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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 are some catalase positive organisms?
S. aureus - E. Coli - aspergillus
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
delayed!

2. What are the two signals to kill for NK cells?
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
heavy chains
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop

3. What is the pathogenesis of chronic granulomatous disease; What is the presentation? What is the labs?
IgG
IL 3; supports growth and differentiation of bone marrow stem cells
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Liver! (they are proteins circulating in the blood)

4. other than C3a - what other complement acts as an anaphyloxin?
C5a
Kill them because they have CD16 on them that recognize the FcG portion
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
No because no peptide fragment!

5. In thymic development - What is the positive selection? negative selections?
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
When you select for which MHC it will have; take out the lymphs that self react
Digeorge syndrome - 22q11 deletion resulting in failure to develop 3rd and 4th pharyngeal pouches; cardiac and great vessel congenital defects - tetany from hypocalcemia - recurrent viral/fungal infections from T cell deficiency; hypoPTH - hypoCa - a
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop

6. 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?
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
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
IL 15; IL 12 - interferon Beta and interferon alpha
Negative nitroblue tetrazolium reduction test

7. What is the clinical use for sirolimus? what should you combine it with?
Activates cytotoxic CD 8 T cells as second signal
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Barrel hoop basement membrane fenestrations

8. How is the antigen loaded onto a MHC II?
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)
Anti Jo -1
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

9. what happens in a deficiency of C1 esterase inhibitor? DAF?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
NK cells
2 heavy chains and two light chains
Hereditary angioedema; PNH

10. What are HEV? Where are they found? Where does the vasculature of the lymph node travel to?
Antihistone
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)
neutrophilia!
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

11. What bugs can actually infect the lymph node itself?
If there is class switching and plasma cell production (that is when memory cells are produced)
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Immunosuppression after kidney transplantation
Fab portion

12. describe the pathogenesis of delayed type IV hypersensitivity
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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
Not thymus - BM
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

13. What is the pathogenesis of HyperIgE syndrome? What are the labs?
encapsulated
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
IgG
Th cells fail to produce interferon gamma; a lot of IgE

14. 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
Inferior mesenteric
CRP - C3b - IgM
IgG

15. Which MHC presents intracellular peptides? how so?
MHC I; from RER with help of the B2 microglobulin
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
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs

16. What is the main cytokine released by T cells? What does it do
IL 3; supports growth and differentiation of bone marrow stem cells
Bind FcG for antibody dependent cellular cytotoxicity
IgM and IgD
Tetanus - Botulinum - HBV - Rabies

17. Which disease is associated with DR3?
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
DM type I
pathogenesis
mesenchymal

18. What is the most common example of passive immunity?
IgAs in mothers breast milk!
Increases expression of MHC I and MHC II and also activates NK cells
Superficial inguinal
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens

19. Which diseases are associated with DR4?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
DM type I and RA
Chronic granulomatous disease
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve

20. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
active complement pathway
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
Antibody mediated cytotoxicity; either complement dependent or complement independent
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

21. How do you test for type III hypersensitivity?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Paracortex; viral infection
Immunoflourescent staining of tissue biopsies
A recomb cytokine of IL 2; RCC and metastatic melanoma

22. How do endotoxin/LPS of gram negative bacteria stimulate the immune system if they do not have a peptide fragment?
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
Th cells fail to produce interferon gamma; a lot of IgE
Previous transfusion; pregnant woman whose fetus had paternal antigens
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

23. What are the PALS?
Lack of NADPH oxidase results in a lack of respiratory burst in neutrophils; susceptibility to catalase positive organisms (S. aureus - E. Coli - Aspergillus)
Influenza; antigenic shift; antigenic drift
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

24. The two heavy chains of an antibody contribute to the...
T cell dysfunction
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
Fab portion
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

25. what else does interferon gamma do other than inducing ribonuclease production - activating NK cells - inducing increased MHC expression?
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
Activate macrophages
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
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!

26. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
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
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
opsonizes

27. What is the marginal zone of the spleen? what happens there?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
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

28. How is the thymus organized? what happens in each section?
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow
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
IgE; by activating eosinophils
Popliteal

29. So antibodies are the effectors for the humoral response. List some of their functions.
Inferior mesenteric
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
Acts as second signal on B cells to induce class switching to IgE and IgG
type four

30. What does IL 5 do?
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Interferon gamma; Th1
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils

31. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
...
Antihistone
If there is class switching and plasma cell production (that is when memory cells are produced)

32. What lymph node drains the testes?
Barrel hoop basement membrane fenestrations
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Cyclosporine - OKT3
Para aortic

33. what cytokine does basophils secrete?
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
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
IgAs in mothers breast milk!
IL 4

34. What are the autoantibodies for type I diabetes mellitus?
Anti glutamate carboxylase and anti insulin
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 :(
MS - hay fever - SLE - goodpastures
heavy chains

35. What is the pathology seen in chronic transplant rejection?
Hereditary angioedema; PNH
Rheumatic arthritis
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening

36. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
Bind FcG for antibody dependent cellular cytotoxicity
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
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

37. In general What are T cells good for?
Anti viral and anti tumor
Cross link
Pernicious Anemia and Hashimotos
Th2; Th1

38. other than eat and bite RBCs what else do Macrophages of spleen do>
Remove encapsulated bacateria
MHC II - B7
T cell precursor
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 :(

39. What lymph node drains the rectum (above the pectinate line)?
The patient could become cyanotic in the OR!
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
Internal iliac
mesenchymal

40. What is colostrum?
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
The igA found in breast milk
Negative selection
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

41. What lymph node drains the duodenum - jejunum?
Superior mesenteric
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Antibody mediated cytotoxicity; either complement dependent or complement independent
Macrophages - Dendritic cells - B cells

42. IgM can fix complement but...
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Superficial inguinal
IgG
cannot cross placenta

43. How is sirolimus different from tacrolimus?
T cell activation; no with CD 4 or CD 8
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
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!

44. The secondary follicles have __________; primary follicles are dense
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
pale central germinal centers

45. what will NK cells do to cells covered in IgG Ab? why?
Axillary
Kill them because they have CD16 on them that recognize the FcG portion
Found in the red pulp; contains the cords of billroth or the splenic parenchyma that have APCs/Macrophages that closely interact with the basement membrane of the vasculature and where RBCs squeeze through into the parenchyma and interact with Macrop
not Ab mediated

46. Which disease is associated with HLA A3?
Hemochromatosis
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
Graves

47. What is MHC I made out of? Where is it found? What does it bind to? What type of antigens does it present?
Previous transfusion; pregnant woman whose fetus had paternal antigens
An alpha chain and a B2 microglobulin; on all nucleated cells; TCR and CD8; intracellular antigens
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Daclizumab; prevent ACUTE rejection of renal transplant

48. in which immunodef order do you see a lot of pus? no pus?
IL 5
Receiving preformed Antibodies
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Delayed type hypersensitivity

49. Which disease is associated with B8?
Basophils! THey want IG E class switch!
Graves
B - T - and NK cells
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles

50. 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?
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
Liver! (they are proteins circulating in the blood)
MS - hay fever - SLE - goodpastures
Activates cytotoxic CD 8 T cells as second signal