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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. The lymphocytes are ________ origin
mesenchymal
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Fab portion
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

2. What are the two signals required for B cell class switching? Which is the second signal?
heavy chains
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
pathogenesis
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2

3. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
IL 3; supports growth and differentiation of bone marrow stem cells
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
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

4. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Kill them because they have CD16 on them that recognize the FcG portion
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Immunoflourescent staining of tissue biopsies

5. What is passive immunity?
Receiving preformed Antibodies
Superficial inguinal
MS
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

6. What are the autoantibodies for polymyositis and dermatomyositis?
cannot cross placenta
Anti Jo -1
Wiskott Aldrich syndrome
Type IV

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

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8. How is i Th1 helper cell inhibited?
MHC class molecules bind to KIRS or CD94 to prevent killing
Cytokine IL 10 secreted by Th2
...
encapsulated

9. The secondary follicles have __________; primary follicles are dense
IgAs in mothers 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
pale central germinal centers
A chemotactic factor for neutrophils

10. What is an example of a parasite showing antigenic variation?
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
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)
Macrophages - Dendritic cells - B cells
False! B cell class switching requires a second signal

11. What does Interferon alpha and beta do? how?
Th2; Th1
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Carbohydrate

12. What is the white pulp of the spleen?
Humoral
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
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

13. What is the main function of IL 12? other than macrophages who else can release IL 12?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
2 heavy chains and two light chains
A j chain
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells

14. What happens when a T helper cell in the paracortical section encounters an antigen? a cytotoxic t cell? a B cell in the cortical section?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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
MHC class molecules bind to KIRS or CD94 to prevent killing
B - T - and NK cells

15. what mediates the type II hypersensitivity? What are the two different methods?
Negative selection
Antibody mediated cytotoxicity; either complement dependent or complement independent
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
carboxy terminal

16. what characterizes an arthus reaction?
Edema and necrosis in that region
NK cells
A j chain
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)

17. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
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 :(
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
Anti U1 RNP (ribonucleoprotein)

18. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
Anti Ach receptor
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
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!
Immunosuppression after kidney transplantation

19. __________ are a part of the innate system.
NK cells
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions

20. What does granzyme do? who secretes it?
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
B - T - and NK cells
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Its a serine protease that activates apoptosis; NK and CD8

21. What are the autoantibodies for pernicious anemia?
...
T cell dysfunction
Its a serine protease that activates apoptosis; NK and CD8
Anti IF

22. Which TCR MHC system is important for viral immunity? neoplastic? donor graft cells?
Carbohydrate
All MHC 1/CD8
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
C5a

23. What does IL 10 do? who is secreted by?
delayed!
When you select for which MHC it will have; take out the lymphs that self react
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class

24. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
IgA
False! B cell class switching requires a second signal

25. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
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
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
...

26. In general What are T cells good for?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti viral and anti tumor
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!

27. So antibodies are the effectors for the humoral response. List some of their functions.
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
IgE; by activating eosinophils
mesenchymal

28. 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!)
Para aortic
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
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

29. What is the clinical use for sirolimus? what should you combine it with?
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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
IgG

30. 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)?
Th cells fail to produce interferon gamma; a lot of IgE
Internal iliac
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
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

31. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
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
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
IgM and IgD

32. What happens in a secondary follicle?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Popliteal
TNF alpha and IL1
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

33. what bacteria are a splenectomy patient most susceptible to? why?
Thrombocytopenia
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
Fc
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

34. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
pathogenesis
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
IgG
By transcytosis

35. What are the autoantibodies for other vasculitides?
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
encapsulated
Anti alpha subunit 3 of collagen on type IV bm

36. 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)
IL 15; IL 12 - interferon Beta and interferon alpha
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
except hyperacute

37. What are the autoantibodies for autoimmune hepatitis?
Anti smooth muscle
MS
IgM and IgA
Daclizumab; prevent ACUTE rejection of renal transplant

38. What do mature naive B lymphocytes express?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Cross link
Sinusitis - otitis media - pneumonia
IgM and IgD

39. 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
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
IL 4 - 5 - 10 - 6
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

40. Describe the Mannose Lectin pathway
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
Th cells fail to produce interferon gamma; a lot of IgE
Axillary
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

41. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Anti topoisomerase
Anti TSh receptor

42. which of the hypersensitivity reactions is not Ab mediated?
Barrel hoop basement membrane fenestrations
acute phase reactants
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Type IV

43. What does it mean if there are igM in the serum at birth?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
In the germinal center of secondary follicles (In the paler center)
Type IV
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

44. What is chronic mucocutaneous candidiasis d/t?
T cell dysfunction
IL 4
By transcytosis
IL 3; supports growth and differentiation of bone marrow stem cells

45. What is the presentation of scid? treatment?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
secondary
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

46. which of the transplant rejections is antibody mediated? why does it occur?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Increases expression of MHC I and MHC II and also activates NK cells
IgG

47. give an example of how influenza does a major antigenic shift.
Antidote for digoxin intoxication
Stimulate the liver to release acute phase reactants
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
RNA segment reassortment

48. What is the common variable immunodeficiency ? How is it different from Brutons?
CD56
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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

49. Which disease is associated with HLA A3?
Immunosuppression after kidney transplantation
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
Hemochromatosis
IgM and IgD

50. What are the autoantibodies for sjorgens syndrome?
A j chain
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
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
Anti SS- A (anti RO) and Anti SS- B