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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 pathology seen in chronic transplant rejection?
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
TGF beta and IL 10
Barrel hoop basement membrane fenestrations
DM type I

2. What lymph node drains the upper limb?
Severe recurrent pyogenic sinus and resp tract And increased susceptibility to type III hypersensitivity like SLE
Axillary
In the germinal center of secondary follicles (In the paler center)
pale central germinal centers

3. Which antibody mediates immunity to worms? how?
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
Increases expression of MHC I and MHC II and also activates NK cells
Lymphocytes
IgE; by activating eosinophils

4. what characterizes an arthus reaction?
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Type III hypersensitivity where an internal antigen antibody complexes activate classical complement pathway resulting in C3a neutrophilic chemotaxis and neutrophilic lysosomal death. SLE
Edema and necrosis in that region
Para aortic

5. What are the autoantibodies for scleroderma (CREST)? scleroderma diffuse?
Axillary
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
Influenza; antigenic shift; antigenic drift
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)

6. The two heavy chains of an antibody contribute to the...
IgM and IgA
Activate macrophages
Histamine; post capillary venules - vasodilation
Fab portion

7. Which are the only two antiinflammatory cytokines?
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
TGF beta and IL 10
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
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7

8. are Th cells involved in trapping of antigens of endotoxin/LPS?
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
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
The antibodies (igM or IgG) either neutralize the target directly (cytoxic!) or recruit leukocytes (Neutrophils and Macrophages!) to incite tissue damage
No because no peptide fragment!

9. What are howell jolly bodies?
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
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
Fever - urticaria - arthralgias - proteinuria - lymphadenopathy
Recomb cytokine of GCSF (granulocyte macrophage colony stimulating factor; for recovery of bone marrow

10. Which disease is associated with DR7?
Lymphocytes
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
Steroid responsive nephrotic syndrome
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

11. What do multimeric antibodies require for assembly?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
Rheumatic arthritis
Adaptive uses classic pathway to kill; innate uses alternative pathway to kill
A j chain

12. Name 5 ways Antibody diversity is generated?
No because no peptide fragment!
cannot cross placenta
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
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

13. What can cause a lymph node enlargement?
Popliteal
Th cells fail to produce interferon gamma; a lot of IgE
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Local infection/inflammation; infection of the ln itself; metastasis

14. Which cytokines do Th2 release and For what?
Normal pro B (CD 19 +) - no mature B cells results in decreased total B cell level - and decreased amount of immunoglobulins in each class
Superior mesenteric
Anti topoisomerase
IL 4 -5 -6 for B cell class switching - IL 10 to inhibit TH1

15. 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?
CD56
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
Leukocyte adhesion defect; ataxia telangietasia; ataxia telangiectasia; chediak higashi syndrome; IgA def; Digeorge syndrome; Jobs; Chediak Higashi

16. What lymph node drains the duodenum - jejunum?
Delayed type hypersensitivity
An anaphylactic immediate reaction; atopy refers to the inherited propensity to develop asthmatic or allergic reactions
Superior mesenteric
All MHC 1/CD8

17. What are the two signals required for Th1 cells? what happens after then activated?
Bind FcG for antibody dependent cellular cytotoxicity
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Fibrosis of blood vessels and graft tissue from ischemia; obliterative vascular fibrosis with intimal thickening
MHC II/CD4 and B7 (on APC) and CD28 (on Th cell); releases cytokines to kill those extracellular buggers!

18. What happens in a secondary follicle?
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!
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Internal iliac
Rheumatic arthritis

19. with failed maturation of B cells in Brutons agammaglobulinemia - What is its effect on immune pathways and why?
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
Its main effect is a defect in Ab opsonization for killing
A j chain
A chemotactic factor for neutrophils

20. Describe the Mannose Lectin pathway
IgM and IgG
IgA
IgM and IgA
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

21. __________ are a part of the innate system.
NK cells
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
lowest concentration
Suppresses immune response (also specifically Th1 cells) and activates Th2; regulatory T cells

22. What are the two signals required for T cells? what happens after?
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
MS - hay fever - SLE - goodpastures

23. What part of the lymph node specifically expands during a cellular immune response? when would this occur?
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
Complement activation (active in both)
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Paracortex; viral infection

24. What does Interferon alpha and beta do? how?
Antimicrosomal and antithyroglobulin
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells
Antimicrobial also secreted by CD8 and NK cells that induces apoptsosis
Delayed type hypersensitivity

25. What is the mode of inheritance of Chediak Higashi syndrome? What is the disease d/t? What does it result in? What is the presentation?
Steroid responsive nephrotic syndrome
AR; defect in MT function results in decreased transport and phagocytosis; recurrent pyogenic infections by staphylococci and streptococci - partial albinism - and peripheral neuropathy
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
C3b; coating of a pathogen with molecules that promotes phagocytosis; IgG and CRP

26. What are MHC's necessary for? By themselves?
T cell activation; no with CD 4 or CD 8
If there is class switching and plasma cell production (that is when memory cells are produced)
...
CGD; Jobs syndrome (defect in Neutrophil chemotactic response)

27. What are the autoantibodies for Celiac disease?
Antigliadin - antiendomysial (both are IgAs - anti tissue transgluataminase igA)
Induces fever - chemokine secretion to recruit - activates adhesion molecules; macrophages
Influenza; antigenic shift; antigenic drift
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

28. which of the hypersensitivity reactions is not Ab mediated?
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E
C5a
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
Type IV

29. which antibody is involved in the primary response or immediate response to an antigen?
Lack of response from lymphocytes when activated; because they are self reactive - this is a form of tolerance
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
By transcytosis
IgM

30. What is the defect in Brutons agammaglobulinemia? What is its effect on B cells? What is its inheritance pattern?
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)
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

31. How does the alternative pathway lead to MAC activation?
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Receiving preformed Antibodies
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
An alpha and beta chain; only on APCs; TCR and CD4; extracellular (phagocytosed by APCs)

32. What are the autoantibodies for systemic sclerosis?
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Anti topoisomerase
Kill them because they have CD16 on them that recognize the FcG portion
T cell precursor

33. In order to produce Antibodies - does the antigen have to be phagocytosed? give an example with a bug and an autoimmune (type II hypersensitivity for example).
Cytokine IL 10 secreted by Th2
A recomb cytokine of IL 2; RCC and metastatic melanoma
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!
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 :(

34. What are the autoantibodies for drug induced lupus?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
Antihistone
MHC class molecules bind to KIRS or CD94 to prevent killing
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

35. What is the pathogenesis of a hypersensitivity reaction?
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
Fc
Receiving preformed Antibodies
Cytokine IL 10 secreted by Th2

36. The secondary follicles have __________; primary follicles are dense
Humoral
pale central germinal centers
MS
Viral neutralization of igM and IgG!

37. what mediates the type II hypersensitivity? What are the two different methods?
IL 15; IL 12 - interferon Beta and interferon alpha
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
Antibody mediated cytotoxicity; either complement dependent or complement independent
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)

38. What is epo used for?
Histamine; post capillary venules - vasodilation
Anemias (esp due to renal failure)
Hereditary angioedema; PNH
Defect in CD40L results in inability to class switch; a lot of IgM and no IgG - A - E

39. which type of immunity is slow but long lasting? as opposed to...
Interferon gamma; Th1
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
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!
Active; passive - fast but short half life (3 weeks!)

40. What is passive immunity?
Receiving preformed Antibodies
Superficial inguinal
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
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

41. What is chronic mucocutaneous candidiasis d/t?
IgAs in mothers breast milk!
DM type I
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
T cell dysfunction

42. other than mediating shock - what else does TNF alpha do? who releases it mainly?
Acts as second signal on B cells to induce class switching to IgE and IgG
Tumor cells and virally infected cells; perforin pore to secrete granzymes through it; apoptosis
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
Activates Th1 helper cells; Macrophages

43. Which type of selection of thymic development provides central tolerance?
Daclizumab; prevent ACUTE rejection of renal transplant
Secretory component
Negative selection
Scratch test - histamine mediated wheal; radioimmunosorbent assay (detects specific IgEs in serum)

44. What does IgE do on the surface of the mast cell to induce inflammatory mediator release?
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!
The patient could become cyanotic in the OR!
RNA segment reassortment
Cross link

45. Which disease is associated withB B27?
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
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
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Steroid responsive nephrotic syndrome

46. How is the antigen loaded onto a MHC II?
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
Basophils! THey want IG E class switch!
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA
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

47. All transplant rejections - _____________ are mediated by Type IV hypersensitivity
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Stimulate the liver to release acute phase reactants
Cytokine release syndrome due to initial release from initial binding (fever etc) and hypersensitivity reaction
except hyperacute

48. What are the autoantibodies for myasthenia gravis?
Anti Ach receptor
RNA segment reassortment
T cell activation; no with CD 4 or CD 8
heavy chains

49. Often bacteria are associated with being killed by humoral immunity. Name some bugs that require cell mediated immunity because they evade humoral response
Legionella - N. gonorrhea - L. monocytogenes - viruses - protozoa (leismaniasis)
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
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
Th1; interferon gamma; IL 2 for cytotoxic T cell activation

50. What is the pathogenesis of a candida skin test?
Anti Ach receptor
Delayed type hypersensitivity
Surrounds the red pulp and begins with PALS and then turns into follicles with B cells/follicles
opsonizes