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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 happens in order for class switching to occur (after being activated by IL and cd40 L)?
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
Pernicious Anemia and Hashimotos
Anti IF
Alternative splicing of mRNA

2. What does interferon gamma do to be antiviral?
Liver! (they are proteins circulating in the blood)
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
Increases expression of MHC I and MHC II and also activates NK cells
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

3. when can graft versus host disease? What is the result?
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
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
TLR ad nuclear receptors
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

4. What is the general structure of an Ab?
2 heavy chains and two light chains
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
isotype

5. The secondary follicles have __________; primary follicles are dense
except hyperacute
B - T - and NK cells
pale central germinal centers
Intracellular pathogens (acute and chronic viruses and virally induced cancers)

6. What is anergy? why does this occur?
heavy chains
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Influenza; antigenic shift; antigenic drift
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance

7. What are MHC's necessary for? By themselves?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Anti mitochondrial
T cell activation; no with CD 4 or CD 8
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation

8. What is recomb alpha interferon used for?
A - B - C; all the D's
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
opsonizes
MHC I - CD16 - CD56

9. What is the difference of IgE AIHA and IgG AIHA if they are both complement dependent type II hypersensitivities?
Anti alpha subunit 3 of collagen on type IV bm
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
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
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock

10. What are the autoantibodies for drug induced lupus?
The igA found in breast milk
Fab portion
Steroid responsive nephrotic syndrome
Antihistone

11. What is epo used for?
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Anemias (esp due to renal failure)
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
CD56

12. What are the mediators that mast cells release?
Not thymus - BM
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

13. The MALT/GALT are not...
Influenza; antigenic shift; antigenic drift
IgG
Its a serine protease that activates apoptosis; NK and CD8
encapsulated

14. What is the late phase reaction of anaphylaxis allergy? what mediates it?
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)
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
Anti alpha subunit 3 of collagen on type IV bm

15. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
IgM
Not thymus - BM
Delayed type hypersensitivity
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

16. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
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)
Complement activation (active in both)
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 CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

17. Which cytokines do Th2 release and For what?
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
IgE; by activating eosinophils
Cells that stil have weird parts of their membrane that macrophages usually bite off

18. What amine is the main chemical mediator released by mast cells? Where does it act What does it result in?
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
Histamine; post capillary venules - vasodilation
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Superior mesenteric

19. 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
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
Lymphocytes
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

20. What is the white pulp of the spleen?
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
Histamine; post capillary venules - vasodilation
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!
Para aortic

21. What are the autoantibodies for graves?
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
Superior mesenteric
Anti TSh receptor
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

22. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
2 heavy chains and two light chains
Its main effect is a defect in Ab opsonization for killing
Activate macrophages
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

23. What is the toxicity of azathioprine?
Hemochromatosis
...
IgG
encapsulated

24. What is the defect in hyper IgM syndrome? What are the lab results?
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

25. What is muromonab - CD3 (OKT3)
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Activate macrophages
Previous transfusion; pregnant woman whose fetus had paternal antigens
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

26. What two ways do you test for a type 1 hypersensitivity reaction? what will you see?
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
If there is class switching and plasma cell production (that is when memory cells are produced)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

27. What lymph node drains the testes?
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Para aortic
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

28. What is the clinical use for azathioprine?
Recom IL 11; thrombocytopenia
MHC class molecules bind to KIRS or CD94 to prevent killing
isotype
...

29. which cytokine inhibits TH2 cells? secreted by who?
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
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
CD56
Interferon gamma; Th1

30. What are the three types of Type III hypersensitivity ? What is the common mechanism between them?
Anti smooth muscle
...
active complement pathway
Immune complex - Arthus reaction and Serum sickness; they are all a result of antibody- antigen complex deposition resulting in complement activation

31. what bacteria are a splenectomy patient most susceptible to? why?
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
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
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
MHC class molecules bind to KIRS or CD94 to prevent killing

32. What is the antimetabolite precursor of 6 mercaptopurine? What is the result?
Type IV
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
...
IgE; by activating eosinophils

33. DTH (delayed type hypersensitivity) is the ________ of a PPD reaction
Remove encapsulated bacateria
type four
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
pathogenesis

34. Which is the most abundant antibody in blood?
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
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
IgG
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

35. What is Aldesleukin? What is it used for
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Th cells fail to produce interferon gamma; a lot of IgE
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
A recomb cytokine of IL 2; RCC and metastatic melanoma

36. What are the autoantibodies for hashimotos?
Antimicrosomal and antithyroglobulin
The igA found in breast milk
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Steroid responsive nephrotic syndrome

37. What is an autograft? syngeneic graft? allograft? xenograft? What is an ex of an allograft? xenograft?
Anti alpha subunit 3 of collagen on type IV bm
Humoral
From self; from identical twin or clone; from nonidentical individual of same species; from different species; fetus; pig valve
A - B - C; all the D's

38. Which helper T cells' development is induced by IL 4? IL 12?
Pernicious Anemia and Hashimotos
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi
Th2; Th1
TNF alpha and IL1

39. What portion of the lymph node is not well developed in DiGeorge Syndrome?
Internal iliac
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
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
Paracortex

40. describe the pathogenesis of delayed type IV hypersensitivity
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
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
Hemochromatosis
Monoclonal Ab to CD3- blocks cellular transduction and signaling of T cells

41. What is thrombopoietin used for?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Type IV
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
Thrombocytopenia

42. What is the clinical use of Muromonab?
IL 4 - 5 - 10 - 6
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Immunosuppression after kidney transplantation
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

43. How do you test for chronic granulomatous disease?
Negative nitroblue tetrazolium reduction test
Interferon gamma and IL 2
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Axillary

44. What is digoxin immune Fab used for?
Antidote for digoxin intoxication
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
IgG
Hemochromatosis

45. In general What are T cells good for?
Anti viral and anti tumor
secondary
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Cyclosporine - OKT3

46. What is the presentation of scid? treatment?
Previous transfusion; pregnant woman whose fetus had paternal antigens
T cell dysfunction
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
Para aortic

47. How does igA cross the epithelium?
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
By transcytosis
T cell activation; no with CD 4 or CD 8
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

48. What is ataxia telangectasia? What is it caused by? What is the triad of presentation? and its labs?
...
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
Anti viral and anti tumor
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP

49. What is chronic mucocutaneous candidiasis d/t?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
T cell dysfunction
...
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE

50. What do mature naive B lymphocytes express?
IgM and IgD
Active; passive - fast but short half life (3 weeks!)
IL 1 - IL 6 - IL 12 - TNF alpha; IL 6- Th2 cells; IL 12- B cells
Hemochromatosis