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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 is the mechanism for sirolimus? what else it known as?
IgG
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
T
...

2. What is a type I hypersensitivity reaction? What is atopic?
If there is class switching and plasma cell production (that is when memory cells are produced)
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)

3. The alternative pathway is the only constutively...
Secretory component
Acts as second signal on B cells to induce class switching to IgE and IgG
active complement pathway
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

4. What lymph node drains the rectum (above the pectinate line)?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Type IV
Internal iliac

5. What are some catalase positive organisms?
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
Anti IF
S. aureus - E. Coli - aspergillus
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

6. Which diseases are associated with DR4?
DM type I and RA
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Cross link
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

7. What are the symptoms of serum sickness?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
Internal iliac
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

8. What is the most common example of passive immunity?
IgAs in mothers breast milk!
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
2 heavy chains and two light chains
Th cells fail to produce interferon gamma; a lot of IgE

9. Which is the main antibody that provides passive immunity to infants?
IgM and IgA
IgG
Not thymus - BM
CD56

10. Which diseases are associated with DR2?
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
MS - hay fever - SLE - goodpastures
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

11. What is recomb alpha interferon used for?
Inferior mesenteric
IL 4 - 5 - 10 - 6
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata

12. what secretes IL 4?
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
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Superficial inguinal
Basophils! THey want IG E class switch!

13. What are the two signals required for B cell class switching? Which is the second signal?
Its main effect is a defect in Ab opsonization for killing
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
A chemotactic factor for neutrophils
Anti IF

14. explain the process from beginning (ie phagocytosis of the peptide) to end of how Abs are formed in Goodpasteurs.
C5a
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
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Severe pyogenic infections early in life

15. What are the autoantibodies for primary biliary cirrhosis?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Anti mitochondrial
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
CD56

16. What are the autoantibodies for Mixed connective tissue disease?
Anti U1 RNP (ribonucleoprotein)
Fc
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
Negative!

17. What is the white pulp of the spleen?
Th cells fail to produce interferon gamma; a lot of IgE
Anti glutamate carboxylase and anti insulin
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
SP infections

18. What type of cells do NK cells attack? with What tools? by necrosis or apoptosis?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
IL 15; IL 12 - interferon Beta and interferon alpha
lowest concentration

19. Name two endogenous pyrogens
Cytokine IL 10 secreted by Th2
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
2 heavy chains and two light chains
IL 1 and IL 6

20. What is the most common selective Ig deficiency? What is the presentation?
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IL 4 - 5 - 10 - 6

21. From where do cytokines come from?
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
Lymphocytes
Anti viral and anti tumor
Superficial inguinal

22. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
RNA segment reassortment
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

23. what cell surface marker is used for NK cells as it is unique to them?
CD56
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Humoral
Alternative splicing of mRNA

24. What does IL 5 do?
Superficial inguinal
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
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

25. describe the classic complement pathway.
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
cannot cross placenta
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

26. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
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
If there is class switching and plasma cell production (that is when memory cells are produced)
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy

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

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28. What are the major functions of Antibodies?
Opsonize bacteria (for enhanced phagocytosis) - neutralize viruses (igG) - activate complement (igM and igG) - sensitize mast cells (igE)
Influenza; antigenic shift; antigenic drift
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
Viral neutralization of igM and IgG!

29. What is the clinical use for azathioprine?
...
opsonizes
Its a serine protease that activates apoptosis; NK and CD8
delayed!

30. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
not Ab mediated
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
T cell activation; no with CD 4 or CD 8
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant

31. what results in symptoms of shock in an acute hemolytic transfusion reaction?
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Its a serine protease that activates apoptosis; NK and CD8
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!

32. What does granulysin do?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Negative nitroblue tetrazolium reduction test
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
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

33. What are the cell surface proteins for Macrophages? which two are for opsonins?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Secretory component
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

34. How do we use thymus dependent antigens to prevent infection from organisms that lack a peptide component?
dimer
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
CRP - C3b - IgM
Local infection/inflammation; infection of the ln itself; metastasis

35. What are the autoantibodies for other vasculitides?
IL 4
Anti IF
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
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear

36. What is the pathogenesis of acute transplant rejection? When does it occur?
IgM and IgD
IL 5
Anti U1 RNP (ribonucleoprotein)
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after

37. which antibody is involved in the primary response or immediate response to an antigen?
IgM
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
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
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

38. 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?
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
...
MHC I - CD16 - CD56
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

39. what characterizes an arthus reaction?
IL 5
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
Superficial inguinal
Edema and necrosis in that region

40. What is colostrum?
Complement activation (active in both)
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
The igA found in breast milk
S. aureus - E. Coli - aspergillus

41. The ______ in the BM are DN - the DP are in the cortex of thymus
T cell precursor
In the germinal center of secondary follicles (In the paler center)
S. aureus - E. Coli - aspergillus
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

42. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
secondary
Cross link
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

43. What is digoxin immune Fab used for?
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Antidote for digoxin intoxication
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
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

44. What is three common causes of severe combined immunodef? What is the result of all three?
When you select for which MHC it will have; take out the lymphs that self react
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)

45. can igG cross the placenta?
Yes
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
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
pathogenesis

46. 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!)
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Histamine; post capillary venules - vasodilation

47. What is muromonab - CD3 (OKT3)
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells
IgG
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
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

48. other than C3a - what other complement acts as an anaphyloxin?
C5a
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)
Salmonella - 2 flagellar variants; Borrelia (relapsing fever); and Neisseria gonorrhoaea - pilus protein

49. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
pale central germinal centers
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
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
TNF alpha and IL1

50. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Sinusitis - otitis media - pneumonia
Anti glutamate carboxylase and anti insulin
carboxy terminal
Rheumatic arthritis