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USMLE Step 1 Immunology

Subjects : health-sciences, usmle-step-1

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Answer 50 questions in 15 minutes.
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Match each statement with the correct term.
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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. where do somatic hypermutation and class switching occur?
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
In the germinal center of secondary follicles (In the paler center)
Histamine; post capillary venules - vasodilation
Sinusitis - otitis media - pneumonia

2. Which is the most abundant antibody in blood?
active complement pathway
Influenza; antigenic shift; antigenic drift
IgG
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

3. What is the pathogenesis of chronic transplant rejection? When does it occur? is it reversible?
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
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 :(
Wiskott Aldrich syndrome
Decreased Th1 response; disseminated mycobacterial infections; decreased interferon gamma

4. Name the three opsonins
Popliteal
CRP - C3b - IgM
Fab portion
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak

5. What type of fenestrations are found in the red pulp of the spleen?
pentamer
Anti alpha subunit 3 of collagen on type IV bm
Since cant cross placenta most likely means that child was forced early to produce due to an infection (most likely CMV)
Barrel hoop basement membrane fenestrations

6. What is the pathogenesis of IgG AIHA ABO hemolytic disease of a newborn? describe what happens.
pale central germinal centers
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
Inferior mesenteric
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

7. What is the main function of IL 12? other than macrophages who else can release IL 12?
Induce differentiation of T cells into Th1 helper cells and activates NK cells also; B cells
IL 4 - 5 - 10 - 6
P - ANCA (antimyeloperoxidase); in neutrophil; p= perinuclear
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

8. In general What are T cells good for?
...
Th2; Th1
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
Anti viral and anti tumor

9. T/F B cells do not require a second signal
False! B cell class switching requires a second signal
Lymphocytes
Sinusitis - otitis media - pneumonia
Interferon gamma; Th1

10. describe the classic complement pathway.
Negative nitroblue tetrazolium reduction test
neutrophilia!
IgG and IgM bind to pathogens activating C1 convertase and leads to C2 and C4 and then C3 convertase activated
Macrophages - Dendritic cells - B cells

11. What are C1 - C2 - C3 - C4 important for?
B - T - and NK cells
Daclizumab; prevent ACUTE rejection of renal transplant
Viral neutralization of igM and IgG!
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

12. What is the thymus ? Where is it located? is it encapsulated? How many lobes does it have?
Cross link antigens which increases their phagocytability; activate complement for MAC attack; opsonization; neutralization
The place of T cell diff and maturation; ant mediastinum above heart; yes; 2
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Trypanosomes with programmed rearrangement (results in recurring fever -- sleeping sickness!)

13. What is chronic mucocutaneous candidiasis d/t?
pentamer
Type IV
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
T cell dysfunction

14. Type IV hypersensitivity is i...
not Ab mediated
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
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

15. Which disease is associated with B8?
MS
Recurrent sinopulmonary bacterial infections after 6 months (d/t mothers igGs transplacental) due to opsonization defect
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
Graves

16. What happens in a secondary follicle?
Graves
T cell activation; no with CD 4 or CD 8
Isotype switching (activated by Th2 cell signals and cytokines) - somatic hypermutation
The patient could become cyanotic in the OR!

17. 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
Mediates septic shock; activates the endothelium for adhesion and dilation and leukocyte recruitment results in vascular leak
Tetanus - Botulinum - HBV - Rabies
MHC II - B7

18. where do NK cells develop?
Not thymus - BM
Lack of MHC class I constant region which it binds or a nonspecific activation signal (TLR)
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
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)

19. what cytokine does basophils secrete?
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Th cells fail to produce interferon gamma; a lot of IgE
IL 4
IgM and IgG

20. what happens in a deficiency of C1 esterase inhibitor? DAF?
Sinusitis - otitis media - pneumonia
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
Hereditary angioedema; PNH

21. What is the arthus reaction? What is the difference between arthus and serum sickness? give an example. How do you test for it?
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
Nuclear remnants that are usually taken out of RBC before complete maturation by Macrophages
active complement pathway
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )

22. which antibodies prevent antigens from binding mucosal surfaces?
Cyclosporine - OKT3
IgA
Ig - CD19 - CD20 - CD21 - CD40 - MHC II - B7
Defect in BTK a tyrosine kinase gene; failed maturation of B cells; X linked recessive

23. What is the main function of IL 8?
By transcytosis
Receiving preformed Antibodies
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
A chemotactic factor for neutrophils

24. which antibodies can bind complement?
Anti TSh receptor
IgM and IgG
IL 15; IL 12 - interferon Beta and interferon alpha
IgM and IgD

25. what happens in a deficiency of C5- C8? why dont you get recurrent pyogenic infections like in C3 def?
Interferon gamma; Th1
Septicemia with neisseria; because at least you have C3 to act like a neutrophilic chemotactic and an acute phase reactant
IgA
encapsulated

26. What is the pathology of acute transplant rejection? is it reversible?
Mycobacterium Tuberculosis - Mycobacterium Avium Intracellulare; Toxoplasmosis Gondii
Vasculitis of graft vessels with dense interstitial lymphocytic infiltrate; yes! with immunosuppressants
Antibody mediated cytotoxicity; either complement dependent or complement independent
Make antibody - allergy type 1 (igE) - Cytotoxic and immunecomplex hypersensitivity type II and III (igG); hyperacute organ rejection is Ab mediated

27. What lymph node drains the duodenum - jejunum?
Anticentromere; anti Scl -70 (anti DNA topoisomerase I)
Superior mesenteric
Receiving preformed Antibodies
Recom IL 11; thrombocytopenia

28. What is the presentation of common variable immunodef? and What are the labs?
Since it is a comp dependent type II hypersensitivity reaction; C3a brings anaphylotoxins that bring in mediators of shock
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
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
mesenchymal

29. What is recomb gamma interferon used for?
Chronic granulomatous disease
DM type I and RA
Graves
...

30. Which antibodies can be multimeric?
IgM and IgA
Hyperacute; presence of preformed antibodies in the recipient ( to blood groups or HLA )
Anti alpha subunit 3 of collagen on type IV bm
Superficial inguinal

31. What is the clinical use for sirolimus? what should you combine it with?
Inferior mesenteric
Graves
Psoriasis - Ankylosis Spondylitis - IBD - Reiters; all seronegative spondylopathies
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids

32. what ensure that a memory response is generated?
If there is class switching and plasma cell production (that is when memory cells are produced)
Opsonization (Brutons agammaglobulinemia) - adhesion (Leukocyte adhesion defect) - phagocytosis (chediak higashi syndrome) - respiratory burst (chronic granulomatous disease)
MS
Superficial inguinal

33. How does the alternative pathway lead to MAC activation?
No because no peptide fragment!
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
Bind FcG for antibody dependent cellular cytotoxicity
MHC I - CD16 - CD56

34. The pathogenesis of contact dermatitis is ________ hypersensitivity
Immunosuppression after kidney transplantation in combination with cyclosporine and corticosteroids
type four
Receiving preformed Antibodies
Antiviral by inducing ribonuclease which degrades only viral mRNA (prevents protein synthesis) and activates NK cells to kill virus infected cells

35. What is recomb alpha interferon used for?
HBV - HBC - Kaposis - leukemias - malignant melanoma - hairy cell leukemia and condyluma accuminata
B - T - and NK cells
except hyperacute
MS - hay fever - SLE - goodpastures

36. What are the T cell functions?
Anemias (esp due to renal failure)
Activate B cells - activate Macrophages - kill viruses directly - delayed cell mediated hypersensitivity - acute and chronic rejection
No because no peptide fragment!
Sinusitis - otitis media - pneumonia

37. The two heavy chains of an antibody contribute to the...
MHC II - B7 - CD40 and CD14; CD40 and D14 for FcG and C3b resp
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
Fab portion
IL 3; supports growth and differentiation of bone marrow stem cells

38. Monomer in circulation - ___ when secreted
dimer
Fab portion
Bind FcG for antibody dependent cellular cytotoxicity
IgAs in mothers breast milk!

39. what characterizes an arthus reaction?
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
IL 15; IL 12 - interferon Beta and interferon alpha
Edema and necrosis in that region
IgA; sinus and lung infections from lack of secretory defense - milk allergies and diarrhea from giardiasis; Anaphylasix on exposure to blood products with igA

40. What are the two signals required for T cells? what happens after?
except hyperacute
Proteins; IgG - IgM - endotoxin (microbial surfaces in general - nonspecific ones also) - mannose binding Lectin; classic - alternative - MB pathway (resp)
MHC I/CD8 and IL2/IL 2 Receptor (IL 2 is from Th1!); cytoxicity!
pentamer

41. How is sirolimus different from tacrolimus?
MAC (membrane attack complex) Which is activated by C5b - C9 and results in lysis and cytoxicity by creating pores in the target membrane; encapsulated organisms (S. pnuemonia - H.influenzae - B perfussis for example) and other organisms with non pep
Carbohydrate
Both decrease cd8 tcell prolif but one through mtor and the other through calcineurin (resp)
Delayed type hypersensitivity

42. which antibody activate mast cells - basophils - and eosinophils?
TCR - CD4/8 - CD28 (binds B7) - CD3 (for intracellular transduction) - CD40L
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
IgE
Recurrent infections to every type of antigen; bone marrow transplant (be weary of GVH disease!)

43. What are the mediators that mast cells release?
except hyperacute
Cross link
Histamine (causes vasodilation) - leukotrienes (causes bronchoconstriction) - chemotaxins for eos - and heparin (increased blood flow needs to be anticoagulated!)
CD21 on B cells (although there is T cell lymphocytosis in EBV)

44. What kinds of receptors activate innate immunity?
Antibody mediated cytotoxicity; either complement dependent or complement independent
Ischemia and necrosis of graft due to occlusion of vessels and fibrinoid necrosis and thrombosis within the vessels
IgM and IgD
TLR ad nuclear receptors

45. where are complements produced?
Complement activation (active in both)
CD21 on B cells (although there is T cell lymphocytosis in EBV)
Liver! (they are proteins circulating in the blood)
IgG

46. which of the IL2 inhibitors produce nephrotoxicity? thrombocytopenia/leukopenia?
IgE; by activating eosinophils
MHC II - B7
Cyclosporine and tacrolimus; sirolimus (as well as hyperlipidemia)
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith

47. What does granzyme do? who secretes it?
type four
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!
Its a serine protease that activates apoptosis; NK and CD8
Interferon gamma and IL 2

48. Which diseases are associated with DR2?
Anti nuclear Antibodies (ANA); Anti dsDNA - anti Smith
Cell mediated due to T cell cytotoxicity reacting to foreign MHCs; few weeks after
MS - hay fever - SLE - goodpastures
DAF and C1 esterase inhibitor on cells prevent complement activation on their surfaces (microbial surfaces lack this)

49. The alternative pathway is the only constutively...
Complement activation (active in both)
Anti topoisomerase
MHC II - B7
active complement pathway

50. What does IL 4 do?
Adenosine deaminase deficiency (AR) - defective IL 2 receptor (X linked) - and failure to synthesize MHC II; both humoral and cell mediated deficiency
Acts as second signal on B cells to induce class switching to IgE and IgG
Cytokine IL 10 secreted by Th2
Edema and necrosis in that region

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USMLE Step 1 Immunology

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