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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 main function of TNF alpha? How does it do this?
IL 4 - 5 - 10 - 6
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
IgG
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

2. What are the autoantibodies for drug induced lupus?
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
Kill them because they have CD16 on them that recognize the FcG portion
Interferon gamma; Th1
Antihistone

3. __________ are a part of the innate system.
Anti alpha subunit 3 of collagen on type IV bm
NK cells
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)
cannot cross placenta

4. Give an example of someone who could get hyperacute transplant rejection.
encapsulated
Previous transfusion; pregnant woman whose fetus had paternal antigens
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
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants

5. What is Aldesleukin? What is it used for
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
A recomb cytokine of IL 2; RCC and metastatic melanoma

6. in which immunodef order do you see a lot of pus? no pus?
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated

7. what cytokine does basophils secrete?
Hemochromatosis
IL 4
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1
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

8. What is the presentation of hyperIgM syndrome?
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
B - T - and NK cells
Severe pyogenic infections early in life
Steroid responsive nephrotic syndrome

9. What is wiskott aldrich syndrome? What is its mode of inheritance? What is the pathogenesis of disease? What is its triad of presentation? what labs does it present with?
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
Paracortex
A B and T cell disorder; defect in DNA repair enzymes; ataxia - telangactasia and IgA def; igA def. and increased AFP
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

10. What are MHC's necessary for? By themselves?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
...
carboxy terminal
T cell activation; no with CD 4 or CD 8

11. From where do cytokines come from?
No because no peptide fragment!
T cell precursor
Anti SS- A (anti RO) and Anti SS- B
Lymphocytes

12. IgG...
opsonizes
Complement activation (active in both)
MHC I; from RER with help of the B2 microglobulin
Its a serine protease that activates apoptosis; NK and CD8

13. What is the symptoms involved in graft versus host disease? it What transplant cases does it usually occur? give an example
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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 patient could become cyanotic in the OR!
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

14. How do you test for type III hypersensitivity?
2 heavy chains and two light chains
B - T - and NK cells
Immunoflourescent staining of tissue biopsies
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

15. What is colostrum?
Axillary
IL 15; IL 12 - interferon Beta and interferon alpha
Lymphocytes
The igA found in breast milk

16. Which disease is associated withB B27?
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
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
Severe pyogenic infections early in life
Celiac

17. What are the sinusoids of the spleen? What is the difference between a spleen and a lymph node?
IgM and IgA
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
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
MHC class molecules bind to KIRS or CD94 to prevent killing

18. what prevents NK cells from killing normal cells if their default is to kill?
Coarse Faces - cold (noninflamed d/t inability to attract neutrophils) staph abscesses - retained primary teeth - high igE - dermatologic problems (eczema)
MHC class molecules bind to KIRS or CD94 to prevent killing
A j chain
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

19. What are the cell surface proteins on NK cells?
MHC I - CD16 - CD56
MS
Celiac
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization

20. is IgM an opsonizer?
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
Negative!
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
MHC I; from RER with help of the B2 microglobulin

21. after C3 spontaneously hydrolyzes to C3b and C3a - what happens to C3a?
DM type I
IgG
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Anti viral and anti tumor

22. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
except hyperacute
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Its main effect is a defect in Ab opsonization for killing
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

23. which antibodies prevent antigens from binding mucosal surfaces?
Kill them because they have CD16 on them that recognize the FcG portion
IgA
Negative nitroblue tetrazolium reduction test
T cell precursor

24. Name three things that IL 1 does as a cytokine. other than the liver - who secretes IL 1
IL 4
Activates Macrophages and Th1 cells; suppresses Th2 cells; antiviral and antitumor
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
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages

25. Name 5 ways Antibody diversity is generated?
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
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
CROSS LINK Beta region on TCR of CD4 cells to the MHC class II on APCs this results in uncoordinated release of Interferon gamma from CD4 Th1 cells and subsequent release of IL1 - IL6 and TNF alpha from Macrophages --> toxic shock syndrome; s. pyogen
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.

26. To what disease do the autoantibodies to IgG (rheumatoid factor)?
Paracortex; viral infection
Rheumatic arthritis
DM type I
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells

27. What is the two fates of the RBCs that go through the spleen? what happens eventually to all of them>
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
Th2; Th1
CD21 on B cells (although there is T cell lymphocytosis in EBV)
DM type I

28. What is the result of an IL 12 deficiency? What is the presentation? What are the labs?
A recomb cytokine of IL 2; RCC and metastatic melanoma
Acts as second signal on B cells to induce class switching to IgA; also stimulates eosinophils
Inferior mesenteric
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

29. Complements are...
acute phase reactants
lowest concentration
Humoral
IgM and IgD

30. What are the main symptoms of T cell immunodeficiencies?
Influenza; antigenic shift; antigenic drift
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Intracellular pathogens (acute and chronic viruses and virally induced cancers)
Local infection/inflammation; infection of the ln itself; metastasis

31. 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)?
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
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
Anti mitochondrial

32. IgE has the ___________ in the serum
Bind FcG for antibody dependent cellular cytotoxicity
lowest concentration
S. aureus - E. Coli - aspergillus
Active; passive - fast but short half life (3 weeks!)

33. What are the two signals required for Th1 cells? what happens after then activated?
NK cells
IgA
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
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

34. Which is the main antibody in the delayed or secondary response to an antigen?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Basophils! THey want IG E class switch!
Recom IL 11; thrombocytopenia
IgG

35. 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
MS
IL 4 - 5 - 10 - 6
lowest concentration

36. What do multimeric antibodies require for assembly?
Anti TSh receptor
Anemias (esp due to renal failure)
DM type I and RA
A j chain

37. what ensure that a memory response is generated?
Not thymus - BM
If there is class switching and plasma cell production (that is when memory cells are produced)
Lymphocytes
except hyperacute

38. 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
T cells react to the angtigen and activate leukocyted (macrophage acitivation)
Negative selection
IL 1 and IL 6

39. What bugs can actually infect the lymph node itself?
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Previous transfusion; pregnant woman whose fetus had paternal antigens
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

40. What are the two signals to kill for NK cells?
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
Rheumatic arthritis
DM type I and RA
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)

41. What is a factor that is a predictor for a bad transplantation?
Patient has had previous exposure to blood products which result in presence of preformed anti HLA cytotoxic Abs
Internal iliac
Celiac
Cross link

42. what happens in a deficiency of C1 esterase inhibitor? DAF?
Negative!
Hereditary angioedema; PNH
Antimicrosomal and antithyroglobulin
Kill them because they have CD16 on them that recognize the FcG portion

43. what bacteria are a splenectomy patient most susceptible to? why?
Pernicious Anemia and Hashimotos
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
IgG
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

44. What is chronic mucocutaneous candidiasis d/t?
Periarteriolar lymphatic sheath in the white pulp that surround that dead end of the capillaries in the red pulp - contain T cells
Pernicious Anemia and Hashimotos
lowest concentration
T cell dysfunction

45. describe the classic complement pathway.
T
MS - hay fever - SLE - goodpastures
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Anti glutamate carboxylase and anti insulin

46. other than mediating shock - what else does TNF alpha do? who releases it mainly?
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
IL 4
Activates Th1 helper cells; Macrophages
Axillary

47. What happens in a deficiency of C3?
Its involved in inflammation and results in anaphylaxis and neutrophil chemotaxis.
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Antimicrosomal and antithyroglobulin
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE

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

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49. What is the main function of IL 8?
A chemotactic factor for neutrophils
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
Negative selection
mesenchymal

50. The alternative pathway is the only constutively...
Antiviral for uninfected cells (for future protection) and kills virally infected cells (NK activation)
CD40 (on b cell) CD40 ligand on Th2 cell; and interleukins (4 -5 -6) from Th2 cell; CD40 is actually the second signal
active complement pathway
IgAs in mothers breast milk!