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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 lymph node drains the anal canal (below the pectinate line)?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Alternative splicing of mRNA
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Superficial inguinal

2. What type of side chains are found on Fc region of an antibody?
secondary
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Carbohydrate
Type IV

3. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Antimicrosomal and antithyroglobulin
Chronic granulomatous disease
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
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

4. From where do cytokines come from?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Lymphocytes
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

5. in which immunodef order do you see a lot of pus? no pus?
...
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
If there is class switching and plasma cell production (that is when memory cells are produced)
Barrel hoop basement membrane fenestrations

6. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
IL 1 and IL 6
IL 5
Kill them because they have CD16 on them that recognize the FcG portion
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

7. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
lowest concentration
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

8. Only the _______ contribute to the Fc region
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
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 :(
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
heavy chains

9. describe the classic complement pathway.
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
IgM and IgD
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)

10. 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
IgM and IgG
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
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

11. What are the two signals required for Th1 cells? what happens after then activated?
Barrel hoop basement membrane fenestrations
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Fab portion
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

12. What is passive immunity?
Antidote for digoxin intoxication
By transcytosis
C5a
Receiving preformed Antibodies

13. which cells have more complete tolerance - B or T cells?
IgM and IgA
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Immunoflourescent staining of tissue biopsies
T

14. What are the autoantibodies for graves?
Anti TSh receptor
Increases expression of MHC I and MHC II and also activates NK cells
IgM and IgG
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

15. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
A chemotactic factor for neutrophils
SP infections
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)

16. What are the labs in brutons agammaglobulinemia?
IgE; by activating eosinophils
IL 4 - 5 - 10 - 6
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

17. How fast does it occur?
In IgE AIHA- it results in MAC attack (remember IgE is not an opsonin!) - in IgG AIHA C3b (and IgG) opsonization results in phagocytosis by fixed macrophages in the spleen
IgG
The patient could become cyanotic in the OR!
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp

18. Which type of selection of thymic development provides central tolerance?
Negative selection
DM type I
Glycoproteins; HLA
IgM

19. Which are the only two antiinflammatory cytokines?
carboxy terminal
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
In the germinal center of secondary follicles (In the paler center)
TGF beta and IL 10

20. What bugs can actually infect the lymph node itself?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Basophils! THey want IG E class switch!
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

21. What is the autoantibody for SLE that is nonspecific? Specific?
Anti glutamate carboxylase and anti insulin
C5a
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Negative nitroblue tetrazolium reduction test

22. How is the thymus organized? what happens in each section?
Fab portion
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
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
Alternative splicing of mRNA

23. What happens in a deficiency of C3?
Axillary
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

24. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Fab portion
Anemias (esp due to renal failure)
Viral neutralization of igM and IgG!

25. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
DM type I

26. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Hemochromatosis
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
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 :(
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

27. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
MS
Chronic granulomatous disease
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
Anti TSh receptor

28. What is the general structure of an Ab?
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
Superficial inguinal
2 heavy chains and two light chains
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)

29. What are the function of B cells?
Wiskott Aldrich syndrome
B - T - and NK cells
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

30. which cytokine inhibits TH2 cells? secreted by who?
Immunosuppression after kidney transplantation
Interferon gamma; Th1
Wiskott Aldrich syndrome
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

31. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Fc
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
IL 3; supports growth and differentiation of bone marrow stem cells
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 :(

32. __________ are a part of the innate system.
Pernicious Anemia and Hashimotos
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
Graves
NK cells

33. What does IgA pick up from epithelial cells before being secreted?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Alternative splicing of mRNA
Secretory component
Anti alpha subunit 3 of collagen on type IV bm

34. Which is the main antibody in the delayed or secondary response to an antigen?
type four
Receiving preformed Antibodies
IgG
Liver! (they are proteins circulating in the blood)

35. What are the autoantibodies for myasthenia gravis?
MS - hay fever - SLE - goodpastures
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
encapsulated
Anti Ach receptor

36. other than C3a - what other complement acts as an anaphyloxin?
Increases expression of MHC I and MHC II and also activates NK cells
C5a
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
Immunosuppression after kidney transplantation

37. What are the main cell surface proteins on B cells?
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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
Anti TSh receptor

38. What is Aldesleukin? What is it used for
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
A recomb cytokine of IL 2; RCC and metastatic melanoma
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Bind FcG for antibody dependent cellular cytotoxicity

39. what characterizes an arthus reaction?
Antimicrosomal and antithyroglobulin
Edema and necrosis in that region
Superficial inguinal
MS - hay fever - SLE - goodpastures

40. What are the autoantibodies for systemic sclerosis?
Anti topoisomerase
T
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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

41. can igG cross the placenta?
Yes
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Increases expression of MHC I and MHC II and also activates NK cells
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

42. What are complements in the complement system? What activates them? there seems to be different ones - What are these pathways called?
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
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

43. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Activates Th1 helper cells; Macrophages
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
MHC I; from RER with help of the B2 microglobulin
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

44. Describe the complement independent Type II hypersenstivity reaction. Give an example.
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Increases expression of MHC I and MHC II and also activates NK cells
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)

45. What is the presentation of common variable immunodef? and What are the labs?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
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
Anti IF
Axillary

46. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
type four
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Anti alpha subunit 3 of collagen on type IV bm

47. What does granulysin do?
S. aureus - E. Coli - aspergillus
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
IL 15; IL 12 - interferon Beta and interferon alpha

48. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
Cross link
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
Kill them because they have CD16 on them that recognize the FcG portion

49. What can cause a lymph node enlargement?
Anti TSh receptor
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Local infection/inflammation; infection of the ln itself; metastasis
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

50. Which is the main antibody that provides passive immunity to infants?
pentamer
IgG
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE