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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 does interferon gamma do? What two type of cells does it attack mostly?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
dimer
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
DM type I and RA

2. What are the three immune privileged sites? why are they called that? what happens after infection in these areas?
Activates cytotoxic CD 8 T cells as second signal
Inferior mesenteric
Influenza; antigenic shift; antigenic drift
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

3. The lymphocytes are ________ origin
Antidote for digoxin intoxication
mesenchymal
opsonizes
Influenza; antigenic shift; antigenic drift

4. How is sirolimus different from tacrolimus?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
T cell precursor

5. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
except hyperacute
A chemotactic factor for neutrophils
Liver! (they are proteins circulating in the blood)

6. What are the three types of lymphocytes?
B - T - and NK cells
Barrel hoop basement membrane fenestrations
Steroid responsive nephrotic syndrome
IgM

7. What are the autoantibodies for autoimmune hepatitis?
IgA
Anti smooth muscle
Celiac
Basophils! THey want IG E class switch!

8. What is the main cytokine released by T cells? What does it do
The igA found in breast milk
IL 3; supports growth and differentiation of bone marrow stem cells
Thrombocytopenia
IL 5

9. What is the clinical use of Muromonab?
Thrombocytopenia
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Receiving preformed Antibodies
Immunosuppression after kidney transplantation

10. What is recomb gamma interferon used for?
Chronic granulomatous disease
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Local infection/inflammation; infection of the ln itself; metastasis
Interferon gamma; Th1

11. What does it mean if there are igM in the serum at birth?
Alternative splicing of mRNA
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Celiac
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

12. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
Superior mesenteric
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
IL 4
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

13. Only the _______ contribute to the Fc region
heavy chains
Graves
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages

14. 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
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
IgE
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

15. give an example of how influenza does a major antigenic shift.
C - ANCA (antiproteinase); in neutrophil; c= cytoplasmic
RNA segment reassortment
encapsulated
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

16. Which Thelper cell activated Macrophages? by secreting what? what else does Th1 secrete? For what?
Antihistone
Th1; interferon gamma; IL 2 for cytotoxic T cell activation
Barrel hoop basement membrane fenestrations
Activates Th1 helper cells; Macrophages

17. What are the autoantibodies for primary biliary cirrhosis?
CD56
Anti mitochondrial
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

18. From where do cytokines come from?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Paracortex; viral infection
Lymphocytes
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

19. What is three common causes of severe combined immunodef? What is the result of all three?
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Glycoproteins; HLA
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Anti TSh receptor

20. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
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
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

21. IgG...
By transcytosis
opsonizes
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
T

22. Type Iv hypersensitivity is...
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Stimulate the liver to release acute phase reactants
delayed!
IL 4 - 5 - 10 - 6

23. Leukocyte adhesion defect presents with...
Paracortex; viral infection
neutrophilia!
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Paracortex

24. What is the end result of complement activation? what bugs are this important for? through what pathway and why?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

25. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
NK cells
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
Axillary

26. What is the presentation of scid? treatment?
Alternative splicing of mRNA
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Influenza; antigenic shift; antigenic drift
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

27. What are the autoantibodies for drug induced lupus?
not Ab mediated
Antihistone
Histamine; post capillary venules - vasodilation
MS - hay fever - SLE - goodpastures

28. What type of fenestrations are found in the red pulp of the spleen?
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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
Barrel hoop basement membrane fenestrations

29. What is the main function of interferons?
Aut. Dominant; C1 esterase inhibitor deficiency resulting in continued C1 which results in increased C2 and C4 cleavage products which have anaphyltoxic activity and result in swelling of face and oropharynx
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
CD21 on B cells (although there is T cell lymphocytosis in EBV)

30. How does complement link innate and adaptive?
Cells that stil have weird parts of their membrane that macrophages usually bite off
Anti TSh receptor
TLR ad nuclear receptors
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill

31. What part of the complement system also acts as an opsonin? What is opsonization? can you Name two other opsonins?
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP
Histamine; post capillary venules - vasodilation
Type IV
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

32. What are the autoantibodies for hashimotos?
Antimicrosomal and antithyroglobulin
...
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
Hereditary angioedema; PNH

33. in which immunodef order do you see a lot of pus? no pus?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
IgM and IgA
IL 1 and IL 6
C5a

34. What is the pathogenesis of a candida skin test?
Delayed type hypersensitivity
Its a serine protease that activates apoptosis; NK and CD8
Active; passive - fast but short half life (3 weeks!)
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

35. What are the symptoms of serum sickness?
Its main effect is a defect in Ab opsonization for killing
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Anti glutamate carboxylase and anti insulin
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy

36. Which is the main antibody in the delayed or secondary response to an antigen?
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
carboxy terminal
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
IgG

37. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
IgM and IgD
Anti topoisomerase
Histamine; post capillary venules - vasodilation

38. What are the T cell functions?
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
Antidesmoglein
Antidote for digoxin intoxication
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

39. Which is the most abundant antibody in blood?
IgG
Cross link
Activate macrophages
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction

40. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
IL 3; supports growth and differentiation of bone marrow stem cells
pathogenesis
...

41. What bugs can actually infect the lymph node itself?
Axillary
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
Cross link
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii

42. What is serum sickness? give an example.
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Edema and necrosis in that region
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
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

43. What is the common variable immunodeficiency ? How is it different from Brutons?
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
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 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 :(

44. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
A - B - C; all the D's
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
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L

45. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
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
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
encapsulated
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

46. what happens in order for class switching to occur (after being activated by IL and cd40 L)?
The patient could become cyanotic in the OR!
Alternative splicing of mRNA
TLR ad nuclear receptors
...

47. What lymph node drains the lateral side of the dorsum of the foot?
Popliteal
opsonizes
encapsulated
active complement pathway

48. What is anergy? why does this occur?
Anti IF
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Anti viral and anti tumor

49. which type of immunity is slow but long lasting? as opposed to...
neutrophilia!
Inferior mesenteric
The igA found in breast milk
Active; passive - fast but short half life (3 weeks!)

50. How is the antigen loaded onto a MHC II?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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