

14. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
Pernicious Anemia and Hashimotos
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
neutrophilia!
Superficial inguinal

15. which of the transplant rejections is antibody mediated? why does it occur?
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Anti alpha subunit 3 of collagen on type IV bm
Th2; Th1
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

16. What are the three types of lymphocytes?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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!
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
B - T - and NK cells

17. What are MHC's necessary for? By themselves?
Hereditary angioedema; PNH
The red pulp of the spleen its where the vasculature channels go through and interact with the parenchyma of the spleen (has macrophages) which empty in the sinuses; they are both encapsulated (with trabeculae) secondary lymphoid organs that trap ant
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
T cell activation; no with CD 4 or CD 8

18. What cytokines to Th2 secrete?
IL 4 - 5 - 10 - 6
A chemotactic factor for neutrophils
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Humoral

19. What happens in a deficiency of C3?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Paracortex; viral infection
Complement activation (active in both)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

20. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Rheumatic arthritis
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!
A recomb cytokine of IL 2; RCC and metastatic melanoma

21. What are the autoantibodies for pernicious anemia?
Not thymus - BM
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Anti IF
Pernicious Anemia and Hashimotos

22. What is the clinical use for sirolimus? what should you combine it with?
Hours later (instead of minutes); instead of release of preformed mediators - mast cells synthesize PGs and LTs that mediate the late phase reaction (edema - inflammation - decreased airflow)
Para aortic
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
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

23. What is recomb beta interferon used for?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
MS
active complement pathway
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

24. What is the presentation of hyperIgM syndrome?
Anti U1 RNP (ribonucleoprotein)
Severe pyogenic infections early in life
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Axillary

25. what cytokine does basophils secrete?
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
IL 4
pathogenesis
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis

26. Complements are...
acute phase reactants
Superficial inguinal
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Axillary

27. give an example of a virus that uses antigenic variation. What does a major variation result in? minor?
Influenza; antigenic shift; antigenic drift
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
secondary
Anti glutamate carboxylase and anti insulin

28. What is the clinical use for azathioprine?
The patient could become cyanotic in the OR!
Delayed type hypersensitivity
...
MS - hay fever - SLE - goodpastures

29. What are the function of B cells?
CD56
TLR ad nuclear receptors
A j chain
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

30. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
Histamine; post capillary venules - vasodilation
Anti topoisomerase
False! B cell class switching requires a second signal
Steroid responsive nephrotic syndrome

31. How does complement link innate and adaptive?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Lymphocytes
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

32. What does IL 10 do? who is secreted by?
Macrophages - Dendritic cells - B cells
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
heavy chains
Superficial inguinal

33. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
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

34. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
pathogenesis
Steroid responsive nephrotic syndrome
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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

35. What type of fenestrations are found in the red pulp of the spleen?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Barrel hoop basement membrane fenestrations
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
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

36. T/F B cells do not require a second signal
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
False! B cell class switching requires a second signal

37. What does IL 4 do?
Steroid responsive nephrotic syndrome
Acts as second signal on B cells to induce class switching to IgE and IgG
Delayed type hypersensitivity
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

38. What is the presentation of common variable immunodef? and What are the labs?
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
S. aureus - E. Coli - aspergillus
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

39. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Celiac
Anti IF
Cross link
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

40. The idiotype; the Fc portion determines the...
S. aureus - E. Coli - aspergillus
isotype
...
IL 5

41. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Carbohydrate

42. What is epo used for?
Anemias (esp due to renal failure)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
TGF beta and IL 10
T cell precursor

43. Which disease is associated withB B27?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Its main effect is a defect in Ab opsonization for killing
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
IgM

44. What can cause a lymph node enlargement?
Superficial inguinal
Local infection/inflammation; infection of the ln itself; metastasis
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
IgM and IgD

45. Which HLA's are included in MHC I? MHC II?

46. What is the autoantibody for SLE that is nonspecific? Specific?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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
False! B cell class switching requires a second signal
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

47. Give three examples of bacteria that use antigenic variation and how.
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein
Rheumatic arthritis
Hemochromatosis
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

48. How do you test for type III hypersensitivity?
Immunoflourescent staining of tissue biopsies
Active; passive - fast but short half life (3 weeks!)
Paracortex; viral infection
A chemotactic factor for neutrophils

49. The Fc region is found on the...
Internal iliac
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
carboxy terminal
...

50. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
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
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
...